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| {{Infobox_Disease |
| | #redirect:[[ST elevation myocardial infarction]] |
| Name = Myocardial infarction|
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| Image = AMI scheme.png |
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| Caption = Diagram of a '''myocardial infarction''' (2) of the tip of the [[Sternocostal surface|anterior wall of the heart]] (an ''apical infarct'') after occlusion (1) of a branch of the [[left coronary artery]] (LCA, [[right coronary artery]] = RCA).|
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| DiseasesDB = 8664 |
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| ICD10 = {{ICD10|I|21||i|20}}-{{ICD10|I|22||i|20}} |
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| ICD9 = {{ICD9|410}} |
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| ICDO = |
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| OMIM = |
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| MedlinePlus = 000195 |
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| eMedicineSubj = med |
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| eMedicineTopic = 1567 |
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| eMedicine_mult = {{eMedicine2|emerg|327}} {{eMedicine2|ped|2520}} |
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| MeshID = D009203 |
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| }}
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| {{SI}}
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| {{CMG}}
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| {{EH}}
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| See the page on [[ST elevation myocardial infarction]] and [[non ST elevation myocardial infarction]]
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| ==Overview==
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| A '''heart attack''', known in [[medicine]] as an ('''acute''') '''myocardial infarction''' ('''AMI''' or '''MI'''), occurs when the [[Blood flow|blood supply]] to part of the [[heart]] is interrupted. This is most commonly due to occlusion (blockage) of a [[coronary artery]] following the rupture of a [[Vulnerable plaque|vulnerable atherosclerotic plaque]], which is an unstable collection of [[lipids]] (like [[cholesterol]]) and [[white blood cell]]s (especially [[macrophage]]s) in the wall of an [[artery]]. The resulting [[ischemia]] (restriction in blood supply) and [[Hypoxia (medical)|oxygen shortage]], if left untreated for a sufficient period, can cause damage and/or death (''[[infarction]]'') of heart muscle tissue (''[[myocardium]]'').
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| Classical symptoms of acute myocardial infarction include sudden [[chest pain]] (typically radiating to the left arm or left side of the neck), [[dyspnea|shortness of breath]], [[nausea]], [[vomiting]], [[palpitation]]s, [[sweating]], and [[anxiety]] (often described as a sense of impending doom). Women may experience less typical symptoms than men, most commonly shortness of breath, weakness, a feeling of indigestion, and [[fatigue (physical)|fatigue]].<ref name="Kosuge">{{cite journal | last=Kosuge | first=M | coauthors= Kimura K, Ishikawa T et al. | title=Differences between men and women in terms of clinical features of ST-segment elevation acute myocardial infarction | journal=Circulation Journal | volume=70 | issue=3 | pages=222–226 | date=March 2006 | pmid=16501283 | url=http://www.jstage.jst.go.jp/article/circj/70/3/222/_pdf | accessdate=2008-05-31 | doi=10.1253/circj.70.222 }}</ref> Approximately one quarter of all myocardial infarctions are silent, without chest pain or other symptoms. A heart attack is a [[medical emergency]], and people experiencing chest pain are advised to alert their [[emergency medical services]], because prompt treatment is beneficial.
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| Heart attacks are the leading cause of death for both men and women all over the world.<ref name="WHO-2002">{{cite book | authorlink=http://www.who.int/en/ | title=The World Health Report 2004 - Changing History | publisher=[[World Health Organization]] | date=2004 | pages=120-4 | format=PDF | url=http://www.who.int/entity/whr/2004/en/report04_en.pdf | id= ISBN 92-4-156265-X}}</ref> Important [[risk factor]]s are previous [[cardiovascular disease]] (such as [[Angina pectoris|angina]], a previous heart attack or [[stroke]]), older age (especially men over 40 and women over 50), [[tobacco smoking]], high blood levels of certain lipids ([[triglyceride]]s, [[low-density lipoprotein]] or "bad cholesterol") and low [[high density lipoprotein]] (HDL, "good cholesterol"), [[Diabetes mellitus|diabetes]], [[Hypertension|high blood pressure]], [[obesity]], [[chronic kidney disease]], [[heart failure]], [[Alcohol and cardiovascular disease|excessive alcohol consumption]], the abuse of certain drugs (such as [[cocaine]]), and chronic high stress levels.<ref name="pmid18241872">{{cite journal |author=Bax L, Algra A, Mali WP, Edlinger M, Beutler JJ, van der Graaf Y |title=Renal function as a risk indicator for cardiovascular events in 3216 patients with manifest arterial disease |journal=Atherosclerosis |volume= |issue= |pages= |year=2008 |pmid=18241872 |doi=10.1016/j.atherosclerosis.2007.12.006 |url=http://linkinghub.elsevier.com/retrieve/pii/S0021-9150(07)00768-X}}</ref><ref name="pmid16651468">{{cite journal |author=Pearte CA, Furberg CD, O'Meara ES, ''et al'' |title=Characteristics and baseline clinical predictors of future fatal versus nonfatal coronary heart disease events in older adults: the Cardiovascular Health Study |journal=Circulation |volume=113 |issue=18 |pages=2177–85 |year=2006 |pmid=16651468 |doi=10.1161/CIRCULATIONAHA.105.610352 |url=http://circ.ahajournals.org/cgi/content/full/113/18/2177}}</ref>
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| Immediate treatment for suspected acute myocardial infarction includes [[oxygen therapy|oxygen]], [[aspirin]], and sublingual [[Glyceryl trinitrate (pharmacology)|glyceryl trinitrate]] (colloquially referred to as [[nitroglycerin]] and abbreviated as NTG or GTN). [[Analgesia|Pain relief]] is also often given, classically [[morphine sulfate]].<ref>{{cite journal |author=Erhardt L, Herlitz J, Bossaert L, ''et al'' |title=Task force on the management of chest pain |journal=Eur. Heart J. |volume=23 |issue=15 |pages=1153–76 |year=2002 |pmid=12206127 |doi=10.1053/euhj.2002.3194| url=http://eurheartj.oxfordjournals.org/cgi/reprint/23/15/1153|format=PDF}}</ref>
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| The patient will receive a number of diagnostic tests, such as an [[electrocardiogram]] (ECG, EKG), a chest [[X-ray]] and [[blood test]]s to detect elevations in [[cardiac markers]] (blood tests to detect heart muscle damage). The most often used markers are the [[creatine kinase]]-MB (CK-MB) fraction and the [[troponin]] I (TnI) or [[troponin]] T (TnT) levels. On the basis of the ECG, a distinction is made between '''ST elevation MI''' (STEMI) or '''non-ST elevation MI''' (NSTEMI). Most cases of STEMI are treated with [[thrombolysis]] or if possible with [[percutaneous coronary intervention]] (PCI, angioplasty and stent insertion), provided the hospital has facilities for [[coronary angiography]]. NSTEMI is managed with medication, although PCI is often performed during hospital admission. In patients who have multiple blockages and who are relatively stable, or in a few extraordinary emergency cases, [[Coronary artery bypass surgery|bypass surgery]] of the blocked coronary artery is an option.
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| The phrase "heart attack" is sometimes used incorrectly to describe [[sudden cardiac death]], which may or may not be the result of acute myocardial infarction. A heart attack is different from, but can be the cause of [[cardiac arrest]], which is the stopping of the heartbeat, and [[cardiac arrhythmia]], an abnormal heartbeat. It is also distinct from [[heart failure]], in which the pumping action of the heart is impaired; severe myocardial infarction may lead to heart failure, but not necessarily.
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| ==Epidemiology==
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| Myocardial infarction is a common presentation of [[ischemic heart disease]]. The WHO estimated that in 2002, 12.6 percent of deaths worldwide were from ischemic heart disease.<ref name=WHO-2002/> Ischemic heart disease is the leading cause of death in developed countries, but third to [[AIDS]] and [[lower respiratory infection]]s in developing countries.<ref name="UCatlas">{{cite web | title=Cause of Death - UC Atlas of Global Inequality | publisher=Center for Global, International and Regional Studies (CGIRS) at the University of California Santa Cruz | url=http://ucatlas.ucsc.edu/cause.php | accessmonthday=December 7 | accessyear=2006}}</ref>
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| In the United States, [[Heart disease|diseases of the heart]] are the [[List of causes of death by rate|leading cause of death]], causing a higher [[death|mortality]] than [[cancer]] ([[malignant]] [[Neoplasia|neoplasms]]).<ref name="causesofdeath">{{cite web | title=Deaths and percentage of total death for the 10 leading causes of death: United States, 2002-2003 | publisher=National Center of Health Statistics | format=[[PDF]] | url=http://www.cdc.gov/nchs/data/hestat/leadingdeaths03_tables.pdf | accessmonthday=April 17 | accessyear=2007}}</ref> [[Coronary heart disease]] is responsible for 1 in 5 deaths in the U.S.. Some 7,200,000 men and 6,000,000 women are living with some form of coronary heart disease. 1,200,000 people suffer a (new or recurrent) coronary attack every year, and about 40% of them die as a result of the attack.<ref name="AHAstats">{{cite web | title=Heart Attack and Angina Statistics | publisher=[[American Heart Association]] | date=2003 | url=http://www.americanheart.org/presenter.jhtml?identifier=4591 | accessmonthday=December 7 | accessyear=2006}}</ref> This means that roughly every 65 seconds, an American dies of a coronary event.
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| In India, cardiovascular disease (CVD) is the leading cause of death.<ref name="mukhPred">{{cite journal | author=Mukherjee AK. | title=Prediction of coronary heart disease using risk factor categories. | journal= J Indian Med Assoc | year=1995 | pmid=8713248}}</ref> The deaths due to CVD in India were 32% of all deaths in 2007 and are expected to rise from 1.17 million in 1990 and 1.59 million in 2000 to 2.03 million in 2010.<ref name="ghafBurd">{{cite journal | author=Ghaffar A, Reddy KS and Singhi M | title=Burden of non-communicable diseases in South Asia. | journal= BMJ | year=2004 | volume=328 | pages=807–810 | format=[[PDF]] | url=http://www.bmj.com/cgi/reprint/328/7443/807.pdf | doi=10.1136/bmj.328.7443.807 | pmid=15070638}}</ref> Although a relatively new epidemic in India, it has quickly become a major health issue with deaths due to CVD expected to double during 1985-2015.<ref name="rastPhys">{{cite journal | author=Rastogi T, Vaz M, Spiegelman D, Reddy KS, Bharathi AV, Stampfer MJ, Willett WC and Ascherio1 A | title=Physical activity and risk of coronary heart disease in India. | journal=Int. J. Epidemiol | year=2004 | volume=33 | pages=1–9 | format=[[PDF]] | url=http://ije.oxfordjournals.org/cgi/reprint/33/4/759.pdf | doi = 10.1093/ije/dyh042 | pmid=15044412}}</ref><ref name="GuptEsca">{{cite journal | author=Gupta R. | title=Escalating Coronary Heart Disease and Risk Factors in South Asians. | journal=Indian Heart Journal | year=2007 | pages=214–17 | format=[[PDF]] | url=http://indianheartjournal.com/editorial007.pdf}}</ref> Mortality estimates due to CVD vary widely by state, ranging from 10% in Meghalaya to 49% in Punjab (percentage of all deaths). Punjab (49%), Goa (42%), Tamil Nadu (36%) and Andhra Pradesh (31%) have the highest CVD related mortality estimates.<ref name="guptCorr">{{cite journal | author=Gupta R, Misra A, Pais P, Rastogi P and Gupta VP. | title=Correlation of regional cardiovascular disease mortality in India with lifestyle and nutritional factors. | journal=International Journal of Cardiology | year=2006 | volume=108 | issue=3 | pages=291–300 | format=[[PDF]] | url=http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6T16-4GFV5CY-4-3&_cdi=4882&_user=209690&_orig=search&_coverDate=04%2F14%2F2006&_sk=998919996&view=c&wchp=dGLzVlz-zSkzV&md5=050edf99a813f475b985c8d590c86228&ie=/sdarticle.pdf | doi = 10.1016/j.ijcard.2005.05.044}}</ref> State-wise differences are correlated with prevalence of specific dietary risk factors in the states. Moderate physical exercise is associated with reduced incidence of CVD in India (those who exercise have less than half the risk of those who don't).<ref name="rastPhys">{{cite journal | author=Rastogi T, Vaz M, Spiegelman D, Reddy KS, Bharathi AV, Stampfer MJ, Willett WC and Ascherio1 A | title=Physical activity and risk of coronary heart disease in India. | journal=Int. J. Epidemiol | year=2004 | volume=33 | pages=1–9 | format=[[PDF]] | url=http://ije.oxfordjournals.org/cgi/reprint/33/4/759.pdf | doi = 10.1093/ije/dyh042 | pmid=15044412}}</ref> CVD also affects Indians at a younger age (in their 30s and 40s) than is typical in other countries.
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| ===Risk factors===
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| Risk factors for [[atherosclerosis]] are generally risk factors for myocardial infarction:
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| *[[Old age|Older age]]
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| *[[Male]] sex<ref name="Framingham1998">{{cite journal | author=Wilson PW, D'Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. | title=Prediction of coronary heart disease using risk factor categories. | journal=Circulation | year=1998 | volume=97 | issue=18 | pages=1837–47 | format=[[PDF]] | url=http://circ.ahajournals.org/cgi/reprint/97/18/1837.pdf | pmid=9603539}}</ref>
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| *[[Tobacco smoking]]
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| *[[Hypercholesterolemia]] (more accurately [[hyperlipoproteinemia]], especially high [[low density lipoprotein]] and low [[high density lipoprotein]])
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| *[[Hyperhomocysteinemia]] (high [[homocysteine]], a toxic blood [[amino acid]] that is elevated when intakes of [[vitamins]] B2, B6, B12 and [[folic acid]] are insufficient)
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| *[[Diabetes mellitus|Diabetes]] (with or without [[insulin resistance]])
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| *[[Hypertension|High blood pressure]]
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| *[[Obesity]]<ref name="Yusuf-2005">{{cite journal | author=Yusuf S, Hawken S, Ounpuu S, Bautista L, Franzosi MG, Commerford P, Lang CC, Rumboldt Z, Onen CL, Lisheng L, Tanomsup S, Wangai P Jr, Razak F, Sharma AM, Anand SS; INTERHEART Study Investigators. | title=Obesity and the risk of myocardial infarction in 27,000 participants from 52 countries: a case-control study. | journal=Lancet | year=2005 | volume=366 | issue=9497 | pages=1640–9 | pmid=16271645 | doi = 10.1016/S0140-6736(05)67663-5}}</ref> (defined by a [[body mass index]] of more than 30 kg/m², or alternatively by waist circumference or [[waist-hip ratio]]).
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| *[[Workplace stress|Stress]] Occupations with high stress index are known to have susceptibility for atherosclerosis.
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| Many of these risk factors are modifiable, so many heart attacks can be prevented by maintaining a healthier lifestyle. Physical activity, for example, is associated with a lower risk profile.<ref name="Jensen-1991">{{cite journal | author=Jensen G, Nyboe J, Appleyard M, Schnohr P. | title=Risk factors for acute myocardial infarction in Copenhagen, II: Smoking, alcohol intake, physical activity, obesity, oral contraception, diabetes, lipids, and blood pressure. | journal=Eur Heart J | year=1991 | volume=12 | issue=3 | pages=298–308 | pmid=2040311}}</ref> Non-modifiable risk factors include age, sex, and family history of an early heart attack (before the age of 60), which is thought of as reflecting a [[genetic predisposition]].<ref name="Framingham1998"/>
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| [[Socioeconomics|Socioeconomic]] factors such as a shorter [[education]] and lower income (particularly in women), and living with a partner may also contribute to the risk of MI.<ref name="Nyboe-1989">{{cite journal | author=Nyboe J, Jensen G, Appleyard M, Schnohr P. | title=Risk factors for acute myocardial infarction in Copenhagen. I: Hereditary, educational and socioeconomic factors. Copenhagen City Heart Study. | journal=Eur Heart J | year=1989 | volume=10 | issue=10 | pages=910–6 | pmid=2598948}}</ref> To understand epidemiological study results, it's important to note that many factors associated with MI mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and marital status.<ref name="Nyboe-1989"/>
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| Women who use [[combined oral contraceptive pill]]s have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking.<ref name="Khader-2003">{{cite journal | author=Khader YS, Rice J, John L, Abueita O. | title=Oral contraceptives use and the risk of myocardial infarction: a meta-analysis. | journal=Contraception | year=2003 | volume=68 | issue=1 | pages=11–7 | pmid=12878281 | doi = 10.1016/S0010-7824(03)00073-8}}</ref>
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| Inflammation is known to be an important step in the process of [[Atheroma|atherosclerotic plaque]] formation.<ref name="Wilson-2006">{{cite journal | author=Wilson AM, Ryan MC, Boyle AJ. | title=The novel role of C-reactive protein in cardiovascular disease: risk marker or pathogen. | journal=Int J Cardiol | year=2006 | volume=106 | issue=3 | pages=291–7 | pmid=16337036 | doi = 10.1016/j.ijcard.2005.01.068}}</ref> [[C-reactive protein]] (CRP) is a sensitive but non-specific [[Biomarker (medicine)|marker]] for [[inflammation]]. Elevated CRP blood levels, especially measured with high sensitivity assays, can predict the risk of MI, as well as [[stroke]] and development of diabetes.<ref name="Wilson-2006"/> Moreover, some drugs for MI might also reduce CRP levels.<ref name="Wilson-2006"/> The use of high sensitivity CRP assays as a means of [[Screening (medicine)|screening]] the general population is advised against, but it may be used optionally at the physician's discretion, in patients who already present with other risk factors or known [[coronary artery disease]].<ref name="Pearson-2003">{{cite journal | author=Pearson TA, Mensah GA, Alexander RW, Anderson JL, Cannon RO 3rd, Criqui M, Fadl YY, Fortmann SP, Hong Y, Myers GL, Rifai N, Smith SC Jr, Taubert K, Tracy RP, Vinicor F; Centers for Disease Control and Prevention; American Heart Association. | title=Markers of inflammation and cardiovascular disease: application to clinical and public health practice: A statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. | journal=Circulation | year=2003 | volume=107 | issue=3 | pages=499–511 | format=[[PDF]] | url=http://circ.ahajournals.org/cgi/reprint/107/3/499.pdf | pmid=12551878 | doi = 10.1161/01.CIR.0000052939.59093.45}}</ref> Whether CRP plays a direct role in atherosclerosis remains uncertain.<ref name="Wilson-2006"/>
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| Inflammation in [[Periodontium|periodontal]] disease may be linked coronary heart disease, and since [[periodontitis]] is very common, this could have great consequences for [[public health]].<ref name="Janket-2003">{{cite journal | author=Janket SJ, Baird AE, Chuang SK, Jones JA. | title=Meta-analysis of periodontal disease and risk of coronary heart disease and stroke. | journal=Oral Surg Oral Med Oral Pathol Oral Radiol Endod. | year=2003 | volume=95 | issue=5 | pages=559–69 | pmid=12738947 | doi=10.1038/sj.ebd.6400272}}</ref> [[Serology|Serological]] studies measuring [[antibody]] levels against typical periodontitis-causing [[bacteria]] found that such antibodies were more present in subjects with coronary heart disease.<ref name="Pihlstrom-2005">{{cite journal | author=Pihlstrom BL, Michalowicz BS, Johnson NW. | title=Periodontal diseases. | journal=Lancet | year=2005 | volume=366 | issue=9499 | pages=1809–20 | pmid=16298220 | doi = 10.1016/S0140-6736(05)67728-8}}</ref> Periodontitis tends to increase blood levels of CRP, [[fibrinogen]] and [[cytokines]];<ref name="Scannapieco-2003">{{cite journal | author=Scannapieco FA, Bush RB, Paju S. | title=Associations between periodontal disease and risk for atherosclerosis, cardiovascular disease, and stroke. A systematic review. | journal=Ann Periodontol | year=2003 | volume=8 | issue=1 | pages=38–53 | pmid=14971247 | doi = 10.1902/annals.2003.8.1.38}}</ref> thus, periodontitis may mediate its effect on MI risk via other risk factors.<ref name="D'Aiuto-2006">{{cite journal | author=D'Aiuto F, Parkar M, Nibali L, Suvan J, Lessem J, Tonetti MS. | title=Periodontal infections cause changes in traditional and novel cardiovascular risk factors: results from a randomized controlled clinical trial. | journal=Am Heart J | year=2006 | volume=151 | issue=5 | pages=977–84 | pmid=16644317 | doi=10.1016/j.ahj.2005.06.018}}</ref> [[Medical research|Preclinical research]] suggests that periodontal bacteria can promote aggregation of [[platelets]] and promote the formation of [[foam cell]]s.<ref name="Lourbakos-2001">{{cite journal | author=Lourbakos A, Yuan YP, Jenkins AL, Travis J, Andrade-Gordon P, Santulli R, Potempa J, Pike RN. | title=Activation of protease-activated receptors by gingipains from Porphyromonas gingivalis leads to platelet aggregation: a new trait in microbial pathogenicity. | journal=Blood | year=2001 | volume=97 | issue=12 | pages=3790–7 | format=[[PDF]] | url=http://bloodjournal.hematologylibrary.org/cgi/reprint/97/12/3790.pdf | pmid=11389018 | doi = 10.1182/blood.V97.12.3790}}</ref><ref name="Qi-2003">{{cite journal | author=Qi M, Miyakawa H, Kuramitsu HK. | title=Porphyromonas gingivalis induces murine macrophage foam cell formation. | journal=Microb Pathog | year=2003 | volume=35 | issue=6 | pages=259–67 | pmid=14580389 | doi = 10.1016/j.micpath.2003.07.002}}</ref> A role for specific periodontal bacteria has been suggested but remains to be established.<ref name="Spahr-2006">{{cite journal | author=Spahr A, Klein E, Khuseyinova N, Boeckh C, Muche R, Kunze M, Rothenbacher D, Pezeshki G, Hoffmeister A, Koenig W. | title=Periodontal infections and coronary heart disease: role of periodontal bacteria and importance of total pathogen burden in the Coronary Event and Periodontal Disease (CORODONT) study. | journal=Arch Intern Med | year=2006 | volume=166 | issue=5 | pages=554–9 | pmid=16534043 | doi = 10.1001/archinte.166.5.554}}</ref>
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| [[Calcium]] deposition is another part of atherosclerotic plaque formation. Calcium deposits in the coronary arteries can be detected with [[CT scan]]s. Several studies have shown that coronary calcium can provide predictive information beyond that of classical risk factors.<ref name="JAMAcalc">Greenland P, LaBree L, Azen SP, Doherty TM, Detrano RC. Coronary artery calcium score combined with Framingham score for risk prediction in asymptomatic individuals. ''JAMA''. 2004;291:210-215. PMID 14722147</ref><ref name="NEJMcalc">Detrano R, Guerci AD, Carr JJ, ''et al''. Coronary calcium as a predictor of coronary events in four racial or ethnic groups. ''N Engl J Med''. 2008;358(13):1336-45. PMID 18367736</ref><ref name="ACCcalc">Arad Y, Goodman K, Roth M, Newstein D, Guerci AD. Coronary calcification, coronary disease risk factors, C-reactive protein, and atherosclerotic cardiovascular disease events: the St. Francis Heart Study. ''J Am Coll Cardiol''. 2005;46:158-165. PMID 15992651</ref>
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| [[Baldness]], [[Grey hair|hair greying]], a diagonal [[Earlobe|earlobe crease]]<ref name="Lichstein-1974">{{cite journal | author=Lichstein E, Chadda KD, Naik D, Gupta PK. | title=Diagonal ear-lobe crease: prevalence and implications as a coronary risk factor. | journal=N Engl J Med | year=1974 | volume=290 | issue=11 | pages=615–6 | pmid=4812503}}</ref> and possibly other [[skin]] features are independent risk factors for MI. Their role remains controversial; a common denominator of these signs and the risk of MI is supposed, possibly genetic. <ref name="Miric-1998">{{cite journal | author=Miric D, Fabijanic D, Giunio L, Eterovic D, Culic V, Bozic I, Hozo I. | title=Dermatological indicators of coronary risk: a case-control study. | journal=Int J Cardiol | year=1998 | volume=67 | issue=3 | pages=251–5 | pmid=9894707 | doi=10.1016/S0167-5273(98)00313-1}}</ref>
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| ==Pathophysiology==<!-- This section is linked from [[Myocardial infarction]] -->
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| [[Image:Heart attack diagram.png|left|thumb|350px|A myocardial infarction occurs when an [[atherosclerosis|atherosclerotic]] [[Atheroma|plaque]] slowly builds up in the inner lining of a [[coronary artery]] and then suddenly ruptures, totally occluding the artery and preventing blood flow downstream.]]
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| {{main|Acute coronary syndrome}}
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| Acute myocardial infarction refers to two subtypes of [[acute coronary syndrome]], namely '''non-ST-elevated myocardial infarction''' and '''ST-elevated myocardial infarction''', which are most frequently (but not always) a manifestation of [[coronary artery disease]]. The most common triggering event is the disruption of an [[Atherosclerosis|atherosclerotic]] [[Atheroma|plaque]] in an epicardial coronary artery, which leads to a clotting cascade, sometimes resulting in total occlusion of the artery. Atherosclerosis is the gradual buildup of [[cholesterol]] and fibrous tissue in plaques in the wall of [[artery|arteries]] (in this case, the [[coronary artery|coronary arteries]]), typically over decades. Blood stream column irregularities visible on angiography reflect artery [[lumen]] narrowing as a result of decades of advancing atherosclerosis. Plaques can become unstable, rupture, and additionally promote a [[thrombus]] (blood clot) that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coronary vasculature, it leads to myocardial infarction (necrosis of downstream myocardium).
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| If impaired blood flow to the heart lasts long enough, it triggers a process called the [[ischemic cascade]]; the heart cells die (chiefly through [[necrosis]]) and do not grow back. A [[collagen]] [[scar]] forms in its place. Recent studies indicate that another form of cell death called [[apoptosis]] also plays a role in the process of tissue damage subsequent to myocardial infarction.<ref name="Krijnen-2002">{{cite journal | author=Krijnen PA, Nijmeijer R, Meijer CJ, Visser CA, Hack CE, Niessen HW. | title=Apoptosis in myocardial ischaemia and infarction. | journal=J Clin Pathol | year=2002 | volume=55 | issue=11 | pages=801–11 | pmid=12401816 | doi = 10.1136/jcp.55.11.801}}</ref> As a result, the patient's heart will be permanently damaged. This scar tissue also puts the patient at risk for potentially life threatening arrhythmias, and may result in the formation of a ventricular aneurysm that can rupture with catastrophic consequences.
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| Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in conduction velocity between injured and uninjured tissue can trigger [[Cardiac arrhythmia#Re-entry|re-entry]] or a feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is [[ventricular fibrillation]] (''V-Fib''/VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac death. Another life threatening arrhythmia is [[ventricular tachycardia]] (''V-Tach''/VT), which may or may not cause sudden cardiac death. However, ventricular tachycardia usually results in rapid heart rates that prevent the heart from pumping blood effectively. [[Cardiac output]] and [[blood pressure]] may fall to dangerous levels, which can lead to further coronary ischemia and extension of the infarct.
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| The [[defibrillator|cardiac defibrillator]] is a device that was specifically designed to terminate these potentially fatal arrhythmias. The device works by delivering an electrical shock to the patient in order to depolarize a critical mass of the heart muscle, in effect "[[reboot]]ing" the heart. This therapy is time dependent, and the odds of successful defibrillation decline rapidly after the onset of cardiopulmonary arrest.
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| ==Triggers==
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| Heart attack rates are higher in association with intense exertion, be it [[stress (psychology)|psychological stress]] or physical exertion, especially if the exertion is more intense than the individual usually performs.<ref name="Framingham1998">Wilson PW, D'Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. "[http://circ.ahajournals.org/cgi/content/full/97/18/1837 Prediction of coronary heart disease using risk factor categories]". ''Circulation'' 1998; '''97'''(18): 1837-47. PMID 9603539</ref> Quantitatively, the period of intense exercise and subsequent recovery is associated with about a 6-fold higher myocardial infarction rate (compared with other more relaxed time frames) for people who are physically very fit.<ref name="Framingham1998">Wilson PW, D'Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. "[http://circ.ahajournals.org/cgi/content/full/97/18/1837 Prediction of coronary heart disease using risk factor categories]". ''Circulation'' 1998; '''97'''(18): 1837-47. PMID 9603539</ref> For those in poor physical condition, the rate differential is over 35-fold higher.<ref name="Framingham1998">Wilson PW, D'Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. "[http://circ.ahajournals.org/cgi/content/full/97/18/1837 Prediction of coronary heart disease using risk factor categories]". ''Circulation'' 1998; '''97'''(18): 1837-47. PMID 9603539</ref> One observed mechanism for this phenomenon is the increased arterial pulse pressure stretching and relaxation of arteries with each heart beat which, as has been observed with [[intravascular ultrasound]], increases mechanical "shear stress" on [[atheroma]]s and the likelihood of plaque rupture.<ref name="Framingham1998">Wilson PW, D'Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. "[http://circ.ahajournals.org/cgi/content/full/97/18/1837 Prediction of coronary heart disease using risk factor categories]". ''Circulation'' 1998; '''97'''(18): 1837-47. PMID 9603539</ref>
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| Acute severe infection, such as [[pneumonia]], can trigger myocardial infarction. A more controversial link is that between ''[[Chlamydophila pneumoniae]]'' infection and atherosclerosis.<ref name="Saikku-1992">{{cite journal | author=Saikku P, Leinonen M, Tenkanen L, Linnanmaki E, Ekman MR, Manninen V, Manttari M, Frick MH, Huttunen JK. | title=Chronic Chlamydia pneumoniae infection as a risk factor for coronary heart disease in the Helsinki Heart Study. | journal=Ann Intern Med | year=1992 | volume=116 | issue=4 | pages=273–8 | pmid=1733381}}</ref> While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor.<ref name="Saikku-1992">{{cite journal | author=Saikku P, Leinonen M, Tenkanen L, Linnanmaki E, Ekman MR, Manninen V, Manttari M, Frick MH, Huttunen JK. | title=Chronic Chlamydia pneumoniae infection as a risk factor for coronary heart disease in the Helsinki Heart Study. | journal=Ann Intern Med | year=1992 | volume=116 | issue=4 | pages=273–8 | pmid=1733381}}</ref> Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.<ref name="Andraws-2005">{{cite journal | author=Andraws R, Berger JS, Brown DL. | title=Effects of antibiotic therapy on outcomes of patients with coronary artery disease: a meta-analysis of randomized controlled trials. | journal=JAMA | year=2005 | volume=293 | issue=21 | pages=2641–7 | pmid=15928286 | doi = 10.1001/jama.293.21.2641}}</ref>
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| There is an association of an increased incidence of MI in the morning hours<ref name="pmid2865677">{{cite journal |author=Muller JE, Stone PH, Turi ZG, ''et al'' |title=Circadian variation in the frequency of onset of acute myocardial infarction |journal=[[N. Engl. J. Med.]] |volume=313 |issue=21 |pages=1315–22 |year=1985 |pmid=2865677 |doi=}}</ref><ref name="pmid3673917">{{cite journal |author=Beamer AD, Lee TH, Cook EF, ''et al'' |title=Diagnostic implications for myocardial ischemia of the circadian variation of the onset of chest pain |journal=[[Am. J. Cardiol.]] |volume=60 |issue=13 |pages=998–1002 |year=1987 |pmid=3673917 |doi=}}</ref><ref name="pmid9036740">{{cite journal |author=Cannon CP, McCabe CH, Stone PH, ''et al'' |title=Circadian variation in the onset of unstable angina and non-Q-wave acute myocardial infarction (the TIMI III Registry and TIMI IIIB) |journal=[[Am. J. Cardiol.]] |volume=79 |issue=3 |pages=253–8 |year=1997 |pmid=9036740 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914997007431}}</ref>. Some investigators have noticed that the ability of platelets to aggregate varies according to a circadian rhythm, although they have not proven causation.<ref name="pmid3587281">{{cite journal |author=Tofler GH, Brezinski D, Schafer AI, ''et al'' |title=Concurrent morning increase in platelet aggregability and the risk of myocardial infarction and sudden cardiac death |journal=[[N. Engl. J. Med.]] |volume=316 |issue=24 |pages=1514–8 |year=1987 |pmid=3587281 |doi=}}</ref> Some investigators theorize that this increased incidence may be related to the circadian variation in cortisol production affecting the concentrations of various cytokines and other mediators of inflammation.<ref name="pmid12027868">{{cite journal |author=Fantidis P, Perez De Prada T, Fernandez-Ortiz A, ''et al'' |title=Morning cortisol production in coronary heart disease patients |journal=[[Eur. J. Clin. Invest.]] |volume=32 |issue=5 |pages=304–8 |year=2002 |pmid=12027868 |doi= |url=http://www.blackwell-synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=0014-2972&date=2002&volume=32&issue=5&spage=304}}</ref>
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| ==Classification==
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| Acute myocardial infarction is a type of [[acute coronary syndrome]], which is most frequently (but not always) a manifestation of [[coronary artery disease]]. The acute coronary syndromes include ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and [[unstable angina]] (UA).
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| ===By zone===
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| Depending on the location of the obstruction in the [[coronary circulation]], different zones of the heart can become injured. Using the [[anatomical terms of location]] corresponding to areas perfused by major coronary arteries, one can describe anterior, inferior, lateral, apical, septal, posterior, and right-ventricular infarctions (and combinations, such as anteroinferior, anterolateral, and so on).<ref name="MedicalDictionary">{{cite web | title=Dorland's Illustrated Medical Dictionary | publisher=WB Saunders, an Elsevier imprint | url=http://www.mercksource.com/pp/us/cns/cns_hl_dorlands.jspzQzpgzEzzSzppdocszSzuszSzcommonzSzdorlandszSzdorlandzSzdmd_i_07zPzhtm | accessmonthday=November 25 | accessyear=2006}}</ref>
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| * For example, an occlusion of the [[left anterior descending coronary artery]](LAD) will result in an ''anterior wall'' myocardial infarct.<ref name=rubin525>{{cite book | coauthors = Emanuel Rubin, Fred Gorstein, Raphael Rubin, Roland Schwarting, David Strayer | title = Rubin's Pathology - Clinicopathological Foundations of Medicine | publisher = Lippincott Williams & Wilkins | date = 2001 | location = Maryland | pages = 525 | id = ISBN 0-7817-4733-3 }}</ref>
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| * Infarcts of the ''lateral wall'' are caused by occlusion of the [[left circumflex coronary artery]](LCx) or its oblique marginal branches (or even large diagonal branches from the LAD.)
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| * Both ''inferior wall'' and ''posterior wall'' infarctions may be caused by occlusion of either the [[right coronary artery]] or the left circumflex artery, depending on which feeds the [[posterior descending artery]].
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| * Right ''ventricular wall'' infarcts are also caused by [[right coronary artery]] occlusion.
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| ===Subendocardial vs. transmural===
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| Another distinction is whether a MI is subendocardial, affecting only the inner third to one half of the heart muscle, or transmural, damaging (almost) the entire wall of the heart.<ref name=rubin's-p545>{{cite book | coauthors = Emanuel Rubin, Fred Gorstein, Raphael Rubin, Roland Schwarting, David Strayer | title = Rubin's Pathology - Clinicopathological Foundations of Medicine | publisher = Lippincott Williams & Wilkins | date = 2001 | location = Maryland | pages = p. 545 | id = ISBN 0-7817-4733-3 }}</ref> The inner part of the heart muscle is more vulnerable to oxygen shortage, because the coronary arteries run inward from the [[epicardium]] to the [[endocardium]], and because the blood flow through the heart muscle is hindered by the [[Systole (medicine)|heart contraction]].<ref name=rubin525/>
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| The phrases transmural and subendocardial infarction were previously considered synonymous with Q-wave and non-Q-wave myocardial infarction respectively, based on the presence or absence of Q waves on the ECG. It has since been shown that there is no clear [[correlation]] between the presence of Q waves with a transmural infarction and the absence of Q waves with a subendocardial infarction,<ref name="Moon-2004">{{cite journal | author=Moon JC, De Arenaza DP, Elkington AG, Taneja AK, John AS, Wang D, Janardhanan R, Senior R, Lahiri A, Poole-Wilson PA, Pennell DJ. | title=The pathologic basis of Q-wave and non-Q-wave myocardial infarction: a cardiovascular magnetic resonance study. | journal=J Am Coll Cardiol | year=2004 | volume=44 | issue=3 | pages=554–60 | pmid=15358019 | doi = 10.1016/j.jacc.2004.03.076}}</ref> but Q waves are associated with larger infarctions, while the lack of Q waves is associated with smaller infarctions. The presence or absence of Q-waves also has clinical importance,<ref name="Yang-2004">{{cite journal | author=Yang H, Pu M, Rodriguez D, Underwood D, Griffin BP, Kalahasti V, Thomas JD, Brunken RC | title=Ischemic and viable myocardium in patients with non-Q-wave or Q-wave myocardial infarction and left ventricular dysfunction: a clinical study using positron emission tomography, echocardiography, and electrocardiography. | journal=J Am Coll Cardiol | year=2004 | volume=43 | issue=4 | pages=592–8 | pmid=14975469 | doi = 10.1016/j.jacc.2003.07.052}}</ref> with improved outcomes associated with a lack of Q waves.<ref name="Goodman-1998">{{cite journal | author=Goodman SG, Langer A, Ross AM, Wildermann NM, Barbagelata A, Sgarbossa EB, Wagner GS, Granger CB, Califf RM, Topol EJ, Simoons ML, Armstrong PW. | title=Non-Q-wave versus Q-wave myocardial infarction after thrombolytic therapy: angiographic and prognostic insights from the global utilization of streptokinase and tissue plasminogen activator for occluded coronary arteries-I angiographic substudy. GUSTO-I Angiographic Investigators. | journal=Circulation | year=1998 | volume=97 | issue=5 | pages=444–50 | pmid=9490238}}</ref>
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| ==Symptoms==
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| [[Image:AMI pain front.png|right|thumb|150px|Rough diagram of pain zones in myocardial infarction (dark red = most typical area, light red = other possible areas, view of the chest).]]
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| [[Image:AMI pain back.png|right|thumb|150px|Back view.]]
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| The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous.<ref name=warningsigns>[[National Heart, Lung and Blood Institute]]. [http://www.nhlbi.nih.gov/actintime/haws/haws.htm Heart Attack Warning Signs]. Retrieved November 22, 2006.</ref> [[Chest pain]] is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Chest pain due to [[ischemia]] (a lack of blood and hence oxygen supply) of the heart muscle is termed [[angina pectoris]]. Pain radiates most often to the left [[arm]], but may also radiate to the lower [[jaw]], [[neck]], right arm, [[Human back|back]], and [[epigastrium]], where it may mimic [[heartburn]]. [[Levine's sign]], in which the patient localizes the chest pain by clenching their fist over the sternum, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed that it had a poor positive predictive value.<ref name="pmid17208083">{{cite journal |author=Marcus GM, Cohen J, Varosy PD, ''et al'' |title=The utility of gestures in patients with chest discomfort |journal=[[Am. J. Med.]] |volume=120 |issue=1 |pages=83–9 |year=2007 |pmid=17208083 |doi=10.1016/j.amjmed.2006.05.045 |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9343(06)00668-1}}</ref>
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| Shortness of breath ([[dyspnea]]) occurs when the damage to the heart limits the [[Cardiac output|output]] of the [[left ventricle]], causing [[left ventricular failure]] and consequent [[pulmonary edema]]. Other symptoms include [[diaphoresis]] (an excessive form of [[sweating]]), weakness, [[light-headedness]], [[nausea]], [[vomiting]], and [[palpitation]]s. These symptoms are likely induced by a massive surge of [[catecholamines]] from the [[sympathetic nervous system]]<ref name="pmid3524599">{{cite journal |author=Little RA, Frayn KN, Randall PE, ''et al'' |title=Plasma catecholamines in the acute phase of the response to myocardial infarction |journal=[[Arch Emerg Med]] |volume=3 |issue=1 |pages=20–7 |year=1986 |pmid=3524599 |doi=}}</ref> which occurs in response to pain and the hemodynamic abnormalities that result from cardiac dysfunction. [[Unconsciousness|Loss of consciousness]] (due to inadequate cerebral perfusion and cardiogenic shock) and even [[sudden cardiac death|sudden death]] (frequently due to the development of ventricular fibrillation) can occur in myocardial infarctions.
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| Women often experience markedly different symptoms from men. The most common symptoms of MI in women include dyspnea, weakness, and [[fatigue (physical)|fatigue]]. Fatigue, sleep disturbances, and [[dyspnea]] have been reported as frequently occurring symptoms which may manifest as long as one month before the actual clinically manifested ischemic event. In women, [[chest pain]] may be less predictive of coronary [[ischemia]] than in men.<ref name=McSweeney>{{cite journal | author=McSweeney JC, Cody M, O'Sullivan P, Elberson K, Moser DK, Garvin BJ | title=Women's early warning symptoms of acute myocardial infarction | journal=Circulation | year=2003 | pages=2619–23 | volume=108 | issue=21 | pmid=14597589 | doi = 10.1161/01.CIR.0000097116.29625.7C}}</ref>
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| Approximately half of all MI patients have experienced warning symptoms such as chest pain prior to the infarction.<ref name=MedicineNet>D Lee, D Kulick, J Marks. [http://www.medicinenet.com/heart_attack/article.htm Heart Attack (Myocardial Infarction)] by MedicineNet.com . Retrieved November 28, 2006.</ref>
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| Approximately one fourth of all myocardial infarctions are silent, without chest pain or other symptoms.<ref name="Kannel-1986">{{cite journal | author=Kannel WB. | title=Silent myocardial ischemia and infarction: insights from the Framingham Study. | journal=Cardiol Clin | year=1986 | volume=4 | issue=4| pages=583–91 | pmid=3779719}}</ref> These cases can be discovered later on electrocardiograms or at autopsy without a prior history of related complaints. A silent course is more common in the [[elderly]], in patients with [[diabetes mellitus]]<ref name="Diabetologica2004-David">{{cite journal | author=Davis TM, Fortun P, Mulder J, Davis WA, Bruce DG | title=Silent myocardial infarction and its prognosis in a community-based cohort of Type 2 diabetic patients: the Fremantle Diabetes Study | journal=Diabetologia | year=2004 | pages=395–9 | volume=47 | issue=3 | pmid=14963648 | doi = 10.1007/s00125-004-1344-4}} </ref> and after [[heart transplantation]], probably because the [[Organ donation|donor]] heart is not connected to nerves of the host.<ref name=rubin's>{{cite book | coauthors = Emanuel Rubin, Fred Gorstein, Raphael Rubin, Roland Schwarting, David Strayer | title = Rubin's Pathology - Clinicopathological Foundations of Medicine | publisher = Lippincott Williams & Wilkins | date = 2001 | location = Maryland | pages = p. 549 | id = ISBN 0-7817-4733-3 }}</ref> In diabetics, differences in [[pain threshold]], [[autonomic neuropathy]], and [[psychology|psychological]] factors have been cited as possible explanations for the lack of symptoms.<ref name="Diabetologica2004-David"/>
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| Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are called an [[acute coronary syndrome]].<ref name=ACS>[http://www.americanheart.org/presenter.jhtml?identifier=3010002 Acute Coronary Syndrome]. [[American Heart Association]]. Retrieved November 25, 2006.</ref>
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| The [[differential diagnosis]] includes other catastrophic causes of chest pain, such as [[pulmonary embolism]], [[aortic dissection]], [[pericardial effusion]] causing [[cardiac tamponade]], [[tension pneumothorax]], and [[esophageal rupture]].<ref name="pmid16199332">{{cite journal |author=Boie ET |title=Initial evaluation of chest pain |journal=[[Emerg. Med. Clin. North Am.]] |volume=23 |issue=4 |pages=937–57 |year=2005 |pmid=16199332 |doi=10.1016/j.emc.2005.07.007 |url=http://linkinghub.elsevier.com/retrieve/pii/S0733-8627(05)00059-3}}</ref>
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| ==Diagnosis==
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| The diagnosis of myocardial infarction is made by integrating the history of the presenting illness and physical examination with [[electrocardiogram]] findings and [[cardiac marker]]s ([[blood test]]s for [[Cardiac muscle|heart muscle]] [[cell (biology)|cell]] damage).<ref name=GPnotebook_MI>[http://www.gpnotebook.co.uk/simplepage.cfm?ID=892665874&linkID=23278&cook=yes Myocardial infarction: diagnosis and investigations] - [[GPnotebook]], retrieved November 27, 2006.</ref> A [[Coronary catheterization|coronary angiogram]] allows visualization of narrowings or obstructions on the heart vessels, and therapeutic measures can follow immediately. At [[autopsy]], a [[pathologist]] can diagnose a myocardial infarction based on [[Anatomical pathology|anatomopathological]] findings.
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| A [[chest radiograph]] and routine blood tests may indicate complications or precipitating causes and are often performed upon arrival to an [[emergency department]]. New regional wall motion abnormalities on an [[Medical ultrasonography|echocardiogram]] are also suggestive of a myocardial infarction. Echo may be performed in equivocal cases by the on-call cardiologist.<ref name=eMedicineEMERG>''DE Fenton et al.'' [http://www.emedicine.com/EMERG/topic327.htm#section~workup Myocardial infarction] - [[eMedicine]], retrieved November 27, 2006.</ref> In stable patients whose symptoms have resolved by the time of evaluation, technetium-99m 2-methoxyisobutylisonitrile (Tc99m MIBI) or [[thallium chloride|thallium-201 chloride]] can be used in [[nuclear medicine]] to visualize areas of reduced blood flow in conjunction with physiologic or pharmocologic stress.<ref name=eMedicineEMERG/><ref name=heartscanpage>[http://www.ucl.ac.uk/nuclear-medicine/Patient_Information/Scans/Cardiac.htm HEART SCAN] - Patient information from [[University College London]]. Retrieved November 27, 2006.</ref> Thallium may also be used to determine viability of tissue, distinguishing whether non-functional myocardium is actually dead or merely in a state of hibernation or of being stunned.<ref name="pmid9885104">{{cite journal |author=Skoufis E, McGhie AI |title=Radionuclide techniques for the assessment of myocardial viability |journal=[[Tex Heart Inst J]] |volume=25 |issue=4 |pages=272–9 |year=1998 |pmid=9885104 |doi=}}</ref>
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| ===Diagnostic criteria===
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| WHO criteria<ref name=Gillum>Gillum RF, Fortmann SP, Prineas RJ, Kottke TE. International diagnostic criteria for acute myocardial infarction and acute stroke. ''Am Heart J'' 1984;108:150-8. PMID 6731265</ref> have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:
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| # Clinical history of ischaemic type chest pain lasting for more than 20 minutes
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| # Changes in serial ECG tracings
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| # Rise and fall of serum cardiac biomarkers such as [[creatine kinase]]-MB fraction and [[troponin]]
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| The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers.<ref name="Alpert-2000"/> According to the new guidelines, a cardiac [[troponin]] rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI.
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| ===Physical examination===
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| The general appearance of patients may vary according to the experienced symptoms; the patient may be comfortable, or restless and in severe distress with an increased [[respiratory rate]]. A cool and [[pallor|pale skin]] is common and points to [[vasoconstriction]]. Some patients have low-grade fever (38–39 °C). [[Blood pressure]] may be elevated or decreased, and the [[pulse]] can be become [[Cardiac arrhythmia|irregular]].<ref name=emedicine>S. Garas ''et al.''. [http://www.emedicine.com/med/topic1567.htm Myocardial Infarction]. [[eMedicine]]. Retrieved November 22, 2006.</ref><ref name=harrisons-p1444>Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL. ''Harrison's Principles of Internal Medicine''. p. 1444. New York: McGraw-Hill, 2005. ISBN 0-07-139140-1.</ref>
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| If heart failure ensues, elevated [[jugular venous pressure]] and [[hepatojugular reflux]], or swelling of the legs due to peripheral [[edema]] may be found on inspection. Rarely, a cardiac bulge with a pace different from the pulse rhythm can be felt on [[precordial examination]]. Various abnormalities can be found on [[auscultation]], such as a third and fourth [[heart sounds|heart sound]], [[Heart murmur|systolic murmurs]], paradoxical splitting of the second heart sound, a [[Pericardium|pericardial]] friction rub and [[rales]] over the lung.<ref name=emedicine/><ref name=harrisons-p1450>Kasper DL, ''et al.'' ''Harrison's Principles of Internal Medicine''. p. 1450.</ref>
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| [[Image:12 Lead EKG ST Elevation tracing color coded.jpg|thumb|400px|12-lead [[electrocardiogram]] showing ST-segment elevation (orange) in I, aVL and V1-V5 with reciprocal changes (blue) in the inferior leads, indicative of an anterior wall myocardial infarction.]]
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| [[Image:ECG 001.jpg|thumb|400px|12-lead [[electrocardiogram]] (ECG) showing acute inferior ST segment elevation MI (STEMI). Note the ST segment elevation in leads II, III, and aVF along with reciprocal ST segment depression in leads I and aVL.]]
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| ===Electrocardiogram===
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| {{main|Electrocardiogram}}
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| The primary purpose of the [[electrocardiogram]] is to detect [[ischemia]] or acute coronary injury in broad, symptomatic [[emergency department]] populations. However, the standard 12 lead [[electrocardiogram|ECG]] has several limitations. An [[electrocardiogram|ECG]] represents a brief sample in time. Because unstable ischemic syndromes have rapidly changing supply versus demand characteristics, a single ECG may not accurately represent the entire picture.<ref name=Cannon_175>Cannon CP at al. ''Management of Acute Coronary Syndromes''. p. 175. New Jersey: Humana Press, 1999. ISBN 0-89603-552-2.</ref> It is therefore desirable to obtain ''serial'' 12 lead ECGs, particularly if the first ECG is obtained during a pain-free episode. Alternatively, many [[emergency department]]s and chest pain centers use computers capable of continuous ST segment monitoring.<ref name="NHAAP_1997">{{cite journal |author=Selker HP, Zalenski RJ, Antman EM, ''et al'' |title=An evaluation of technologies for identifying acute cardiac ischemia in the emergency department: executive summary of a National Heart Attack Alert Program Working Group Report |journal=Ann Emerg Med |volume=29 |issue=1 |pages=1–12 |year=1997 |month=January |pmid=8998085 |doi=10.1016/S0196-0644(97)70297-X}}</ref> The standard 12 lead ECG also does not directly examine the [[right ventricle]], and is relatively poor at examining the posterior basal and lateral walls of the [[left ventricle]]. In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG.<ref name=Cannon_175/> The use of additional ECG leads like right-sided leads V3R and V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. In spite of these limitations, the 12 lead ECG stands at the center of risk stratification for the patient with suspected acute myocardial infarction. Mistakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the quality of patient care.<ref name="EDQMI_2006">{{cite journal |author=Masoudi FA, Magid DJ, Vinson DR, ''et al'' |title=Implications of the failure to identify high-risk electrocardiogram findings for the quality of care of patients with acute myocardial infarction: results of the Emergency Department Quality in Myocardial Infarction (EDQMI) study |journal=Circulation |volume=114 |issue=15 |pages=1565–71 |year=2006 |month=October |pmid=17015790 |doi=10.1161/CIRCULATIONAHA.106.623652 |url=http://circ.ahajournals.org/cgi/content/full/114/15/1565}}</ref>
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| The 12 lead ECG is used to classify patients into one of three groups:<ref name="ECC_2005_ACS">{{cite journal | title=2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - Part 8: Stabilization of the Patient With Acute Coronary Syndromes | journal=Circulation | year=2005 | volume=112 | pages=IV–89–IV–110 | doi=10.1161/CIRCULATIONAHA.105.166561 | url=http://circ.ahajournals.org/cgi/content/full/112/24_suppl/IV-89}}</ref>
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| # those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with [[thrombolysis|thrombolytics]] or primary [[percutaneous coronary intervention|PCI]]),
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| # those with ST segment depression or T wave inversion (suspicious for ischemia), and
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| # those with a so-called non-diagnostic or normal ECG.
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| A normal ECG does not rule out acute myocardial infarction. Sometimes the earliest presentation of acute myocardial infarction is the hyperacute T wave, which is treated the same as ST segment elevation.<ref name=Hyperacute2002>{{cite journal |author=Somers MP, Brady WJ, Perron AD, Mattu A |title=The prominant T wave: electrocardiographic differential diagnosis |journal=Am J Emerg Med |volume=20 |issue=3 |pages=243–51 |year=2002 |month=May |pmid=11992348 |doi=10.1053/ajem.2002.32630}}</ref> In practice this is rarely seen, because it only exists for 2-30 minutes after the onset of infarction.<ref name="ACS_Clin_NA">{{cite journal |author=Smith SW, Whitwam W |title=Acute coronary syndromes |journal=Emerg. Med. Clin. North Am. |volume=24 |issue=1 |pages=53–89, vi |year=2006 |month=February |pmid=16308113 |doi=10.1016/j.emc.2005.08.008}}</ref> Hyperacute T waves need to be distinguished from the peaked T waves associated with [[hyperkalemia]].<ref name="ECG_Noncardiac">{{cite journal |author=Van Mieghem C, Sabbe M, Knockaert D |title=The clinical value of the ECG in noncardiac conditions |journal=Chest |volume=125 |issue=4 |pages=1561–76 |year=2004 |month=April |pmid=15078775 |doi= |url=http://www.chestjournal.org/cgi/content/full/125/4/1561}}</ref> The current guidelines for the ECG diagnosis of acute myocardial infarction require at least 1 mm (0.1 mV) of ST segment elevation in the limb leads, and at least 2 mm elevation in the precordial leads. These elevations must be present in anatomically contiguous leads.<ref name="ECC_2005_ACS"/> (I, aVL, V5, V6 correspond to the lateral wall; V1-V4 correspond to the anterior wall; II, III, aVF correspond to the inferior wall.) This criterion is problematic, however, as acute myocardial infarction is not the most common cause of ST segment elevation in [[chest pain]] patients.<ref name="Cause_ST_ED">{{cite journal |author=Brady WJ, Perron AD, Martin ML, Beagle C, Aufderheide TP |title=Cause of ST segment abnormality in ED chest pain patients |journal=Am J Emerg Med |volume=19 |issue=1 |pages=25–8 |year=2001 |month=January |pmid=11146012 |doi=10.1053/ajem.2001.18029 |url=}}</ref> Over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation in at least one precordial lead.<ref name="ST_Other_MI">{{cite journal |author=Wang K, Asinger RW, Marriott HJ |title=ST-segment elevation in conditions other than acute myocardial infarction |journal=N. Engl. J. Med. |volume=349 |issue=22 |pages=2128–35 |year=2003 |month=November |pmid=14645641 |doi=10.1056/NEJMra022580 |url=}}</ref> The clinician must therefore be well versed in recognizing the so-called ECG mimics of acute myocardial infarction, which include [[left ventricular hypertrophy]], [[left bundle branch block]], [[artificial pacemaker|paced rhythm]], [[early repolarization]], [[pericarditis]], [[hyperkalemia]], and ventricular aneurysm.<ref name="ECG_Confound">Brady WJ, Chan TC, Pollack M. "Electrocardiographic manifestations: patterns that confound the EKG diagnosis of acute myocardial infarction-left bundle branch block, ventricular paced rhythm, and left ventricular hypertrophy." ''J Emerg Med'' 2000; '''18(1)''': 71-8. PMID 10645842</ref><ref name="STE_AMI_non-AMI">"Electrocardiographic ST-segment elevation: correct identification of acute myocardial infarction (AMI) and non-AMI syndromes by emergency physicians." ''Acad Emerg Med'' 2001; '''8(4)''': 349-60. PMID 11282670</ref><ref name="ST_Other_MI">"ST-segment elevation in conditions other than acute myocardial infarction." ''New Engl J Med'' 2003; '''349(22)''': 2128-35. PMID 14645641</ref>
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| [[Left bundle branch block]] and [[artificial pacemaker|pacing]] interferes with the electrocardiographic diagnosis of acute myocadial infarction by making the ST segment uninterpretable. The GUSTO investigators Sgarbossa et al. developed a set of criteria for identifying acute myocardial infarction in the presence of left bundle branch block and paced rhythm. They include concordant ST segment elevation > 1 mm (0.1 mV), discordant ST segment elevation > 5 mm (0.5 mV), and concordant ST segment depression in the left precordial leads.<ref name="NEJM_Sgarbossa">Sgarbossa EB, Pinski SL, Barbagelata A, Underwood DA, Gates KB, Topol EJ, Califf RM, Wagner GS. "Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle branch block." ''N Engl J Med'' 1996; '''334''' (8): 481-7. PMID 8559200</ref> The presence of reciprocal changes on the 12 lead ECG may help distinguish true acute myocardial infarction from the mimics of acute myocardial infarction. The contour of the ST segment may also be helpful, with a straight or upwardly convex (non-concave) ST segment favoring the diagnosis of acute myocardial infarction.<ref name="Contour_ST">"Electrocardiographic ST-segment elevation: the diagnosis of acute myocardial infarction by morphologic analysis of the ST segment." ''Acad Emerg Med'' 2001; '''8(10)''': 961-7. PMID 11581081</ref>
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| The constellation of leads with ST segment elevation enables the clinician to identify what area of the heart is injured, which in turn helps predict the so-called culprit artery.
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| {| class=wikitable border="1" cellspacing="0" cellpadding="5" align="center"
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| ! Wall Affected
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| ! Leads Showing ST Segment Elevation
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| ! Leads Showing Reciprocal ST Segment Depression
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| ! Suspected Culprit Artery
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| |-
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| | Septal
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| | V<sub>1</sub>, V<sub>2</sub>
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| | None
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| | [[Anterior interventricular branch of left coronary artery|Left Anterior Descending (LAD)]]
| |
| |-
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| | Anterior
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| | V<sub>3</sub>, V<sub>4</sub>
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| | None
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| | [[Anterior interventricular branch of left coronary artery|Left Anterior Descending (LAD)]]
| |
| |-
| |
| | Anteroseptal
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| | V<sub>1</sub>, V<sub>2</sub>, V<sub>3</sub>, V<sub>4</sub>
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| | None
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| | [[Anterior interventricular branch of left coronary artery|Left Anterior Descending (LAD)]]
| |
| |-
| |
| | Anterolateral
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| | V<sub>3</sub>, V<sub>4</sub>, V<sub>5</sub>, V<sub>6</sub>, I, aVL
| |
| | II, III, aVF
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| | [[Anterior interventricular branch of left coronary artery|Left Anterior Descending (LAD)]], [[Circumflex branch of left coronary artery|Circumflex (LCX)]], or [[Left marginal artery|Obtuse Marginal]]
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| |-
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| | Extensive anterior (Sometimes called Anteroseptal with Lateral extension)
| |
| | V<sub>1</sub>,V<sub>2</sub>,V<sub>3</sub>, V<sub>4</sub>, V<sub>5</sub>, V<sub>6</sub>, I, aVL
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| | II, III, aVF
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| | [[Left coronary artery|Left main coronary artery (LCA)]]
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| |-
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| | [[Diaphragmatic surface of heart|Inferior]]
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| | II, III, aVF
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| | I, aVL
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| | [[Right coronary artery|Right Coronary Artery (RCA) or Circumflex (LCX)]]
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| |-
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| | Lateral
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| | I, aVL</sub>, V<sub>5</sub>, V<sub>6</sub>
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| | II, III, aVF
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| | [[Circumflex branch of left coronary artery|Circumflex (LCX)]] or [[Left marginal artery|Obtuse Marginal]]
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| |-
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| | Posterior (Usually associated with Inferior or Lateral but can be isolated)
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| | V<sub>7</sub>, V<sub>8</sub>, V<sub>9</sub>
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| | V<sub>1</sub>,V<sub>2</sub>,V<sub>3</sub>, V<sub>4</sub>
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| | [[Posterior descending artery|Posterior Descending (PDA)]] (branch of the [[right coronary artery|RCA]] or [[circumflex artery|Circumflex (LCX)]])
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| |-
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| | [[Right ventricle|Right ventricular]] (Usually associated with Inferior)
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| | II, III, aVF, V<sub>1</sub>, V<sub>4</sub>R
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| | I, aVL
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| | [[Right coronary artery|Right Coronary Artery (RCA)]]
| |
| |-
| |
| |}
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| As the myocardial infarction evolves, there may be loss of R wave height and development of pathological Q waves (defined as Q waves deeper than 1 mm and wider than 1 mm.) T wave inversion may persist for months or even permanently following acute myocardial infarction.<ref>{{cite journal | author = Morris F, Brady W | title = ABC of clinical electrocardiography: Acute myocardial infarction-Part I. | journal = BMJ | volume = 324 | issue = 7341 | pages = 831–4 | year = 2002 | pmid = 1934778 | doi = 10.1136/bmj.324.7341.831}} {{PMC|1122768}}</ref> Typically, however, the T wave recovers, leaving a pathological Q wave as the only remaining evidence that an acute myocardial infarction has occurred.
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| ===Cardiac markers===
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| {{main|Cardiac marker}}
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| Cardiac markers or cardiac enzymes are proteins from cardiac tissue found in the blood. These proteins are released into the bloodstream when damage to the heart occurs, as in the case of a myocardial infarction. Until the 1980s, the enzymes [[Aspartate transaminase|SGOT]] and [[lactate dehydrogenase|LDH]] were used to assess cardiac injury. Then it was found that disproportional elevation of the ''MB'' subtype of the enzyme [[creatine kinase]] (CK) was very specific for myocardial injury. Current guidelines are generally in favor of [[troponin]] sub-units I or T, which are very specific for the heart muscle and are thought to rise before permanent injury develops.<ref>{{cite journal | author = Eisenman A | title = Troponin assays for the diagnosis of myocardial infarction and acute coronary syndrome: where do we stand? | journal = Expert Rev Cardiovasc Ther | volume = 4 | issue = 4 | pages = 509–14 | year = 2006 | pmid = 16918269 | doi = 10.1586/14779072.4.4.509}}</ref> Elevated troponins in the setting of chest pain may accurately predict a high likelihood of a myocardial infarction in the near future.<ref>{{cite journal | author = Aviles RJ, Askari AT, Lindahl B, Wallentin L, Jia G, Ohman EM, Mahaffey KW, Newby LK, Califf RM, Simoons ML, Topol EJ, Berger P, Lauer MS | title = [[Troponin]] T levels in patients with acute coronary syndromes, with or without renal dysfunction. | journal = N Engl J Med | volume = 346 | issue = 26 | pages = 2047–52 | year = 2002 | pmid = 12087140 | doi = 10.1056/NEJMoa013456}}. [http://www.cmaj.ca/cgi/content/full/167/6/671 Summary for laymen]</ref> New markers such as [[glycogen phosphorylase isoenzyme BB]] are under investigation.<ref name="pmid15774573">{{cite journal |author=Apple FS, Wu AH, Mair J, ''et al'' |title=Future biomarkers for detection of ischemia and risk stratification in acute coronary syndrome |journal=Clin. Chem. |volume=51 |issue=5 |pages=810–24 |year=2005 |pmid=15774573 |doi=10.1373/clinchem.2004.046292|url=http://www.clinchem.org/cgi/content/full/51/5/810}}</ref>
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| The diagnosis of myocardial infarction requires two out of three components (history, ECG, and enzymes). When damage to the heart occurs, levels of cardiac markers rise over time, which is why [[blood test]]s for them are taken over a 24-hour period. Because these enzyme levels are not elevated immediately following a heart attack, patients presenting with chest pain are generally treated with the assumption that a myocardial infarction has occurred and then evaluated for a more precise diagnosis.<ref name="Braunwald-2002">{{cite journal | author=Braunwald E, Antman EM, Beasley JW, Califf RM, Cheitlin MD, Hochman JS, Jones RH, Kereiakes D, Kupersmith J, Levin TN, Pepine CJ, Schaeffer JW, Smith EE III, Steward DE, Théroux P. | title=ACC/AHA 2002 guideline update for the management of patients with unstable angina and non–ST-segment elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina). | journal=J Am Coll Cardiol | year=2002 | volume=40 | pages=1366–74 | pmid=12383588 | format=[[PDF]] | url=http://www.acc.org/qualityandscience/clinical/guidelines/unstable/incorporated/UA_incorporated.pdf}}</ref>
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| ===Angiography===
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| [[Image:Ha1.jpg|thumb|250px|[[Angiogram]] of the coronary arteries.]]
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| {{main|Coronary catheterization}}
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| In difficult cases or in situations where intervention to restore blood flow is appropriate, coronary [[angiography]] can be performed. A [[catheter]] is inserted into an artery (usually the [[femoral artery]]) and pushed to the vessels supplying the heart. A radio-opaque dye is administered through the catheter and a sequence of x-rays (fluoroscopy) is performed. Obstructed or narrowed arteries can be identified, and [[angioplasty]] applied as a therapeutic measure (see below). Angioplasty requires extensive skill, especially in emergency settings. It is performed by a physician trained in [[interventional cardiology]].
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| ===Histopathology===
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| [[Image:Myocardial infarct emmolition phase histopathology.jpg|thumb|300px|Microscopy image (magn. ca 100x, [[H&E stain]]) from autopsy specimen of myocardial infarct (7 days post-infarction).]]
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| [[Image:Infarktiarpea rotan sydämmessä.jpg|right|thumb|300px| Microscopy image of myocardial infarction scar in the heart of a rat]]
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| [[Anatomical pathology|Histopathological]] examination of the heart may reveal infarction at autopsy. Under the microscope, myocardial infarction presents as a circumscribed area of ischemic, coagulative [[necrosis]] (cell death). On gross examination, the infarct is not identifiable within the first 12 hours.<ref name=rubin546>{{cite book | coauthors = Emanuel Rubin, Fred Gorstein, Raphael Rubin, Roland Schwarting, David Strayer | title = Rubin's Pathology - Clinicopathological Foundations of Medicine | publisher = Lippincott Williams & Wilkins | date = 2001 | location = Maryland | pages = p. 546 | id = ISBN 0-7817-4733-3 }}</ref>
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| Although earlier changes can be discerned using [[electron microscopy]], one of the earliest changes under a normal microscope are so-called ''wavy fibers''.<ref name=Eichbaum1975>Eichbaum FW. "'Wavy' myocardial fibers in spontaneous and experimental adrenergic cardiopathies" ''Cardiology'' 1975; '''60'''(6): 358–65. PMID 782705</ref> Subsequently, the myocyte [[cytoplasm]] becomes more [[eosinophilic]] (pink) and the cells lose their transversal striations, with typical changes and eventually loss of the [[cell nucleus]].<ref name=histopathologyIndia>S Roy. [http://www.histopathology-india.net/Heart5.htm Myocardial infarction]. Retrieved November 28, 2006.</ref> The interstitium at the margin of the infarcted area is initially infiltrated with [[neutrophil]]s, then with [[lymphocyte]]s and [[macrophage]]s, who [[phagocytosis|phagocytose]] ("eat") the myocyte debris. The necrotic area is surrounded and progressively invaded by [[granulation tissue]], which will replace the infarct with a fibrous ([[collagen]]ous) [[scar]] (which are typical steps in [[wound healing]]). The interstitial space (the space between cells outside of blood vessels) may be infiltrated with [[red blood cell]]s.<ref name=rubin546/>
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| These features can be recognized in cases where the perfusion was not restored; reperfused infarcts can have other hallmarks, such as contraction band necrosis.<ref name="Fishbein-1990">{{cite journal | author=Fishbein MC. | title=Reperfusion injury. | journal=Clin Cardiol | year=1990 | volume=13 | issue=3 | pages=213–7 | pmid=2182247 | doi=10.1152/ajpheart.00270.2002 | doi_brokendate=2008-06-25}}</ref>
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| == First aid ==
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| As myocardial infarction is a common medical emergency, the signs are often part of [[first aid]] courses. The [[emergency action principles]] also apply in the case of myocardial infarction.
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| ===Immediate care===
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| When symptoms of myocardial infarction occur, people wait an average of three hours, instead of doing what is recommended: [[call for help|calling for help]] immediately.<ref name=FirstAid>[http://www.nlm.nih.gov/medlineplus/ency/article/000063.htm Heart attack first aid]. [[MedlinePlus]]. Retrieved December 3, 2006.</ref><ref name="ActInTime">[http://www.nhlbi.nih.gov/actintime/index.htm Act In Time to Heart Attack Signs] - [[NHLBI]]. Retrieved December 13, 2006.</ref> Acting immediately by calling the emergency services can prevent sustained damage to the heart ("time is muscle").<ref name=TimeIsMuscle>[http://www.ehac.org/st-agnes/EHAC_LifeandDeath/TimeisMuscle.htm TIME IS MUSCLE TIME WASTED IS MUSCLE LOST]. Early Heart Attack Care, St. Agnes Healthcare. Retrieved November 29, 2006.</ref>
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| Certain positions allow the patient to rest in a position which minimizes breathing difficulties. A half-sitting position with knees bent is often recommended. Access to more oxygen can be given by opening the window and widening the collar for easier breathing.
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| [[Aspirin]] can be given quickly (if the patient is not [[allergy|allergic]] to aspirin); but taking aspirin before calling the [[emergency medical services]] may be associated with unwanted delay.<ref name="Brown-2000">{{cite journal | author=Brown AL, Mann NC, Daya M, Goldberg R, Meischke H, Taylor J, Smith K, Osganian S, Cooper L. | title=Demographic, belief, and situational factors influencing the decision to utilize emergency medical services among chest pain patients. Rapid Early Action for Coronary Treatment (REACT) study. | journal=Circulation | year=2000 | volume=102 | issue=2 | pages=173–8 | pmid=10889127}}</ref> Aspirin has an [[Antiplatelet drug|antiplatelet]] effect which inhibits formation of further [[thrombus|thrombi]] (blood clots) that clog arteries. [[Enteric coating|Non-enteric coated]] or soluble preparations are preferred. If chewed or dissolved, respectively, they can be [[Absorption (pharmacokinetics)|absorbed]] by the body even quicker. If the patient cannot swallow, the aspirin can be used sublingually. U.S. guidelines recommend a dose of 162 – 325 mg.<ref name=Antman-2004>{{cite journal | author = Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, Hochman JS, Krumholz HM, Kushner FG, Lamas GA, Mullany CJ, Ornato JP, Pearle DL, Sloan MA, Smith SC Jr | year = 2004 | title = ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction) | journal=J Am Coll Cardiol | volume=44 | pages=671–719 | pmid=15358045 | url=http://www.acc.org/qualityandscience/clinical/guidelines/stemi/Guideline1/index.htm}}</ref> Australian guidelines recommend a dose of 150 – 300 mg.<ref name=Rossi>Rossi S, editor. [[Australian Medicines Handbook]] 2006. Adelaide: Australian Medicines Handbook; 2006. ISBN 0-9757919-2-3.</ref>
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| [[Glyceryl trinitrate (pharmacology)|Glyceryl trinitrate]] (nitroglycerin) [[sublingual]]ly (under the tongue) can be given if available.
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| If an Automated External Defibrillator (AED) is available the rescuer should immediately bring the AED to the patient's side and be prepared to follow its instructions, especially should the victim lose consciousness.
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| If possible the rescuer should obtain basic information from the victim, in case the patient is unable to answer questions once [[emergency medical technician]]s arrive. The victim's name and any information regarding the nature of the victim's pain will be useful to health care providers. The exact time that these symptoms started may be critical for determining what interventions can be safely attempted once the victim reaches the medical center. Other useful pieces of information include what the patient was doing at the onset of symptoms, and anything else that might give clues to the pathology of the chest pain. It is also very important to relay any actions that have been taken, such as the number or dose of aspirin or nitroglycerin given, to the EMS personnel.
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| Other general first aid principles include monitoring pulse, breathing, level of consciousness and, if possible, the blood pressure of the patient. In case of [[cardiac arrest]], [[cardiopulmonary resuscitation]] (CPR) can be administered.
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| ===Automatic external defibrillation (AED)===
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| Since the publication of data showing that the availability of [[automated external defibrillator]]s (AEDs) in public places may significantly increase chances of survival, many of these have been installed in public buildings, public transport facilities, and in non-ambulance emergency vehicles (e.g. police cars and fire engines). AEDs analyze the heart's rhythm and determine whether the rhythm is amenable to [[defibrillation]] ("shockable"), as in [[ventricular tachycardia]] and [[ventricular fibrillation]].
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| ===Emergency services===
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| [[Emergency medical services|Emergency Medical Services]] (EMS) Systems vary considerably in their ability to evaluate and treat patients with suspected acute myocardial infarction. Some provide as little as first aid and early defibrillation. Others employ highly trained paramedics with sophisticated technology and advanced protocols.<ref name="ACC_AHA_STEMI">Antman et al. "ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction—Executive Summary - A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction)" ''J Am Coll Cardiol'' 2004;44:671-719.</ref> Early access to [[emergency medical services|EMS]] is promoted by a 9-1-1 system currently available to 90% of the population in the United States.<ref name="ACC_AHA_STEMI"/> Most are capable of providing [[oxygen]], IV access, sublingual [[nitroglycerine]], [[morphine]], and [[aspirin]]. Some are capable of providing [[thrombolysis|thrombolytic therapy]] in the prehospital setting.<ref name="ER_TIMI_19">Morrow, Antman, Sayah, et al. "Evaluation of the time saved by prehospital initiation of reteplase for ST-elevation myocardial infarction: results of The Early Retavase-Thrombolysis in Myocardial Infarction (ER-TIMI) 19 trial." ''J Am Coll Cardiol'' 2002;40(1):71-7. PMID 12103258</ref><ref name="Morrison-2000">{{cite journal | author=Morrison LJ, Verbeek PR, McDonald AC, Sawadsky BV, Cook DJ. | title=Mortality and prehospital thrombolysis for acute myocardial infarction: A meta-analysis. | journal=JAMA | year=2000 | volume=283 | issue=20 | pages=2686–92 | format=[[PDF]] | url=http://jama.ama-assn.org/cgi/reprint/283/20/2686.pdf?ijkey=c72b289825a3fd6ace7545ef61cd70936485e7e1 | pmid=10819952 | doi = 10.1001/jama.283.20.2686}}</ref>
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| With [[percutaneous coronary intervention|primary PCI]] emerging as the preferred therapy for ST segment elevation myocardial infarction, [[emergency medical services|EMS]] can play a key role in reducing [[door to balloon]] intervals (the time from presentation to a hospital [[emergency department|ER]] to the restoration of coronary artery blood flow) by performing a 12 lead [[ECG]] in the field and using this information to triage the patient to the most appropriate medical facility.<ref>{{cite journal |author=Rokos IC, Larson DM, Henry TD, ''et al'' |title=Rationale for establishing regional ST-elevation myocardial infarction receiving center (SRC) networks |journal=Am. Heart J. |volume=152 |issue=4 |pages=661–7 |year=2006 |pmid=16996830 |doi=10.1016/j.ahj.2006.06.001}}</ref><ref name="EMS_PCI_Boston">Moyer, Feldman, Levine, et al. "Implications of the Mechanical (PCI) vs Thrombolytic Controversy for ST Segment Elevation Myocardial Infarction on the Organization of Emergency Medical Services: The Boston EMS Experience" ''Crit Path Cardiol'' 2004;3:53-61.</ref><ref name="EMS_PCI">Terkelsen, Lassen, Norgaard, et al. "Reduction of treatment delay in patients with ST-elevation myocardial infarction: impact of pre-hospital diagnosis and direct referral to primary percutanous coronary intervention" ''Eur Heart J'' 2005;26(8):770-7.</ref><ref name="PCI_STEMI_National_Policy">Henry, Atkins, Cunningham, et al. "ST-Segment Elevation Myocardial Infarction: Recommendations on Triage of Patients to Heart Attack Centers - Is it Time for a National Policy for the Treatment of ST-Segment Elevation Myocardial Infarction?" ''J Am Coll Cardiol'' 2006;47:1339-1345.</ref> In addition, the 12 lead ECG can be transmitted to the receiving hospital, which enables time saving decisions to be made prior to the patient's arrival. This may include a "cardiac alert" or "STEMI alert" that calls in off duty personnel in areas where the [[Coronary catheterization|cardiac cath lab]] is not staffed 24 hours a day.<ref>Rokos I. and Bouthillet T., [http://www.stemisystems.org/PDF/STEMIsystems_issue2.pdf "The emergency medical systems-to-balloon (E2B) challenge: building on the foundations of the D2B Alliance,"] ''STEMI Systems'', Issue Two, May 2007. Accessed June 16, 2007.</ref> Even in the absence of a formal alerting program, prehospital 12 lead ECGs are independently associated with reduced door to treatment intervals in the emergency department.<ref name=Cannon_176>Cannon CP at al. ''Management of Acute Coronary Syndromes''. p. 176. New Jersey: Humana Press, 1999. ISBN 0-89603-552-2.</ref>
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| ===Wilderness first aid===
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| In [[wilderness first aid]], a possible heart attack justifies [[patient evacuation|evacuation]] by the fastest available means, including [[MEDEVAC]], even in the earliest or precursor stages. The patient will rapidly be incapable of further exertion and have to be carried out.
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| ===Air travel===
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| Certified personnel traveling by commercial aircraft may be able to assist an MI patient by using the on-board [[first aid kit]], which may contain some cardiac drugs (such as [[glyceryl trinitrate]] spray, [[aspirin]], or [[opioid]] painkillers), an AED,<ref>{{cite web|last=Youngwith|first=Janice|title=Saving hearts in the air|url=http://www.dailyherald.com/special/americanheartmonth/2008/index.asp?id=11|publisher=Dailyherald.com|date=2008-02-06|accessdate=2008-06-12}}</ref> and [[oxygen]]. Pilots may divert the flight to land at a nearby airport. [[Cardiac monitors]] are being introduced by some airlines, and they can be used by both on-board and ground-based physicians.<ref name=aircraft>Dowdall N. "'Is there a doctor on the aircraft?' Top 10 in-flight medical emergencies." ''BMJ'' 2000; '''321'''(7272):1336-7. PMID 11090520. {{PMC|1119071}}</ref>
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| == Treatment ==
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| A heart attack is a [[medical emergency]] which demands both immediate attention and activation of the [[emergency medical services]]. The ultimate goal of the management in the acute phase of the disease is to salvage as much myocardium as possible and prevent further complications. As time passes, the risk of damage to the heart muscle increases; hence the phrase that in myocardial infarction, "time is muscle," and time wasted is muscle lost.<ref name="TimeIsMuscle"/>
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| The treatments itself may have complications. If attempts to restore the blood flow are initiated after a critical period of only a few hours, the result is [[reperfusion injury]] instead of amelioration.<ref name=Faxon2005>Faxon DP. "Coronary interventions and their impact on post myocardial infarction survival." ''Clin Cardiol'' 2005; '''28'''(11 Suppl 1):I38-44. PMID 16450811</ref> Other treatment modalities may also cause complications; the use of antithrombotics for example carries an increased risk of [[bleeding]].
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| ===First line===
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| [[oxygen first aid|Oxygen]], [[aspirin]], [[glyceryl trinitrate (pharmacology)|glyceryl trinitrate]] (nitroglycerin) and [[analgesia]] (usually [[morphine]], although experts often argue this point), hence the popular [[mnemonic]] ''MONA'', ''morphine, oxygen, nitro, aspirin'') are administered as soon as possible. In many areas, first responders can be trained to administer these prior to arrival at the hospital. Morphine is classically the preferred pain relief drug due to its ability to dilate blood vessels, which aids in blood flow to the heart as well as its pain relief properties. However, morphine can also cause hypotension (usually in the setting of hypovolemia), and should be avoided in the case of right ventricular infarction. Moreover, the CRUSADE trial also demonstrated an increase in mortality with administering morphine in the setting of NSTEMI.<ref name="pmid15976786">{{cite journal |author=Meine TJ, Roe MT, Chen AY, ''et al'' |title=Association of intravenous morphine use and outcomes in acute coronary syndromes: results from the CRUSADE Quality Improvement Initiative |journal=Am Heart J |volume=149 |issue=6 |pages=1043–9 |year=2005 |pmid=15976786 |doi=10.1016/j.ahj.2005.02.010 |url=http://linkinghub.elsevier.com/retrieve/pii/S0002870305001493}}</ref>
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| Of the first line agents, only aspirin has been proven to decrease [[death|mortality]].<ref name="Lancet1988-ISIS2">{{cite journal | author=ISIS-2 Collaborative group | title=Randomized trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. | journal=Lancet | year=1988 | pages=349–60 | issue=2 | pmid=2899772}}</ref>
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| Once the diagnosis of myocardial infarction is confirmed, other pharmacologic agents are often given. These include [[beta blocker]]s,<ref name="ISIS-1">{{cite journal | author=ISIS-1 Collaborative Group | title=Randomised trial of intravenous atenolol among 16 027 cases of suspected acute myocardial infarction: ISIS-1 | journal=Lancet | year=1986 | volume=2 | issue=8498 | pages=57–66 | pmid=2873379}}</ref><ref name="TIMI-2">{{cite journal | author=The TIMI Study Group | title=Comparison of invasive and conservative strategies after treatment with intravenous tissue plasminogen activator in acute myocardial infarction. | journal=N Engl J Med | year=1989 | volume=320 | issue=10 | pages=618–27 | pmid=2563896}}</ref> anticoagulation (typically with [[heparin]]),<ref name="Antman-2004"/> and possibly additional antiplatelet agents such as [[clopidogrel]].<ref name="Antman-2004"/> These agents are typically not started until the patient is evaluated by an emergency room physician or under the direction of a cardiologist. These agents can be used regardless of the reperfusion strategy that is to be employed. While these agents can decrease mortality in the setting of an acute myocardial infarction, they can lead to complications and potentially death if used in the wrong setting.
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| ===Reperfusion===
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| The concept of reperfusion has become so central to the modern treatment of acute myocardial infarction, that we are said to be in the reperfusion era.<ref name="Reperfusion_Era_30_Day_Mortality">Lee KL, Woodlief LH, Topol EJ, et al. "Predictors of 30-Day Mortality in the Era of Reperfusion for Acute Myocardial Infarction." ''Circulation'' 1995; '''91''': 1659-1668. PMID 7882472</ref><ref name="Reperfusion_Era_PAMI">Stone GW, Grines CL, Browne KF, et al. "Predictors of in-hospital and 6-month outcome after acute myocardial infarction in the reperfusion era: the Primary Angioplasty in Myocardial Infarction (PAMI) trail." ''J Am Coll Cardiol'' 1995; '''25''': 370-377. PMID 14645641</ref> Patients who present with suspected acute myocardial infarction and ST segment elevation (STEMI) or new bundle branch block on the 12 lead [[ECG]] are presumed to have an occlusive thrombosis in an epicardial coronary artery. They are therefore candidates for immediate reperfusion, either with [[thrombolysis|thrombolytic therapy]], [[percutaneous coronary intervention]] (PCI) or when these therapies are unsuccessful, [[Coronary artery bypass surgery|bypass surgery]].
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| Individuals without ST segment elevation are presumed to be experiencing either unstable angina (UA) or non-ST segment elevation myocardial infarction (NSTEMI). They receive many of the same initial therapies and are often stabilized with [[antiplatelet drug]]s and [[Anticoagulant|anticoagulated]]. If their condition remains ([[Hemodynamics|hemodynamically]]) stable, they can be offered either late [[Coronary catheterization|coronary angiography]] with subsequent restoration of blood flow (revascularization), or [[Minimally invasive procedure|non-invasive]] [[Cardiac stress test|stress testing]] to determine if there is significant ischemia that would benefit from revascularization. If hemodynamic instability develops in individuals with NSTEMIs, they may undergo urgent coronary angiography and subsequent revascularization. The use of thrombolytic agents is contraindicated in this patient subset, however.<ref name="FTT_Lancet">"Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Fibrinolytic Therapy Trialists' (FTT) Collaborative Group." ''Lancet'' 1994; '''343'''(8893): 311-22. PMID 7905143</ref>
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| The basis for this distinction in treatment regimens is that ST segment elevations on an ECG are typically due to complete occlusion of a coronary artery. On the other hand, in NSTEMIs there is typically a sudden narrowing of a coronary artery with preserved (but diminished) flow to the distal myocardium. Anticoagulation and antiplatelet agents are given to prevent the narrowed artery from occluding.
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| At least 10% of patients with STEMI don't develop myocardial necrosis (as evidenced by a rise in cardiac markers) and subsequent Q waves on EKG after reperfusion therapy. Such a successful restoration of flow to the infarct-related artery during an acute myocardial infarction is known as "aborting" the myocardial infarction. If treated within the hour, about 25% of STEMIs can be aborted.<ref name=Verheught2006>Verheugt FW, Gersh BJ, Armstrong PW. "Aborted myocardial infarction: a new target for reperfusion therapy." ''Eur Heart J'' 2006; '''27'''(8): 901-4. PMID 16543251</ref>
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| ====Thrombolytic therapy====
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| {{Main|Thrombolysis}}
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| Thrombolytic therapy is indicated for the treatment of STEMI if the drug can be administered within 12 hours of the onset of symptoms, the patient is eligible based on exclusion criteria, and primary PCI is not immediately available.<ref name="Antman-2004"/> The effectiveness of [[thrombolysis|thrombolytic therapy]] is highest in the first 2 hours. After 12 hours, the risk associated with thrombolytic therapy outweighs any benefit.<ref name="FTT_Lancet"/><ref name="Golden_Hour_Lancet">Boersma E, Maas AC, Deckers JW, Simoons ML. "Early thrombolytic treatment in acute myocardial infarction: reappraisal of the golden hour." ''Lancet'' 1996; '''348''' (9030): 771-5. PMID 8813982</ref> Because irreversible injury occurs within 2–4 hours of the infarction, there is a limited window of time available for reperfusion to work.
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| Thrombolytic drugs are contraindicated for the treatment of unstable angina and NSTEMI<ref name="FTT_Lancet"/><ref name="TIMI_IIIB">"Effects of tissue plasminogen activator and a comparison of early invasive and conservative strategies in unstable angina and non-Q-wave myocardial infarction. Results of the TIMI IIIB Trial. Thrombolysis in Myocardial Ischemia." ''Circulation'' 1994; '''89''' (4): 1545-56. PMID 8149520</ref> and for the treatment of individuals with evidence of [[cardiogenic shock]].<ref name="Hochman-1999">{{cite journal | author=Hochman JS, Sleeper LA, Webb JG, Sanborn TA, White HD, Talley JD, Buller CE, Jacobs AK, Slater JN, Col J, McKinlay SM, LeJemtel TH. | title=Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. | journal=N Engl J Med | year=1999 | volume=341 | issue=9 | pages=625–34 | pmid=10460813}}</ref>
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| Although no perfect thrombolytic agent exists, an ideal thrombolytic drug would lead to rapid reperfusion, have a high sustained patency rate, be specific for recent thrombi, be easily and rapidly administered, create a low risk for intra-cerebral and systemic bleeding, have no antigenicity, adverse hemodynamic effects, or clinically significant drug interactions, and be cost effective.<ref name="Ideal_Thrombolytic">White HD, Van de Werf FJ. "Thrombolysis for acute myocardial infarction.." ''Circulation'' 1998; '''97''' (16): 1632-46. PMID 9593569</ref> Currently available thrombolytic agents include [[streptokinase]], [[urokinase]], and [[alteplase]] (recombinant [[tissue plasminogen activator]], rtPA). More recently, thrombolytic agents similar in structure to rtPA such as [[reteplase]] and [[tenecteplase]] have been used. These newer agents boast efficacy at least as good as rtPA with significantly easier administration. The thrombolytic agent used in a particular individual is based on institution preference and the age of the patient.
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| Depending on the thrombolytic agent being used, [[adjuvant]] anticoagulation with [[heparin]] or [[low molecular weight heparin]] may be of benefit.<ref name="GUSTO-1993-1">{{cite journal | author=The GUSTO investigators | title=An international randomized trial comparing four thrombolytic strategies for acute myocardial infarction. The GUSTO investigators. | journal=N Engl J Med | year=1993 | volume=329 | issue=10 | pages=673–82 | pmid=8204123 | doi=10.1056/NEJM199309023291001}}</ref><ref name="Sabatine-2005">{{cite journal | author=Sabatine MS, Morrow DA, Montalescot G, Dellborg M, Leiva-Pons JL, Keltai M, Murphy SA, McCabe CH, Gibson CM, Cannon CP, Antman EM, Braunwald E; Clopidogrel as Adjunctive Reperfusion Therapy (CLARITY)-Thrombolysis in Myocardial Infarction (TIMI) 28 Investigators. | title=Angiographic and clinical outcomes in patients receiving low-molecular-weight heparin versus unfractionated heparin in ST-elevation myocardial infarction treated with fibrinolytics in the CLARITY-TIMI 28 Trial. | journal=Circulation | year=2005 | volume=112 | issue=25 | pages=3846–54 | pmid=16291601 | doi = 10.1161/CIRCULATIONAHA.105.595397}}</ref> With TPa and related agents (reteplase and tenecteplase), heparin is needed to maintain coronary artery patency. Because of the anticoagulant effect of fibrinogen depletion with streptokinase<ref name="Cowley-1983">{{cite journal | author=Cowley MJ, Hastillo A, Vetrovec GW, Fisher LM, Garrett R, Hess ML. | title=Fibrinolytic effects of intracoronary streptokinase administration in patients with acute myocardial infarction and coronary insufficiency. | journal=Circulation | year=1983 | volume=67 | issue=5 | pages=1031–8 | pmid=6831667}}</ref> and urokinase<ref name="Lourenco-1989">{{cite journal | author=Lourenco DM, Dosne AM, Kher A, Samama M. | title=Effect of standard heparin and a low molecular weight heparin on thrombolytic and fibrinolytic activity of single-chain urokinase plasminogen activator ''in vitro''. | journal=Thromb Haemost | year=1989 | volume=62 | issue=3 | pages=923–6 | pmid=2556812}}</ref><ref name="Van de Werf-1986">{{cite journal | author=Van de Werf F, Vanhaecke J, de Geest H, Verstraete M, Collen D. | title=Coronary thrombolysis with recombinant single-chain urokinase-type plasminogen activator in patients with acute myocardial infarction. | journal=Circulation | year=1986 | volume=74 | issue=5 | pages=1066–70 | pmid=2429783}}</ref><ref name="Bode-1988">{{cite journal | author=Bode C, Schoenermark S, Schuler G, Zimmermann R, Schwarz F, Kuebler W. | title=Efficacy of intravenous prourokinase and a combination of prourokinase and urokinase in acute myocardial infarction. | journal=Am J Cardiol | year=1988 | volume=61 | issue=13 | pages=971–4 | pmid=2452564 | doi = 10.1016/0002-9149(88)90108-7}}</ref> treatment, it is less necessary there.<ref name="GUSTO-1993-1"/>
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| Intracranial bleeding (ICB) and subsequent [[cerebrovascular accident]] (CVA) is a serious side effect of thrombolytic use. The risk of ICB is dependent on a number of factors, including a previous episode of intracranial bleed, age of the individual, and the thrombolytic regimen that is being used. In general, the risk of ICB due to thrombolytic use for the treatment of an acute myocardial infarction is between 0.5 and 1 percent.<ref name="GUSTO-1993-1" />
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| Thrombolytic therapy to abort a myocardial infarction is not always effective. The degree of effectiveness of a thrombolytic agent is dependent on the time since the myocardial infarction began, with the best results occurring if the thrombolytic agent is used within two hours of the onset of symptoms.<ref name="Boersma-1996">{{cite journal | author=Boersma E, Maas AC, Deckers JW, Simoons ML. | title=Early thrombolytic treatment in acute myocardial infarction: reappraisal of the golden hour. | journal=Lancet | year=1996 | volume=348 | issue=9030 | pages=771–5 | pmid=8813982 | doi = 10.1016/S0140-6736(96)02514-7}}</ref><ref name="Morrison-2000"/> If the individual presents more than 12 hours after symptoms commenced, the risk of intracranial bleed are considered higher than the benefits of the thrombolytic agent.<ref name="LATE-1993">{{cite journal | author=LATE trial intestigatos. | title=Late Assessment of Thrombolytic Efficacy (LATE) study with alteplase 6-24 hours after onset of acute myocardial infarction. | journal=Lancet | year=1993 | volume=342 | issue=8874 | pages=759–66 | pmid=8103874 | doi=10.1016/0140-6736(93)91538-W}}</ref> Failure rates of thrombolytics can be as high as 20% or higher.<ref name="Chesebro-1987">{{cite journal | author=Chesebro JH, Knatterud G, Roberts R, Borer J, Cohen LS, Dalen J, Dodge HT, Francis CK, Hillis D, Ludbrook P, et al. | title=Thrombolysis in Myocardial Infarction (TIMI) Trial, Phase I: A comparison between intravenous tissue plasminogen activator and intravenous streptokinase. Clinical findings through hospital discharge | journal=Circulation | year=1987| volume=76 | issue=1 | pages=142–54 | pmid=3109764}}</ref> In cases of failure of the thrombolytic agent to open the infarct-related coronary artery, the patient is then either treated conservatively with anticoagulants and allowed to "complete the infarction" or [[percutaneous coronary intervention]] (PCI, see below) is then performed. Percutaneous coronary intervention in this setting is known as "rescue PCI" or "salvage PCI". Complications, particularly bleeding, are significantly higher with rescue PCI than with primary PCI due to the action of the thrombolytic agent.
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| ====Percutaneous coronary intervention====
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| {{main|Percutaneous coronary intervention}}
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| [[Image:Intracoronary thrombus.png|right|thumb|350px|[[Thrombus]] material (in a cup, upper left corner) removed from a coronary artery during a [[percutaneous coronary intervention]] to abort a myocardial infarction. Five pieces of thrombus are shown (arrow heads).]]
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| The benefit of prompt, expertly performed primary percutaneous coronary intervention over thrombolytic therapy for acute ST elevation myocardial infarction is now well established.<ref name="Keeley-2003">{{cite journal | author=Keeley EC, Boura JA, Grines CL. | title=Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. | journal=Lancet | year=2003 | volume=361 | issue=9351 | pages=13–20 | pmid=12517460 | doi = 10.1016/S0140-6736(03)12113-7}}</ref><ref name="Grines-1993">{{cite journal | author=Grines CL, Browne KF, Marco J, Rothbaum D, Stone GW, O'Keefe J, Overlie P, Donohue B, Chelliah N, Timmis GC, et al. | title=A comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction. The Primary Angioplasty in Myocardial Infarction Study Group. | journal=N Engl J Med | year=1993 | volume=328 | issue=10 | pages=673–9 | pmid=8433725 | doi = 10.1056/NEJM199303113281001}}</ref><ref name="GUSTO-IIb">{{cite journal | author=The Global Use of Strategies to Open Occluded Coronary Arteries in Acute Coronary Syndromes (GUSTO IIb) Angioplasty Substudy Investigators. | title=A clinical trial comparing primary coronary angioplasty with tissue plasminogen activator for acute myocardial infarction. | journal=N Engl J Med | year=1997 | volume=336 | issue=23 | pages=1621–8 | pmid=9173270 | doi=10.1056/NEJM199706053362301}}</ref> When performed rapidly by an experienced team, primary PCI restores flow in the culprit artery in more than 95% of patients.<ref name="Keeley-2003"/> Logistic and economic obstacles seem to hinder a more widespread application of [[angioplasty|percutaneous coronary intervention]] (PCI) via [[cardiac catheterization]],<ref name=Boersma2006>Boersma E; The Primary Coronary Angioplasty vs. Thrombolysis Group. "Does time matter? A pooled analysis of randomized clinical trials comparing primary percutaneous coronary intervention and in-hospital fibrinolysis in acute myocardial infarction patients." ''Eur Heart J'' 2006; '''27'''(7):779-88. PMID 16513663</ref> although the feasibility of regionalized PCI for STEMI is currently being explored in the United States.<ref name=Rokos_2006>Rokos IC, Larson DM, Henry TD, et al.; "Rationale for establishing regional ST-elevation myocardial infarction receiving center (SRC) networks." ''Am Heart J'' 2006; '''152'''(4):661-7. PMID 16996830</ref> The use of percutaneous coronary intervention as a therapy to abort a myocardial infarction is known as primary PCI. The goal of primary PCI is to open the artery as soon as possible, and preferably within 90 minutes of the patient presenting to the emergency room. This time is referred to as the [[door-to-balloon]] time. Few hospitals can provide PCI within the 90 minute interval,<ref name=Doortoballoon>Bradley EH, Herrin J, Wang Y, Barton BA, Webster TR, Mattera JA, Roumanis SA, Curtis JP, Nallamothu BK, Magid DJ, McNamara RL, Parkosewich J, Loeb JM, Krumholz HM. "Strategies for reducing the door-to-balloon time in acute myocardial infarction." ''N Engl J Med'' 2006; '''355'''(22): 2308-20. PMID 17101617</ref> which prompted the American College of Cardiology (ACC) to launch a national Door to Balloon (D2B) Initiative in November of 2006. Over 800 hospitals have joined the D2B Alliance as of March 16, 2007.<ref name="ACC-D2B">{{cite web | title=D2B: An Alliance for Quality | publisher=American College of Cardiology | date=2006 | url=http://d2b.acc.org/ | accessmonthday=April 15 | accessyear=2007}}</ref>
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| One particularly successful implementation of a primary PCI protocol is in the [[Calgary Health Region]] under the auspices of the [[Libin Cardiovascular Institute of Alberta]]. Under this model, EMS teams responding to an emergency electronically transmit the ECG directly to a digital archiving system that allows emergency room physicians and/or cardiologists to immediately confirm the diagnosis. This in-turn allows for redirection of the EMS teams to facilities prepped to conduct time-critical angioplasty, based on the ECG analysis. In an article published in the [[Canadian Medical Association Journal]] in June of 2007, the Calgary implementation resulted in a median time to treatment of 62 minutes.<ref name="De Villiers-2007">{{cite journal | author = De Villiers JS, Anderson T, McMeekin JD, ''et al''. | title = Expedited transfer for primary percutaneous coronary intervention: a program evaluation | journal = CMAJ | volume = 176 | pages = 1833–8 | year = 2007 | pmid = 17576980}}</ref>
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| The current guidelines in the United States restrict primary PCI to hospitals with available emergency bypass surgery as a backup,<ref name="Antman-2004"/> but this is not the case in other parts of the world.<ref name="Aversano-2001">{{cite journal | author = Aversano T ''et al''. | title = Thrombolytic therapy vs primary percutaneous coronary intervention for myocardial infarction in patients presenting to hospitals without on-site cardiac surgery: a randomized controlled trial | journal = JAMA | volume = 287 | issue = 15 | pages = 1943–51 | year = 2002 | pmid = 11960536 | doi = 10.1001/jama.287.15.1943}}</ref>
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| Primary PCI involves performing a coronary [[angiogram]] to determine the anatomical location of the infarcting vessel, followed by balloon [[angioplasty]] (and frequently deployment of an intracoronary stent) of the thrombosed arterial segment. In some settings, an extraction catheter may be used to attempt to aspirate (remove) the thrombus prior to balloon angioplasty. While the use of intracoronary [[stent]]s do not improve the short term outcomes in primary PCI, the use of stents is widespread because of the decreased rates of procedures to treat restenosis compared to balloon angioplasty.<ref name="Grines-1999">{{cite journal | author=Grines CL, Cox DA, Stone GW, Garcia E, Mattos LA, Giambartolomei A, Brodie BR, Madonna O, Eijgelshoven M, Lansky AJ, O'Neill WW, Morice MC. | title=Coronary angioplasty with or without stent implantation for acute myocardial infarction. Stent Primary Angioplasty in Myocardial Infarction Study Group. | journal=N Engl J Med | year=1999 | volume=341 | issue=26 | pages=1949–56 | pmid=10607811}}</ref>
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| Adjuvant therapy during primary PCI include intravenous [[heparin]], [[aspirin]], and [[clopidogrel]]. The use of [[glycoprotein IIb/IIIa inhibitor]]s are often used in the setting of primary PCI to reduce the risk of ischemic complications during the procedure.<ref name="Brener-1998">{{cite journal | author=Brener SJ, Barr LA, Burchenal JE, Katz S, George BS, Jones AA, Cohen ED, Gainey PC, White HJ, Cheek HB, Moses JW, Moliterno DJ, Effron MB, Topol EJ. | title=Randomized, placebo-controlled trial of platelet glycoprotein IIb/IIIa blockade with primary angioplasty for acute myocardial infarction. ReoPro and Primary PTCA Organization and Randomized Trial (RAPPORT) Investigators. | journal=Circulation | year=1998 | volume=98 | issue=8 | pages=734–41 | pmid=9727542}}</ref><ref name="Tcheng-2003-1">{{cite journal | author=Tcheng JE, Kandzari DE, Grines CL, Cox DA, Effron MB, Garcia E, Griffin JJ, Guagliumi G, Stuckey T, Turco M, Fahy M, Lansky AJ, Mehran R, Stone GW; CADILLAC Investigators. | title=Benefits and risks of abciximab use in primary angioplasty for acute myocardial infarction: the Controlled Abciximab and Device Investigation to Lower Late Angioplasty Complications (CADILLAC) trial. | journal=Circulation | year=2003 | volume=108 | issue=11 | pages=1316–23 | pmid=12939213 | doi = 10.1161/01.CIR.0000087601.45803.86}}</ref> Due to the number of antiplatelet agents and anticoagulants used during primary PCI, the risk of bleeding associated with the procedure are higher than during an elective PCI.<ref>{{cite book |title=900 Questions: An Interventional Cardiology Board Review |last=Mukherjee |first=Debabrata |year=2006 |publisher=Lippincott Williams & Wilkins |isbn=0781773490 }} </ref>
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| ====Coronary artery bypass surgery====
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| {{Main|Coronary artery bypass graft surgery}}
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| [[Image:Coronary artery bypass surgery Image 657B-PH.jpg|thumb|right|300px|'''Coronary artery bypass surgery''' during mobilization (freeing) of the [[right coronary artery]] from its surrounding tissue, [[adipose tissue]] (yellow). The tube visible at the bottom is the aortic cannula (returns blood from the [[Heart-lung machine|HLM]]). The tube above it (obscured by the [[cardiac surgeon|surgeon]] on the right) is the venous cannula (receives blood from the body). The patient's [[heart]] is stopped and the [[aorta]] is cross-clamped. The patient's head (not seen) is at the bottom.]]
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| Despite the guidelines, emergency bypass surgery for the treatment of an acute myocardial infarction (MI) is less common then PCI or medical management. In an analysis of patients in the U.S. [[National Registry of Myocardial Infarction]] (NRMI) from January 1995 to May 2004, the percentage of patients with [[cardiogenic shock]] treated with primary PCI rose from 27.4% to 54.4%, while the increase in CABG treatment was only from 2.1% to 3.2%.<ref name=NRMI>Babaev A, Frederick PD, Pasta DJ, Every N, Sichrovsky T, Hochman JS; NRMI Investigators. "Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock." ''JAMA'' 2005; 294(4): 448-54. PMID 16046651</ref>
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| Emergency coronary artery bypass graft surgery (CABG) is usually undertaken to simultaneously treat a mechanical complication, such as a ruptured papillary muscle, or a ventricular septal defect, with ensueing cardiogenic shock.<ref name=Sabiston>{{cite book | last =Townsend | first =Courtney M. | coauthors =Beauchamp D.R., Evers M.B., Mattox K.L. | title =Sabiston Textbook of Surgery - The Biological Basis of Modern Surgical Practice | publisher =Elsevier Saunders | date =2004 | location =Philadelphia, Pennsylvania | pages =1871 | url =http://www.elsevier.com/wps/find/bookdescription.cws_home/701163/description#description | id =ISBN 0-7216-0409-9}}</ref> In uncomplicated MI, the [[mortality rate]] can be high when the surgery is performed immediately following the infarction.<ref name=Timing1>Kaul TK, Fields BL, Riggins SL, Dacumos GC, Wyatt DA, Jones CR. "Coronary artery bypass grafting within 30 days of an acute myocardial infarction." ''Ann Thorac Surg'' 1995; '''59(5)''': 1169-76. PMID 7733715</ref> If this option is entertained, the patient should be stabilized prior to surgery, with supportive interventions such as the use of an [[intra-aortic balloon pump]].<ref name=Timing2>Creswell LL, Moulton MJ, Cox JL, Rosenbloom M. "Revascularization after acute myocardial infarction." ''Ann Thorac Surg'' 1995; '''60(1)''': 19-26. PMID 7598589</ref> In patients developing cardiogenic shock after a myocardial infarction, both PCI and CABG are satisfactory treatment options, with similar survival rates.<ref name=SHOCK>White HD, Assmann SF, Sanborn TA, Jacobs AK, Webb JG, Sleeper LA, Wong CK, Stewart JT, Aylward PE, Wong SC, Hochman JS. "Comparison of percutaneous coronary intervention and coronary artery bypass grafting after acute myocardial infarction complicated by cardiogenic shock: results from the Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock (SHOCK) trial." ''Circulation'' 2005; '''112(13)''': 1992-2001. PMID 16186436</ref><ref name="Hochman-2006">{{cite journal | author=Hochman JS, Sleeper LA, Webb JG, Dzavik V, Buller CE, Aylward P, Col J, White HD; SHOCK Investigators. | title=Early revascularization and long-term survival in cardiogenic shock complicating acute myocardial infarction. | journal=JAMA | year=2006 | volume=295 | issue=21 | pages=2511–5 | pmid=16757723 | doi = 10.1001/jama.295.21.2511}}</ref>
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| Coronary artery bypass surgery involves an artery or vein from the patient being implanted to bypass [[stenosis|narrowings]] or occlusions on the coronary arteries. Several arteries and veins can be used, however [[internal mammary artery]] grafts have demonstrated significantly better long-term patency rates than [[great saphenous vein]] grafts.<ref name=Raja2004>Raja SG, Haider Z, Ahmad M, Zaman H. "Saphenous vein grafts: to use or not to use?" ''Heart Lung Circ'' 2004; '''13'''(4): 403-9. PMID 16352226</ref> In patients with two or more coronary arteries affected, bypass surgery is associated with higher long-term [[survival rate]]s compared to percutaneous interventions.<ref name=Hannan2005>Hannan EL, Racz MJ, Walford G, Jones RH, Ryan TJ, Bennett E, Culliford AT, Isom OW, Gold JP, Rose EA. "Long-term outcomes of coronary-artery bypass grafting versus stent implantation." ''N Engl J Med'' 2005; '''352'''(21): 2174-83. PMID 15917382</ref> In patients with single vessel disease, surgery is comparably safe and effective, and may be a treatment option in selected cases.<ref name=Bourassa2000>Bourassa MG. "Clinical trials of coronary revascularization: coronary angioplasty vs. coronary bypass grafting." ''Curr Opin Cardiol'' 2000; '''15'''(4):281-6. PMID 11139092</ref> Bypass surgery has higher costs initially, but becomes [[Cost-effectiveness|cost-effective]] in the long term.<ref name=Hlatky2004>Hlatky MA, Boothroyd DB, Melsop KA, Brooks MM, Mark DB, Pitt B, Reeder GS, Rogers WJ, Ryan TJ, Whitlow PL, Wiens RD. "Medical costs and quality of life 10 to 12 years after randomization to angioplasty or bypass surgery for multivessel coronary artery disease.";; ''Circulation'' 2004; '''110'''(14):1960-6. PMID 15451795</ref> A surgical bypass graft is more [[Invasive (medical)|invasive]] initially but bears less risk of recurrent procedures (but these may be again [[Minimally invasive procedure|minimally invasive]]).<ref name=Bourassa2000/>
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| ===Monitoring for arrhythmias===
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| Additional objectives are to prevent life-threatening arrhythmias or conduction disturbances. This requires monitoring in a [[coronary care unit]] and protocolised administration of [[antiarrhythmic agent]]s. Antiarrhythmic agents are typically only given to individuals with life-threatening arrhythmias after a myocardial infarction and not to suppress the [[premature ventricular contraction|ventricular ectopy]] that is often seen after a myocardial infarction.<ref name="Echt-1991">{{cite journal | author=Echt DS, Liebson PR, Mitchell LB, Peters RW, Obias-Manno D, Barker AH, Arensberg D, Baker A, Friedman L, Greene HL, ''et al.'' | title= Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial. | journal= N Engl J Med | year= 1991 | volume= 324 | issue= 12 | pages= 781–8 | pmid=1900101}}</ref><ref name="Waldo-1996">{{cite journal | author=Waldo AL, Camm AJ, deRuyter H, Friedman PL, MacNeil DJ, Pauls JF, Pitt B, Pratt CM, Schwartz PJ, Veltri EP. | title=Effect of d-sotalol on mortality in patients with left ventricular dysfunction after recent and remote myocardial infarction. The SWORD Investigators. Survival With Oral d-Sotalol. | journal=Lancet | year=1996 | volume=348 | issue=9019 | pages=7–12 | pmid=8691967 | doi = 10.1016/S0140-6736(96)02149-6}}</ref><ref name="Julian-1997">{{cite journal | author= Julian DG, Camm AJ, Frangin G, Janse MJ, Munoz A, Schwartz PJ, Simon P. | title= Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT. European Myocardial Infarct Amiodarone Trial Investigators. | journal= Lancet | year= 1997 | volume= 349 | issue= 9053 | pages= 667–74 | pmid=9078197 | doi = 10.1016/S0140-6736(96)09145-3}}</ref>
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| ===Rehabilitation===
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| [[Cardiopulmonary rehabilitation|Cardiac rehabilitation]] aims to optimize function and [[quality of life]] in those afflicted with a heart disease. This can be with the help of a physician, or in the form of a cardiac rehabilitation program.<ref name=NHLBIrecovery>[http://www.nhlbi.nih.gov/health/dci/Diseases/HeartAttack/HeartAttack_LivingWith.html Life after a Heart Attack]. U.S. [[National Heart, Lung and Blood Institute]]. Retrieved December 2, 2006.</ref>
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| [[Physical exercise]] is an important part of [[Physical medicine and rehabilitation|rehabilitation]] after a myocardial infarction, with beneficial effects on cholesterol levels, blood pressure, weight, [[Stress (medicine)|stress]] and [[Mood (psychology)|mood]].<ref name=NHLBIrecovery/> Some patients become afraid of exercising because it might trigger another infarct.<ref name=BBCrecovery>Trisha Macnair. [http://www.bbc.co.uk/health/conditions/heartattackrecovery1.shtml Recovering after a heart attack]. [[BBC]], December 2005. Retrieved December 2, 2006.</ref> Patients are stimulated to exercise, and should only avoid certain exerting activities such as shovelling. Local authorities may place limitations on [[driving]] [[Motor vehicle|motorised vehicles]].<ref name="NovaScotia-DrivingRegulations">{{cite web | title=Classification of Drivers' Licenses Regulations | publisher=Nova Scotia Registry of Regulations | date=May 24, 2000 | url=http://www.gov.ns.ca/just/regulations/regs/mvclasdl.htm | accessmonthday=April 22 | accessyear=2007}}</ref> Some people are afraid to have [[Human sexual behavior|sex]] after a heart attack. Most people can resume sexual activities after 3 to 4 weeks. The amount of activity needs to be dosed to the patient's possibilities.<ref name=familyphysician>"[http://familydoctor.org/002.xml Heart Attack: Getting Back Into Your Life After a Heart Attack]". [[American Academy of Family Physicians]], updated March 2005. Retrieved December 4, 2006.</ref>
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| ===Secondary prevention===
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| The risk of a recurrent myocardial infarction decreases with strict blood pressure management and lifestyle changes, chiefly [[smoking cessation]], regular [[Physical exercise|exercise]], a sensible [[Diet and heart disease|diet for patients with heart disease]], and [[Alcoholic beverages — recommended maximum intake|limitation of alcohol intake]].
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| Patients are usually commenced on several long-term medications post-MI, with the aim of preventing secondary cardiovascular events such as further myocardial infarctions, [[congestive heart failure]] or [[cerebrovascular accident]] (CVA). Unless contraindicated, such medications may include:<ref>Smith A, Aylward P, Campbell T, ''et al.'' Therapeutic Guidelines: Cardiovascular, 4th edition. North Melbourne: Therapeutic Guidelines; 2003. ISSN 1327-9513</ref><ref name=Rossi/>
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| * [[Antiplatelet drug]] therapy such as [[aspirin]] and/or [[clopidogrel]] should be continued to reduce the risk of plaque rupture and recurrent myocardial infarction. Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk of cardiovascular events, however the risk of [[hemorrhage]] is increased.<ref name="Peters-2003">{{cite journal | author=Peters RJ, Mehta SR, Fox KA, Zhao F, Lewis BS, Kopecky SL, Diaz R, Commerford PJ, Valentin V, Yusuf S; Clopidogrel in Unstable angina to prevent Recurrent Events (CURE) Trial Investigators. | title=Effects of aspirin dose when used alone or in combination with clopidogrel in patients with acute coronary syndromes: observations from the Clopidogrel in Unstable angina to prevent Recurrent Events (CURE) study. | journal=Circulation | year=2003 | volume= 108 | issue=14 | pages=1682–7 | pmid=14504182 | doi = 10.1161/01.CIR.0000091201.39590.CB}}</ref>
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| * [[Beta blocker]] therapy such as [[metoprolol]] or [[carvedilol]] should be commenced.<ref name=Yusuf>Yusuf S, Peto R, Lewis J, Collins R, Sleight P. Beta blockade during and after myocardial infarction: an overview of the randomized trials. ''Prog Cardiovasc Dis'' 1985;'''27''':335-71. PMID 2858114</ref> These have been particularly beneficial in high-risk patients such as those with [[left ventricle|left ventricular]] dysfunction and/or continuing cardiac [[ischaemia]].<ref name="Dargie-2001">{{cite journal | author=Dargie HJ. | title=Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial. | journal=Lancet | year=2001 | volume=357 | issue=9266 | pages=1385–90 | pmid=11356434 | doi=10.1016/S0140-6736(00)04560-8}}</ref> β-Blockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in NSTEMI.
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| * [[ACE inhibitor]] therapy should be commenced 24–48 hours post-MI in hemodynamically-stable patients, particularly in patients with a history of MI, [[diabetes mellitus]], [[hypertension]], [[anterior]] location of infarct (as assessed by ECG), and/or evidence of left ventricular dysfunction. ACE inhibitors reduce mortality, the development of [[heart failure]], and decrease ventricular remodelling post-MI.<ref name="Pfeffer-1992">{{cite journal | author=Pfeffer MA, Braunwald E, Moye LA, Basta L, Brown EJ Jr, Cuddy TE, Davis BR, Geltman EM, Goldman S, Flaker GC, et al | title=Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. The SAVE Investigators. | journal=N Engl J Med. | year= 1992 | volume= 327 | issue= 10 | pages= 669–77 | pmid=1386652}}</ref>
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| * [[Statin]] therapy has been shown to reduce mortality and morbidity post-MI.<ref name="Sacks-1996">{{cite journal | author=Sacks FM, Pfeffer MA, Moye LA, Rouleau JL, Rutherford JD, Cole TG, Brown L, Warnica JW, Arnold JM, Wun CC, Davis BR, Braunwald E. | title=The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events Trial investigators. | journal=N Engl J Med | year=1996 | volume=335 | issue=14 | pages=1001–9 | pmid=8801446 | doi = 10.1056/NEJM199610033351401}}</ref><ref name="Sacks-1998">{{cite journal | author=Sacks FM, Moye LA, Davis BR, Cole TG, Rouleau JL, Nash DT, Pfeffer MA, Braunwald E. | title=Relationship between plasma LDL concentrations during treatment with pravastatin and recurrent coronary events in the Cholesterol and Recurrent Events trial. | journal=Circulation | year=1998 | volume=97 | issue=15 | pages=1446–52 | pmid=9576424}}</ref> The effects of statins may be more than their LDL lowering effects. The general consensus is that statins have [[Atheroma|plaque]] stabilization and multiple other ("pleiotropic") effects that may prevent myocardial infarction in addition to their effects on blood lipids.<ref name=Ray2005>Ray KK, Cannon CP. "The potential relevance of the multiple lipid-independent (pleiotropic) effects of statins in the management of acute coronary syndromes." ''J Am Coll Cardiol'' 2005;'''46'''(8):1425-33. PMID 16226165</ref>
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| * The [[aldosterone antagonist]] agent [[eplerenone]] has been shown to further reduce risk of cardiovascular death post-MI in patients with heart failure and left ventricular dysfunction, when used in conjunction with standard therapies above.<ref name=Pitt>{{cite journal | author = Keating G, Plosker G | title = Eplerenone: a review of its use in left ventricular systolic dysfunction and heart failure after acute myocardial infarction. | journal = Drugs | volume = 64 | issue = 23 | pages = 2689–707 | year = 2004 | pmid = 15537370 | doi = 10.1157/13089615}}</ref>
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| * [[Omega-3 fatty acid]]s, commonly found in fish, have been shown to reduce mortality post-MI.<ref name="GISSI-Prevenzione-2001">{{cite journal | title=Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto miocardico. | journal=Lancet | year=2001 | volume=354 | issue=9177 | pages=447–55 | pmid=10465168 | doi=10.1016/S0140-6736(99)07072-5}}</ref> While the mechanism by which these fatty acids decrease mortality is unknown, it has been postulated that the survival benefit is due to electrical stabilization and the prevention of [[ventricular fibrillation]].<ref name="Leaf-2005">{{cite journal | author = Leaf A, Albert C, Josephson M, Steinhaus D, Kluger J, Kang J, Cox B, Zhang H, Schoenfeld D | title = Prevention of fatal arrhythmias in high-risk subjects by fish oil n-3 fatty acid intake | journal = Circulation | volume = 112 | issue = 18 | pages = 2762–8 | year = 2005 | pmid = 16267249 | url = http://circ.ahajournals.org/cgi/content/full/112/18/2762 | doi = 10.1161/CIRCULATIONAHA.105.549527}}</ref> However, further studies in a high-risk subset have not shown a clear-cut decrease in potentially fatal arrhythmias due to omega-3 fatty acids.<ref name="Brouwer-2006">{{cite journal | author=Brouwer IA, Zock PL, Camm AJ, Bocker D, Hauer RN, Wever EF, Dullemeijer C, Ronden JE, Katan MB, Lubinski A, Buschler H, Schouten EG; SOFA Study Group. | title=Effect of fish oil on ventricular tachyarrhythmia and death in patients with implantable cardioverter defibrillators: the Study on Omega-3 Fatty Acids and Ventricular Arrhythmia (SOFA) randomized trial. | journal=JAMA | year=2006 | volume=295 | issue=22 | pages=2613–9 | pmid=16772624 | doi = 10.1001/jama.295.22.2613}}</ref><ref name="Raitt-2005">{{cite journal | author=Raitt MH, Connor WE, Morris C, Kron J, Halperin B, Chugh SS, McClelland J, Cook J, MacMurdy K, Swenson R, Connor SL, Gerhard G, Kraemer DF, Oseran D, Marchant C, Calhoun D, Shnider R, McAnulty J. | title=Fish oil supplementation and risk of ventricular tachycardia and ventricular fibrillation in patients with implantable defibrillators: a randomized controlled trial. | journal=JAMA | year=2005 | volume=293 | issue=23 | pages=2284–91 | pmid=15956633 | doi = 10.1001/jama.293.23.2884}}</ref>
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| ===New therapies under investigation===
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| Patients who receive [[Stem cell treatments|stem cell treatment]] by [[coronary artery]] injections of [[Adult stem cell|stem cells]] derived from their own [[bone marrow]] after a myocardial infarction (MI) show improvements in left ventricular [[ejection fraction]] and [[end-diastolic volume]] not seen with [[placebo]]. The larger the initial infarct size, the greater the effect of the infusion. [[Clinical trial]]s of [[progenitor cell]] infusion as a treatment approach to ST elevation MI are proceeding.<ref name=REPAIR2006>{{cite journal | author = Schachinger V, Erbs S, Elsasser A, Haberbosch W, Hambrecht R, Holschermann H, Yu J, Corti R, Mathey DG, Hamm CW, Suselbeck T, Assmus B, Tonn T, Dimmeler S, Zeiher AM; REPAIR-AMI Investigators | title = Intracoronary bone marrow-derived progenitor cells in acute myocardial infarction | year = 2006 | journal = N Engl J Med | volume = 355 | issue = 12 | pages = 1210–21 | pmid = 16990384 | doi = 10.1056/NEJMoa060186}}</ref>
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| There are currently 3 [[biomaterial]] and [[tissue engineering]] approaches for the treatment of MI, but these are in an even earlier stage of [[medical research]], so many questions and issues need to be addressed before they can be applied to patients. The first involves [[polymer]]ic left ventricular restraints in the prevention of [[heart failure]]. The second utilizes ''[[in vitro]]'' engineered cardiac tissue, which is subsequently implanted ''[[in vivo]]''. The final approach entails injecting cells and/or a scaffold into the myocardium to create ''[[in situ]]'' engineered cardiac tissue.<ref name=biomaterials2006>Christman KL, Lee RJ. "Biomaterials for the Treatment of Myocardial Infarction". ''J Am Coll Cardiol'' 2006; '''48'''(5): 907-13. PMID 16949479</ref>
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| ==Complications==
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| Complications may occur immediately following the heart attack (in the [[Acute (medical)|acute]] phase), or may need time to develop (a [[Chronic (medicine)|chronic]] problem). After an infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct.
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| ===Congestive heart failure===
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| {{Main|Congestive heart failure}}
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| A myocardial infarction may compromise the function of the heart as a pump for the [[Circulatory system|circulation]], a state called [[heart failure]]. There are different types of heart failure; left- or right-sided (or bilateral) heart failure may occur depending on the affected part of the heart, and it is a low-output type of failure. If one of the heart valves is affected, this may cause dysfunction, such as [[mitral regurgitation]] in the case of left-sided coronary occlusion that disrupts the blood supply of the papillary muscles. The incidence of heart failure is particularly high in patients with diabetes and requires special management strategies.<ref name="Canto-2000">{{cite journal | author=Canto JG, Shlipak MG, Rogers WJ, Malmgren JA, Frederick PD, Lambrew CT, Ornato JP, Barron HV, Kiefe CI. | title=Prevalence, clinical characteristics, and mortality among patients with myocardial infarction presenting without chest pain. | journal=JAMA | year=2000 | volume=283 | issue=24 | pages=3223–9 | pmid=10866870 | doi = 10.1001/jama.283.24.3223}}</ref>
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| ===Myocardial rupture===
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| {{Main|Myocardial rupture}}
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| [[Myocardial rupture]] is most common three to five days after myocardial infarction, commonly of small degree, but may occur one day to three weeks later. In the modern era of early revascularization and intensive pharmacotherapy as treatment for MI, the incidence of myocardial rupture is about 1% of all MIs.<ref name="Yip-2003">{{cite journal | author=Yip HK, Wu CJ, Chang HW, Wang CP, Cheng CI, Chua S, Chen MC. | title=Cardiac rupture complicating acute myocardial infarction in the direct percutaneous coronary intervention reperfusion era. | journal=Chest | year=2003 | volume=124 | issue=2 | pages=565–71 | format=[[PDF]] | url=http://www.chestjournal.org/cgi/reprint/124/2/565.pdf | pmid=12907544 | doi = 10.1378/chest.124.2.565}}</ref> This may occur in the free walls of the [[ventricles]], the [[septum]] between them, the [[papillary muscles]], or less commonly the [[atria]]. Rupture occurs because of increased pressure against the weakened walls of the heart chambers due to heart muscle that cannot pump blood out effectively. The weakness may also lead to ventricular [[aneurysm]], a localized dilation or ballooning of the heart chamber.
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| Risk factors for myocardial rupture include completion of infarction (no revascularization performed), female sex, advanced age, and a lack of a previous history of myocardial infarction.<ref name="Yip-2003"/> In addition, the risk of rupture is higher in individuals who are revascularized with a thrombolytic agent than with PCI.<ref name="Becker-1996">{{cite journal | author=Becker RC, Gore JM, Lambrew C, Weaver WD, Rubison RM, French WJ, Tiefenbrunn AJ, Bowlby LJ, Rogers WJ. | title=A composite view of cardiac rupture in the United States National Registry of Myocardial Infarction. | journal=J Am Coll Cardiol | year=1996 | volume=27 | issue=6 | pages=1321–6 | pmid=8626938 | doi = 10.1016/0735-1097(96)00008-3}}</ref><ref name="Moreno-2002">{{cite journal | author=Moreno R, Lopez-Sendon J, Garcia E, Perez de Isla L, Lopez de Sa E, Ortega A, Moreno M, Rubio R, Soriano J, Abeytua M, Garcia-Fernandez MA. | title=Primary angioplasty reduces the risk of left ventricular free wall rupture compared with thrombolysis in patients with acute myocardial infarction. | journal=J Am Coll Cardiol | year=2002 | volume=39 | issue=4 | pages=598–603 | pmid=11849857 | doi = 10.1016/S0735-1097(01)01796-X}}</ref> The shear stress between the infarcted segment and the surrounding normal myocardium (which may be hypercontractile in the post-infarction period) makes it a nidus for rupture.<ref name="Shin-1983">{{cite journal | author=Shin P, Sakurai M, Minamino T, Onishi S, Kitamura H. | title=Postinfarction cardiac rupture. A pathogenetic consideration in eight cases. | journal=Acta Pathol Jpn | year=1983 | volume=33 | issue=5 | pages=881–93 | pmid=6650169}}</ref>
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| Rupture is usually a catastrophic event that may result a life-threatening process known as [[cardiac tamponade]], in which blood accumulates within the [[pericardium]] or heart sac, and compresses the heart to the point where it cannot pump effectively. Rupture of the intraventricular septum (the muscle separating the left and right ventricles) causes a [[ventricular septal defect]] with [[Shunt (medical)|shunting]] of blood through the defect from the left side of the heart to the right side of the heart, which can lead to right ventricular failure as well as pulmonary overcirculation. Rupture of the papillary muscle may also lead to acute [[mitral regurgitation]] and subsequent [[pulmonary edema]] and possibly even [[cardiogenic shock]].
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| ===Life-threatening arrhythmia===
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| [[Image:Electrocardiogram of Ventricular Tachycardia.png|right|thumb|300px|A 12 lead [[electrocardiogram]] showing ventricular tachycardia.]]
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| Since the electrical characteristics of the infarcted tissue change (see [[Myocardial infarction#Pathophysiology|pathophysiology section]]), [[arrhythmias]] are a frequent complication.<ref>{{cite book |title=Cardiac Arrhythmia: Mechanisms, Diagnosis, and Management |last=Podrid |first=Philip J. |coauthors=Peter R. Kowey |year=2001 |publisher=Lippincott Williams & Wilkins |isbn=0781724864 }}</ref> The re-entry phenomenon may cause rapid heart rates ([[ventricular tachycardia]] and even [[ventricular fibrillation]]), and ischemia in the [[electrical conduction system of the heart]] may cause a [[Third degree heart block|complete heart block]] (when the impulse from the [[sinoatrial node]], the normal cardiac pacemaker, does not reach the heart chambers).<ref>{{cite book |title=Fundamental Approaches to the Management of Cardiac Arrhythmias |last=Sung |first=Ruey J. |coauthors=Michael R. Lauer |year=2000 |publisher=Springer |isbn=0792365593 }}</ref><ref>{{cite book |title=Clinical Cardiac Electrophysiology: Techniques and Interpretations |last=Josephson |first=Mark E. |year=2002 |publisher=Lippincott Williams & Wilkins |isbn=0683306936 }}</ref>
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| ===Pericarditis===
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| {{Main|Pericarditis}}
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| As a reaction to the damage of the heart muscle, [[Inflammation|inflammatory]] cells are attracted. The inflammation may reach out and affect the heart sac. This is called [[pericarditis]]. In [[Dressler's syndrome]], this occurs several weeks after the initial event.
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| ===Cardiogenic shock===
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| A complication that may occur in the acute setting soon after a myocardial infarction or in the weeks following it is [[cardiogenic shock]]. Cardiogenic shock is defined as a hemodynamic state in which the heart cannot produce enough of a [[cardiac output]] to supply an adequate amount of oxygenated blood to the tissues of the body.
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| While the data on performing interventions on individuals with cardiogenic shock is sparse, trial data suggests a long-term mortality benefit in undergoing revascularization if the individual is less than 75 years old and if the onset of the acute myocardial infarction is less than 36 hours and the onset of cardiogenic shock is less than 18 hours.<ref name="Hochman-1999" /> If the patient with cardiogenic shock is not going to be revascularized, aggressive hemodynamic support is warranted, with insertion of an [[intra-aortic balloon pump]] if not contraindicated.<ref name="Hochman-1999" /> If diagnostic coronary angiography does not reveal a culprit blockage that is the cause of the cardiogenic shock, the prognosis is poor.<ref name="Hochman-1999" />
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| ==Prognosis==
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| The prognosis for patients with myocardial infarction varies greatly, depending on the patient, the condition itself and the given treatment. Using simple [[variable]]s which are immediately available in the [[emergency room]], patients with a higher risk of adverse outcome can be identified. For example, one study found that 0.4% of patients with a low risk profile had died after 90 days, whereas the [[mortality rate]] in high risk patients was 21.1%.<ref name="PEPA">Lopez de Sa E, Lopez-Sendon J, Anguera I, Bethencourt A, Bosch X; Proyecto de Estudio del Pronostico de la Angina (PEPA) Investigators. "Prognostic value of clinical variables at presentation in patients with non-ST-segment elevation acute coronary syndromes: results of the Proyecto de Estudio del Pronostico de la Angina (PEPA)." ''Medicine (Baltimore)'' 2002; '''81'''(6): 434-42. PMID 12441900</ref>
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| Although studies differ in the identified variables, some of the more [[Reproducibility|reproduced]] risk stratifiers include age, [[Hemodynamics|hemodynamic]] parameters (such as [[heart failure]], [[cardiac arrest]] on admission, [[Systole (medicine)|systolic]] [[blood pressure]], or [[Killip class]] of two or greater), ST-segment deviation, [[diabetes mellitus|diabetes]], [[Blood plasma|serum]] [[creatinine]] concentration, [[Peripheral artery occlusive disease|peripheral vascular disease]] and elevation of cardiac markers.<ref name="PEPA"/><ref name="GRACE">Fox KA, Dabbous OH, Goldberg RJ, Pieper KS, Eagle KA, Van de Werf F, Avezum A, Goodman SG, Flather MD, Anderson FA Jr, Granger CB. "Prediction of risk of death and myocardial infarction in the six months after presentation with acute coronary syndrome: prospective multinational observational study (GRACE)." ''BMJ'' 2006; '''333'''(7578):1091. PMID 17032691</ref><ref name="Weir-2006">{{cite journal | author=Weir RA, McMurray JJ, Velazquez EJ. | title=Epidemiology of heart failure and left ventricular systolic dysfunction after acute myocardial infarction: prevalence, clinical characteristics, and prognostic importance. | journal=Am J Cardiol | year=2006 | volume=97 | issue=10A | pages=13F–25F | pmid=16698331 | doi = 10.1016/j.amjcard.2006.03.005}}</ref>
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| Assessment of [[left ventricle|left ventricular]] [[ejection fraction]] may increase the predictive power of some risk stratification models.<ref name="Bosch-2005">{{cite journal | author=Bosch X, Theroux P. | title=Left ventricular ejection fraction to predict early mortality in patients with non-ST-segment elevation acute coronary syndromes. | journal=Am Heart J | year=2005 | volume=150 | issue=2 | pages=215–20 | pmid=16086920 | doi = 10.1016/j.ahj.2004.09.027}}</ref> The prognostic importance of Q-waves is debated.<ref>{{cite journal | author = Nicod P, Gilpin E, Dittrich H, Polikar R, Hjalmarson A, Blacky A, Henning H, Ross J | title = Short- and long-term clinical outcome after Q wave and non-Q wave myocardial infarction in a large patient population. | journal = Circulation | volume = 79 | issue = 3 | pages = 528–36 | year = 1989 | pmid = 2645061}}</ref> Prognosis is significantly worsened if a mechanical complication ([[papillary muscle]] rupture, myocardial free wall rupture, and so on) were to occur.<ref name="Becker-1996"/>
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| There is evidence that case fatality of myocardial infarction has been improving over the years in all ethnicities.<ref name="Liew-2006">{{cite journal | author=Liew R, Sulfi S, Ranjadayalan K, Cooper J, Timmis AD. | title=Declining case fatality rates for acute myocardial infarction in South Asian and white patients in the past 15 years. | journal=Heart | year=2006 | volume=92 | issue=8 | pages=1030–4 | pmid=16387823 | doi = 10.1136/hrt.2005.078634}}</ref>
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| ==Legal implications==
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| At [[common law]], a myocardial infarction is generally a [[disease]], but may sometimes be an [[injury]]. This has implications for no-fault insurance schemes such as [[workers' compensation]]. A heart attack is generally not covered;<ref name=prairieview>[http://www.pvamu.edu/pages/2026.asp Workers' Compensation FAQ]. [[Prairie View A&M University]]. Retrieved November 22, 2006.</ref> however, it may be a [[Industrial injury|work-related injury]] if it results, for example, from unusual emotional stress or unusual exertion.<ref name=biia>[http://www.biia.wa.gov/significantdecisions/contents.htm SIGNIFICANT DECISIONS Subject Index]. Board of Industrial Insurance Appeals. Retrieved November 22, 2006.</ref> Additionally, in some jurisdictions, heart attacks suffered by persons in particular occupations such as [[police officer]]s may be classified as line-of-duty injuries by statute or policy. In some countries or states, a person who has suffered from a myocardial infarction may be prevented from participating in activity that puts other people's lives at risk, for example driving a car, taxi or airplane.<ref name="NovaScotia-DrivingRegulations"/>
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| ==See also==
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| * [[Acute coronary syndrome]]
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| * [[Angina pectoris|Angina]]
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| * [[Cardiac arrest]]
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| * [[Coronary thrombosis]]
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| * [[Hibernating myocardium]]
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| * [[Stunned myocardium]]
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| * [[Ventricular remodeling]]
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| ==References==
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| <div class="references-small" style="-moz-column-count:2; column-count:2;">
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| <references />
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| </div>
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| ==External links==
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| * [http://hp2010.nhlbihin.net/atpiii/calculator.asp?usertype=pub Risk Assessment Tool for Estimating 10-year Risk of Having a Heart Attack] - based on information of the [[Framingham Heart Study]], from the United States [[National Heart, Lung and Blood Institute]]
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| * [http://www.nlm.nih.gov/medlineplus/heartattack.html Heart Attack] - overview of resources from [[MedlinePlus]].
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| *[http://www.americanheart.org/heartattack American Heart Association's Heart Attack web site] - Information and resources for preventing, recognizing and treating heart attack.
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| {{Circulatory system pathology}}
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| {{Electrocardiography}}
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| {{SIB}}
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| [[Category:Aging-associated diseases]]
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| [[Category:Cardiovascular diseases]]
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| [[Category:Causes of death]]
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| [[Category:Ischemic heart diseases]]
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| [[Category:Medical emergencies]]
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| [[ar:احتشاء عضل القلب]]
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| [[bg:Инфаркт на миокарда]]
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| [[ca:Infart miocardíac]]
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| [[cs:Infarkt myokardu]]
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| [[de:Myokardinfarkt]]
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| [[et:Müokardi infarkt]]
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| [[el:Έμφραγμα του μυοκαρδίου]]
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| [[es:Infarto agudo de miocardio]]
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| [[eo:Korinfarkto]]
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| [[eu:Miokardio infartu akutu]]
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| [[fa:سکته قلبی]]
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| [[fr:Infarctus du myocarde]]
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| [[ko:심근경색]]
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| [[hr:Infarkt miokarda]]
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| [[id:Serangan jantung]]
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| [[is:Hjartaáfall]]
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| [[it:Infarto miocardico acuto]]
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| [[he:התקף לב]]
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| [[ku:Mirina masûlkeyên dil]]
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| [[la:Infarctus cordis]]
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| [[lt:Miokardo infarktas]]
| |
| [[hu:Szívinfarktus]]
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| [[mk:Срцев напад]]
| |
| [[nl:Hartinfarct]]
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| [[ja:心筋梗塞]]
| |
| [[no:Hjerteinfarkt]]
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| [[nn:Hjarteåtak]]
| |
| [[pl:Zawał mięśnia sercowego]]
| |
| [[pt:Infarto agudo do miocárdio]]
| |
| [[qu:Sunqu p'itiy]]
| |
| [[ru:Острый инфаркт миокарда]]
| |
| [[sq:Infarkti miokardial]]
| |
| [[simple:Myocardial infarction]]
| |
| [[sr:Срчани удар]]
| |
| [[fi:Sydäninfarkti]]
| |
| [[sv:Hjärtinfarkt]]
| |
| [[vi:Nhồi máu cơ tim]]
| |
| [[tr:Kalp krizi]]
| |
| [[uk:Гострий інфаркт міокарда]]
| |
| [[ur:احتشاء عضل قلب]]
| |
| [[yi:הארץ אטאקע]]
| |
| [[zh:心肌梗死]]
| |
| | |
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