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Latest revision as of 00:17, 30 July 2020

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Several factors have been associated with an increased risk of developing ST elevation myocardial infarction (STEMI). These factors include physical exertion, psychological stress, sexual activity, diurnal (daily) variations in cortisol and platelet aggregation and circannual (yearly) variations in lipids and infectious etiologies, exposure to pollution and or particulate matter, cocaine and ingestion of a recent fatty meal.

Nomenclature

Muller et al have developed the following nomenclature to categorize and analyze data pertaining to triggers of MI ^[1]:

(1) Trigger: An activity that produces short-term physiological changes that may lead directly to onset of acute CVD.

(2) Acute risk factor: A short-term physiological change, such as a surge in arterial pressure or heart rate, an increase in coagulability, or vasoconstriction, that follows a trigger and may result in disease onset.

(3) Hazard period: The time interval after trigger initiation associated with an increased risk of disease onset because of the trigger. The onset and offset times of the hazard period, which could also be designated a “vulnerable period,” may be sharply defined, as in heavy exertion, or less well defined, as with respiratory infection. The duration of the hazard period may also vary, eg from < 1 hour during heavy physical exertion to weeks or months with bereavement.

(4) Triggered acute risk prevention (TARP): Cardiovascular risk reduction that focuses on the short-term increase in risk associated with a trigger.

Putting Relative Risk of MI and Absolute Risk of MI Into Clinical Context

In the following sections, you will read that certain triggers are associated with a dramatic rise in the relative risk of having an MI (e.g. heavy exertion among patients with a sedentary lifestyle increases their risk of an MI 107 fold). These dramatic increases in relative risk, must, however, be placed in the appropriate clinical context.

It must be born in mind that while triggers are frequent events, MI or sudden death are relatively infrequent events. The risk of sudden death with exercise provides a nice example. The relative risk of sudden death within 30 minutes after >/= 6 METS of exercise goes up 16.9 fold. However, because sudden death is so infrequent, this translates into 1 sudden cardiac death for every 1.51 million episodes of heavy exertion. ^[2] The number of absolute events is even lower among nurses in the Nurses Health Study undertaking mild to meoderate exertion: 1 sudden death for every 36.5 hours of exertion. ^[3]

While the presence of triggers increases the relative risk of MI dramatically, the absolute number of MIs attributable to the trigger may be quite low.

A dramatic rise in the relative risk of a very, very, very infrequent event therefore translates clinically into a very small rise in the absolute number of events attributable to the trigger.

Physical Exertion and MI

Physical exertion, especially if the exertion is much more intense than the individual usually performs has been associated with the onset of STEMI. ^[4]^[5]^[6] ^[7] ^[8]^[2]^[3]^[9] The ONSET study demonstrated that intense exertion (defined as >/= 6 metabolic equivalents of METS) within the previous hour was associated with a 5.9 fold rise in the risk of MI ^[6].

Studies linking physical exertion to MI:

The ONSET Study: Relative risk = 5.9 ^[6]
The Stockholm Heart Epidemiology Program (SHEEP): Relative risk = 6.1 ^[7]
The Triggers and Mechanisms of Myocardial Infarction (TRIMM) study: Relative risk = 2.1 ^[4]

Blizzards have often been cited as a trigger of MI, and the physical exertion of snow shoveling has frequently been cited as a contributor. ^[10] ^[11]

Impact of a sedentary lifestyle: The relative risk of MI quoted above increases dramatically among those individuals who lead a sedentary lifestyle. For those in poor physical condition, the relative risk was 107 fold higher in the ONSET study. In contrast, among those individuals who reported that they engaged in physical activity 5 days a week or more, the risk was only doubled.

Mechanism: It has been hypothesized that exertion increases blood pressure, pulse and oscillatory shear which in turn may increase the risk of plaque rupture.

Physical Exertion and Sudden Death

While the above discussion pertains to documented nonfatal MI, approximately a quarter of MI patients may die of sudden death or fatal MI before reaching the hospital. In a cohort of 21,481 male physicians in the United States who by self report who had no prior history of coronary artery disease, there was a 16.9 fold rise in the risk of sudden cardiac death within 30 minutes of intense exertion (>/= 6 METS) ^[2]. Similar to what has been reported with respect to the onset of MI, there was no increase in the risk of sudden death with heavy exertion among those nurses who exercised more than 2 hours per week.

Psychological Stress

Psychological stress associated with anger ^[12], work related stressful events ^[13], wartime bombing ^[14] ^[15] , earthquakes ^[16] and other natural disasters has been associated with an increased risk of onset of myocardial infarction.

Anger

Intense anger (fist / teeth clenched) has been associated with a risk in the risk of MI in the 2 hours following the episode in the following studies:

ONSET: 2.3 fold rise^[12]
SHEEP: 9 fold rise^[17]
Kotton et al: 14 fold rise^[18]

The psychosocial stressors that precipitated the anger were as follows:

Argument with family members (25%)
Conflicts at work (22%)
Legal problems (8%)

Anxiety

If a patient is in the >75th percentile for anxiety, this increases the relative risk of MI 1.6 fold for the 2 hours following the period of anxiety.^[12]

Bereavement and the Broken Heart Syndrome

Stress cardiomyopathy which is also known as Left Ventricular Apical Ballooning Syndrome, Takotsubo cardiomyopathy, or Ampulla-shaped cardiomyopathy is a cardiac syndrome characterized by a reversible transient apical ventricular dysfunction. Since the cardiomyopathy is often triggered by emotional stress, such as the death of a loved one, the condition is sometimes also referred to as the Broken Heart Syndrome. In 2006, the syndrome was renamed Stress Cardiomyopathy, and was classified as an acquired cardiomyopathy. ^[19]

The typical presentation of someone with takotsubo cardiomyopathy is a sudden onset of congestive heart failure or chest pain associated with EKG changes suggestive of an anterior wall acute MI. During the course of evaluation of the patient, a bulging out of the left ventricular apex with a hypercontractile base of the left ventricle is often noted. It is the hallmark bulging out of the apex of the heart with preserved function of the base that earned the syndrome its name "tako tsubo", or octopus trap in Japan, where it was first described. Evaluation of individuals with takotsubo cardiomyopathy typically include a coronary angiogram, which does not reveal any significant blockages that would cause the left ventricular dysfunction. Provided that the individual survives their initial presentation, the left ventricular function improves within days to weeks^[20]. Takotsubo cardiomyopathy is more commonly seen in post-menopausal women^[21]. Often there is a history of a recent severe emotional or physical stress.^[21]

Work Related Stress

Deadlines

An aggressive timeline or deadline at work has been associated with a rise in the risk of MI:

The SHEEP study: 6 fold rise
The ONSET study: 2.3 fold rise

Firing an Employee

The stress of firing an employee has been associated with a rise in the risk of MI:

The ONSET study: 2.2 fold rise

Natural Disasters

Natural disasters have been associated with an increased risk of MI. The best documented association has been with earthquakes. For instance the 1994 earthquake in Los Angeles was associated with a 4 fold rise in the risk of sudden death and a 35% rise in the relative risk of a non-fatal MI. ^[22] ^[23] It is notable that the association of earthquakes with MI is variable depending upon the time of day that the earthquake occurs. The LA earthquake occurred just after 4 A.M., just when platelet aggregation may be at a peak (see below). However, the earthquake that struck San Francisco Bay in 1989 at 5 P.M. was not associated with an increased risk of MI. ^[24]

Wartime Stress and Missile Attacks

9/11/2001

Within 50 miles of the world trade center, there was a 49% increase in the relative risk of an MI in the 60 days following the 9/11 attack: There were 118 MIs in the 60 days after the attack versus 79 MIs in the 60 days before (p=0.01). How much of this is attributable to particulate matter versus psychological stress is not clear. ^[25]

Missile Attacks

The stress of missile attacks has been associated with a doubling in the risk of non fatal MI and sudden death. ^[26]

Sporting Events

The stress of sporting events has been associated with an increased risk of MI in a population. An example that has been cited is the 50% increase in the risk of MI or stroke among Dutch men associated with the loss of Holland to France in the 1996 European football finals. It is notable that no such rise in risk was observed among Dutch women or the French. ^[27] ^[28] The World Cup of soccer has been associated with a doubling of MI incidence. ^[29]

Sexual Activity

The association of sexual activity with the onset of MI may represent components of physical exertion as well as psychologic stress. In both the SHEEP and the ONSET studies, recent sexual activity increased the risk of MI by 2.5 fold ^[30]^[31]. Again, to place this relative risk into clinical context, it should be noted that only 3% of MI patients had had sexual intercourse within the past 2 hours prior to the onset of MI. It should also be noted that the increase in risk of MI with sexual activity did not differ between patients with and without a history of coronary artery disease.

The risk of MI with sexual intercourse is a frequent concern among patients who have coronary artery disease. Again, the data above indicates that recent sexual activity doubles the risk of an MI, and this may on the surface appear to be disconcerting to both a patient and healthcare professional. But again, to place this relative risk into context, the absolute risk must be taken into account. The average risk of an MI in a patient at average risk has been estimated to be about 1 chance in a million during any given hour during middle age. Sexual activity increases that risk to 2 in a million per hour for the 2 hours after sexual intercourse. If the annual risk of MI is about 1%, weekly sexual intercourse will increase this annual risk to just 1.01%. ^[32] As is the case with physical exertion, regular exercise (6 METS >/= 3 times per week) reduced the relative risk of MI with sexual intercourse from 3.0 to 1.2 in the ONSET study.^[30]

Thus, because the risk is small, because the frequency of sexual activity is relatively small, and because the period of increased risk is short (approximately 2 hours) the absolute risk of MI associated with sexual intercourse is quite small.

Air Pollution / Fine Particulate Matter

Exposure to high levels of ambeint air pollution (exposure to fine particulate matter in the past 2 - 24 hours) has been associated with a transient elevation in the risk of myocardial infarction ^[33]. There is a rise in CRP and plasma viscosity following exposure to fine particulate matter and it has been speculated that the pulmonary inflammation that follows such exposure may trigger a systemic state of hypercoagulability ^[34]^[35]. Exposure to fine particulate matter has also been associated with changes in autonomic tone manifested by sinus tachycardia ^[36] ^[37], as well as a reduction in heart rate variability ^[38] ^[39] ^[40]. Finally, ventricular arrhythmias as manifested by firing of AICDs has been associated with exposure to fine particulate matter ^[41].

Antecedent Infection

Acute severe infection, such as pneumonia, can trigger myocardial infarction ^[42]. A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis^[43]. While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor^[43].Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.^[44]

A Heavy Meal

There have been reports of a 4 fold rise in the risk of MI following a heavy meal. ^[45]

This rise in risk may account for a second peak in the circadian variation in the onset of MI around 8 P.M. in the evening. The mechanism underlying the association is not clear. It has been speculated that ingestion of a heavy fatty meal may be associated with a rise in prothrombotic factors and heart rate, and a reduction in vascular reactivity. ^[46] ^[47]

Cocaine

Ingestion of cocaine has been associated with STEMI ^[48].

Marijuana

Marijuana use has been associated with a 4.8 fold rise in the risk of MI. ^[49]

Circadian Variation in the Onset of STEMI

Most MIs occur in the early morning hours when cortisol and adrenaline rise and platelets are more activated. This diurnal variation is obliterated with aspirin therapy, pointing to the putative role of platelets in the initiation of MI. ^[50] ^[51] ^[52] ^[53] ^[54] ^[55] ^[56]

Relative Frequency of Triggers in Association with MI

When a creful history is obtained, approximately half (48%) of MI patients will report a trigger ^[57]. It is notable that 13% of patients will report that there were of 2 or more triggers. The following triggers were most commonly associated with the onset of MI in the Multicenter Investigation of Limitation of Infarct Size (MILIS) study ^[57]:

Emotional upset (18%)
Moderate physical activity (14%)
Heavy physical activity (9%)
Lack of sleep (8%)
Overeating (7%)

STEMI Triggers in Popular Culture

The sudden death of Tim Russert has prompted interest in the triggers of an MI

Following the sudden death of Tim Russert of NBC's Meet the Press on June 13th 2008, many laypeople and physicians alike have asked "what are the triggers of a sudden heart attack"? Barbara Walters speculated that Tim Russert may have died from "the stress of the job". Others were concerned about a recent weight gain and lack of sleep. This chapter reviews the literature pertaining to triggers of acute MI.

References

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↑ ^2.0 ^2.1 ^2.2 Albert CM, Mittleman MA, Chae CU, Lee IM, Hennekens CH, Manson JE (2000). "Triggering of sudden death from cardiac causes by vigorous exertion". N. Engl. J. Med. 343 (19): 1355–61. PMID 11070099. Unknown parameter |month= ignored (help)
↑ ^3.0 ^3.1 Whang W, Manson JE, Hu FB; et al. (2006). "Physical exertion, exercise, and sudden cardiac death in women". JAMA. 295 (12): 1399–403. doi:10.1001/jama.295.12.1399. PMID 16551711. Unknown parameter |month= ignored (help)
↑ ^4.0 ^4.1 Willich SN, Lewis M, Löwel H, Arntz HR, Schubert F, Schröder R (1993). "Physical exertion as a trigger of acute myocardial infarction. Triggers and Mechanisms of Myocardial Infarction Study Group". N. Engl. J. Med. 329 (23): 1684–90. PMID 8232457. Unknown parameter |month= ignored (help)
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↑ ^6.0 ^6.1 ^6.2 Mittleman MA, Maclure M, Tofler GH, Sherwood JB, Goldberg RJ, Muller JE (1993). "Triggering of acute myocardial infarction by heavy physical exertion. Protection against triggering by regular exertion. Determinants of Myocardial Infarction Onset Study Investigators". N. Engl. J. Med. 329 (23): 1677–83. PMID 8232456. Unknown parameter |month= ignored (help)
↑ ^7.0 ^7.1 Hallqvist J, Möller J, Ahlbom A, Diderichsen F, Reuterwall C, de Faire U (2000). "Does heavy physical exertion trigger myocardial infarction? A case-crossover analysis nested in a population-based case-referent study". Am. J. Epidemiol. 151 (5): 459–67. PMID 10707914. Unknown parameter |month= ignored (help)
↑ Giri S, Thompson PD, Kiernan FJ; et al. (1999). "Clinical and angiographic characteristics of exertion-related acute myocardial infarction". JAMA. 282 (18): 1731–6. PMID 10568645. Unknown parameter |month= ignored (help)
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↑ Glass RI, Zack MM (1979). "Increase in deaths from ischaemic heart-disease after blizzards". Lancet. 1 (8114): 485–7. PMID 85066. Unknown parameter |month= ignored (help)
↑ Franklin BA, Bonzheim K, Gordon S, Timmis GC (1996). "Snow shoveling: a trigger for acute myocardial infarction and sudden coronary death". Am. J. Cardiol. 77 (10): 855–8. doi:10.1016/S0002-9149(97)89181-3. PMID 8623739. Unknown parameter |month= ignored (help)
↑ ^12.0 ^12.1 ^12.2 Mittleman MA, Maclure M, Sherwood JB; et al. (1995). "Triggering of acute myocardial infarction onset by episodes of anger. Determinants of Myocardial Infarction Onset Study Investigators". Circulation. 92 (7): 1720–5. PMID 7671353. Unknown parameter |month= ignored (help)
↑ Möller J, Theorell T, de Faire U, Ahlbom A, Hallqvist J (2005). "Work related stressful life events and the risk of myocardial infarction. Case-control and case-crossover analyses within the Stockholm heart epidemiology programme (SHEEP)". J Epidemiol Community Health. 59 (1): 23–30. doi:10.1136/jech.2003.019349. PMC 1763356. PMID 15598722. Unknown parameter |month= ignored (help)
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↑ Trichopoulos D, Katsouyanni K, Zavitsanos X, Tzonou A, Dalla-Vorgia P (1983). "Psychological stress and fatal heart attack: the Athens (1981) earthquake natural experiment". Lancet. 1 (8322): 441–4. PMID 6131167. Unknown parameter |month= ignored (help)
↑ Möller J, Hallqvist J, Diderichsen F, Theorell T, Reuterwall C, Ahlbom A (1999). "Do episodes of anger trigger myocardial infarction? A case-crossover analysis in the Stockholm Heart Epidemiology Program (SHEEP)". Psychosom Med. 61 (6): 842–9. PMID 10593637.
↑ Koton S, Tanne D, Bornstein NM, Green MS (2004). "Triggering risk factors for ischemic stroke: a case-crossover study". Neurology. 63 (11): 2006–10. PMID 15596741. Unknown parameter |month= ignored (help)
↑ Maron BJ, Towbin JA, Thiene G; et al. (2006). "Contemporary definitions and classification of the cardiomyopathies: an American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention". Circulation. 113 (14): 1807–16. doi:10.1161/CIRCULATIONAHA.106.174287. PMID 16567565.
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↑ Leor J, Kloner RA (1996). "The Northridge earthquake as a trigger for acute myocardial infarction". Am. J. Cardiol. 77 (14): 1230–2. PMID 8651102. Unknown parameter |month= ignored (help)
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↑ Brown DL (1999). "Disparate effects of the 1989 Loma Prieta and 1994 Northridge earthquakes on hospital admissions for acute myocardial infarction: importance of superimposition of triggers". Am. Heart J. 137 (5): 830–6. PMID 10220631. Unknown parameter |month= ignored (help)
↑ Allegra JR, Mostashari F, Rothman J, Milano P, Cochrane DG (2005). "Cardiac events in New Jersey after the September 11, 2001, terrorist attack". J Urban Health. 82 (3): 358–63. doi:10.1093/jurban/jti087. PMID 16000653. Unknown parameter |month= ignored (help)
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↑ Pope CA, Verrier RL, Lovett EG; et al. (1999). "Heart rate variability associated with particulate air pollution". Am. Heart J. 138 (5 Pt 1): 890–9. PMID 10539820. Unknown parameter |month= ignored (help)
↑ Gold DR, Litonjua A, Schwartz J; et al. (2000). "Ambient pollution and heart rate variability". Circulation. 101 (11): 1267–73. PMID 10725286. Unknown parameter |month= ignored (help)
↑ Peters A, Liu E, Verrier RL; et al. (2000). "Air pollution and incidence of cardiac arrhythmia". Epidemiology. 11 (1): 11–7. PMID 10615837. Unknown parameter |month= ignored (help)
↑ Smeeth L, Thomas SL, Hall AJ, Hubbard R, Farrington P, Vallance P (2004). "Risk of myocardial infarction and stroke after acute infection or vaccination". N. Engl. J. Med. 351 (25): 2611–8. doi:10.1056/NEJMoa041747. PMID 15602021. Unknown parameter |month= ignored (help)
↑ ^43.0 ^43.1 Saikku P, Leinonen M, Tenkanen L, Linnanmaki E, Ekman MR, Manninen V, Manttari M, Frick MH, Huttunen JK. (1992). "Chronic Chlamydia pneumoniae infection as a risk factor for coronary heart disease in the Helsinki Heart Study". Ann Intern Med. 116 (4): 273–8. PMID 1733381.
↑ Andraws R, Berger JS, Brown DL. (2005). "Effects of antibiotic therapy on outcomes of patients with coronary artery disease: a meta-analysis of randomized controlled trials". JAMA. 293 (21): 2641–7. PMID 15928286.
↑ Lipovetzky N, Hod H, Roth A, Kishon Y, Sclarovsky S, Green MS (2004). "Heavy meals as a trigger for a first event of the acute coronary syndrome: a case-crossover study". Isr. Med. Assoc. J. 6 (12): 728–31. PMID 15609883. Unknown parameter |month= ignored (help)
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↑ Mittleman MA, Mintzer D, Maclure M, Tofler GH, Sherwood JB, Muller JE (1999). "Triggering of myocardial infarction by cocaine". Circulation. 99 (21): 2737–41. PMID 10351966. Unknown parameter |month= ignored (help)
↑ Mittleman MA, Lewis RA, Maclure M, Sherwood JB, Muller JE (2001). "Triggering myocardial infarction by marijuana". Circulation. 103 (23): 2805–9. PMID 11401936. Unknown parameter |month= ignored (help)
↑ Muller JE, Stone PH, Turi ZG; et al. (1985). "Circadian variation in the frequency of onset of acute myocardial infarction". N. Engl. J. Med. 313 (21): 1315–22. PMID 2865677. Unknown parameter |month= ignored (help)
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↑ Marler JR, Price TR, Clark GL; et al. (1989). "Morning increase in onset of ischemic stroke". Stroke. 20 (4): 473–6. PMID 2648651. Unknown parameter |month= ignored (help)
↑ Behar S, Halabi M, Reicher-Reiss H; et al. (1993). "Circadian variation and possible external triggers of onset of myocardial infarction. SPRINT Study Group". Am. J. Med. 94 (4): 395–400. PMID 8475932. Unknown parameter |month= ignored (help)
↑ Tofler GH, Muller JE, Stone PH; et al. (1992). "Modifiers of timing and possible triggers of acute myocardial infarction in the Thrombolysis in Myocardial Infarction Phase II (TIMI II) Study Group". J. Am. Coll. Cardiol. 20 (5): 1049–55. PMID 1401601. Unknown parameter |month= ignored (help)
↑ Ridker PM, Manson JE, Buring JE, Muller JE, Hennekens CH (1990). "Circadian variation of acute myocardial infarction and the effect of low-dose aspirin in a randomized trial of physicians". Circulation. 82 (3): 897–902. PMID 2203556. Unknown parameter |month= ignored (help)
↑ Parker JD, Testa MA, Jimenez AH; et al. (1994). "Morning increase in ambulatory ischemia in patients with stable coronary artery disease. Importance of physical activity and increased cardiac demand". Circulation. 89 (2): 604–14. PMID 8313548. Unknown parameter |month= ignored (help)
↑ ^57.0 ^57.1 Tofler GH, Stone PH, Maclure M; et al. (1990). "Analysis of possible triggers of acute myocardial infarction (the MILIS study)". Am. J. Cardiol. 66 (1): 22–7. PMID 2193495. Unknown parameter |month= ignored (help)

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[pmid1401601-54] Tofler GH, Muller JE, Stone PH; et al. (1992). "Modifiers of timing and possible triggers of acute myocardial infarction in the Thrombolysis in Myocardial Infarction Phase II (TIMI II) Study Group". J. Am. Coll. Cardiol. 20 (5): 1049–55. PMID 1401601. Unknown parameter |month= ignored (help)

[pmid2203556-55] Ridker PM, Manson JE, Buring JE, Muller JE, Hennekens CH (1990). "Circadian variation of acute myocardial infarction and the effect of low-dose aspirin in a randomized trial of physicians". Circulation. 82 (3): 897–902. PMID 2203556. Unknown parameter |month= ignored (help)

[pmid8313548-56] Parker JD, Testa MA, Jimenez AH; et al. (1994). "Morning increase in ambulatory ischemia in patients with stable coronary artery disease. Importance of physical activity and increased cardiac demand". Circulation. 89 (2): 604–14. PMID 8313548. Unknown parameter |month= ignored (help)

[pmid2193495-57] 57.0 ^57.1 Tofler GH, Stone PH, Maclure M; et al. (1990). "Analysis of possible triggers of acute myocardial infarction (the MILIS study)". Am. J. Cardiol. 66 (1): 22–7. PMID 2193495. Unknown parameter |month= ignored (help)

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@@ Line 1: / Line 1: @@
-{{Infobox_Disease |
+__NOTOC__
-  Name           = Myocardial infarction|
+{{ST elevation myocardial infarction}}
-  Image          =russert.jpg|
-  Caption        =The sudden death of Tim Russert has prompted interest in the triggers of an MI|
-  DiseasesDB     = 8664 |
-  ICD10          = {{ICD10|I|21||i|20}}-{{ICD10|I|22||i|20}} |
-  ICD9           = {{ICD9|410}} |
-  ICDO           = |
-  OMIM           = |
-  MedlinePlus    = 000195 |
-  eMedicineSubj  = med |
-  eMedicineTopic = 1567 |
-  eMedicine_mult = {{eMedicine2|emerg|327}} {{eMedicine2|ped|2520}} |
-  MeshID         = |
-}}
-{{SI}}
-{{WikiDoc Cardiology Network Infobox}}
 {{CMG}}
-{{Editor Join}}
-Following the sudden death of Tim Russert of NBC's Meet the Press on June 13th 2008, many laypeople and physicians alike have asked "what are the triggers of a sudden heart attack"? Barbara Walters speculated that Tim Russert may have died from "the stress of the job". Others were concerned about a recent weight gain and lack of sleep. This chapter reviews the literature pertaining to triggers of acute MI.
 ==Overview==
-Several factors have been associated with an increased risk of developing ST elevation myocardial infarction (STEMI). These factors include physical exertion, psychological stress, sexual activity, diurnal (daily) variations in cortisol and platelet aggregation and circannual (yearly) variations in lipids and infectious etiologies, exposure to pollution and or particulate matter, cocaine and ingestion of a recent fatty meal.
+Several factors have been associated with an increased risk of developing ST elevation myocardial infarction (STEMI). These factors include physical exertion, psychological stress, sexual activity, diurnal (daily) variations in [[cortisol]] and platelet aggregation and circannual (yearly) variations in lipids and infectious etiologies, exposure to pollution and or particulate matter, cocaine and ingestion of a recent fatty meal.
 ==Nomenclature==
 Muller et al have developed the following nomenclature to categorize and analyze data pertaining to triggers of MI <ref name="pmid8113568">{{cite journal |author=Muller JE, Abela GS, Nesto RW, Tofler GH |title=Triggers, acute risk factors and vulnerable plaques: the lexicon of a new frontier |journal=J. Am. Coll. Cardiol. |volume=23 |issue=3 |pages=809–13 |year=1994 |month=March |pmid=8113568 |doi= |url=}}</ref>:
-:(1) '''Trigger:''' An activity that produces short-term physiological changes that may lead directly to onset of acute CVD.
+(1) Trigger: An activity that produces short-term physiological changes that may lead directly to onset of acute CVD.
-:(2) '''Acute risk factor:''' A short-term physiological change, such as a surge in arterial pressure or heart rate, an increase in coagulability, or vasoconstriction, that follows a trigger and may result in disease onset.
+(2) Acute risk factor: A short-term physiological change, such as a surge in arterial pressure or heart rate, an increase in coagulability, or vasoconstriction, that follows a trigger and may result in disease onset.
-:(3) '''Hazard period:''' The time interval after trigger initiation associated with an increased risk of disease onset because of the trigger. The onset and offset times of the hazard period, which could also be designated a “vulnerable period,” may be sharply defined, as in heavy exertion, or less well defined, as with respiratory infection. The duration of the hazard period may also vary, eg from < 1 hour during heavy physical exertion to weeks or months with bereavement.
+(3) Hazard period: The time interval after trigger initiation associated with an increased risk of disease onset because of the trigger. The onset and offset times of the hazard period, which could also be designated a “vulnerable period,” may be sharply defined, as in heavy exertion, or less well defined, as with respiratory infection. The duration of the hazard period may also vary, eg from < 1 hour during heavy physical exertion to weeks or months with bereavement.
-:(4) '''Triggered acute risk prevention (TARP):''' Cardiovascular risk reduction that focuses on the short-term increase in risk associated with a trigger.
+(4) Triggered acute risk prevention (TARP): Cardiovascular risk reduction that focuses on the short-term increase in risk associated with a trigger.
 ==Putting Relative Risk of MI and Absolute Risk of MI Into Clinical Context==
@@ Line 48: / Line 28: @@
 A dramatic rise in the relative risk of a very, very, very infrequent event therefore translates clinically into a very small rise in the absolute number of events attributable to the trigger.
-==Differential Diagnosis of Underlying Causes and Triggers of ST Segment Elevation in the Presence of Myonecrosis (STEMI)==
-While plaque rupture is the most common cause of ST segment elevation MI, other conditions can cause ST elevation and myocardial necrosis. In order to expeditiously treat an alternate underlying cause of myonecrosis, it is important to rpadily identify conditions other than plaque rupture that may also cause ST elevation and myonecrosis. Indeed, the management of some of these conditions might be differ substantially from that of plaque rupture: [[cocaine]] induced STEMI would not be treated with [[beta-blocker]]s, and [[myocardial contusion]] would not be treated with an [[antithrombin]]. These conditions include the following:
-{|style="width:60%; height:100px" border="1"
-|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular'''
-|style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | [[Aortic dissection]] more often extends to occlude the ostium of the [[right coronary artery]]
-[[Aortic stenosis]] can cause subendocardial ischemia and infarction if demand grossly exceeds supply
-|-
-|-bgcolor="LightSteelBlue"
-| '''Chemical / poisoning'''
-|bgcolor="Beige"| [[Carbon monoxide poisoning]]
-|-
-|-bgcolor="LightSteelBlue"
-| '''Dermatologic'''
-|bgcolor="Beige"| No underlying causes
-|-
-|-bgcolor="LightSteelBlue"
-| '''Drug Side Effect'''
-|bgcolor="Beige"| [[Oral contraceptive pills]], particularly among women who smoke
-[[Anabolic steroids]]
-|-
-|-bgcolor="LightSteelBlue"
-| '''Ear Nose Throat'''
-|bgcolor="Beige"| A recent [[upper respiratory tract infection]]s has been associated with a 4.9 fold rise in the risk of [[trigger of MI|MI]]
-|-
-|-bgcolor="LightSteelBlue"
-| '''Endocrine'''
-|bgcolor="Beige"| [[Thyrotoxicosis]]
-|-
-|-bgcolor="LightSteelBlue"
-| '''Environmental'''
-|bgcolor="Beige"| Blizzards and snow shoveling, and inhalation of fine particulate matter in areas with air pollution and high traffic have been identified as [[triggers of MI]].
-|-
-|-bgcolor="LightSteelBlue"
-| '''Gastroenterologic'''
-|bgcolor="Beige"| A heavy meal has been associated with a 4 fold rise in the risk of [[trigger of MI|MI]], and it is not clear if this is mediated by hyperadrenergic tone <ref> Lipovetsky N, Hod H, Roth A, Kishon Y, Sclarovsky S, Green MS. Heavy meals as a trigger for a first event of the acute coronary syndrome:a case-crossover study. Isr Med Assoc J. 2004;6:728 –731.</ref>;
-|-
-|-bgcolor="LightSteelBlue"
-| '''Genetic'''
-|bgcolor="Beige"| [[Familial hypercholesterolemia]]
-|-
-|-bgcolor="LightSteelBlue"
-| '''Hematologic'''
-|bgcolor="Beige"| [[Disseminated intravascular coagulation]] ([[DIC]])
-[[Hypercoagulable states]]
-[[Polycythemia vera]]
-[[Thrombocytosis]]
-|-
-|-bgcolor="LightSteelBlue"
-| '''Iatrogenic'''
-|bgcolor="Beige"| [[Epinephrine]] overdose
-Sudden withdrawal of [[Beta blockers]] or [[nitrates]]
-|-
-|-bgcolor="LightSteelBlue"
-| '''Infectious Disease'''
-|bgcolor="Beige"| A recent [[upper respiratory tract infection]]s has been associated with a 4.9 fold rise in the risk of [[trigger of MI|MI]]
-[[Infectious endocarditis]] may STEMI as a result of embolization
-|-
-|-bgcolor="LightSteelBlue"
-| '''Musculoskeletal / Ortho'''
-|bgcolor="Beige"| No underlying causes
-|-
-|-bgcolor="LightSteelBlue"
-| '''Neurologic'''
-|bgcolor="Beige"| No underlying causes
-|-
-|-bgcolor="LightSteelBlue"
-| '''Nutritional / Metabolic'''
-|bgcolor="Beige"| A heavy meal has been associated with a 4 fold rise in the risk of [[trigger of MI|MI]] and it is not clear if this is mediated by hyperadrenergic tone<ref name="pmid15609883">{{cite journal |author=Lipovetzky N, Hod H, Roth A, Kishon Y, Sclarovsky S, Green MS |title=Heavy meals as a trigger for a first event of the acute coronary syndrome: a case-crossover study |journal=Isr. Med. Assoc. J. |volume=6 |issue=12 |pages=728–31 |year=2004 |month=December |pmid=15609883 |doi= |url=}}</ref>;
-[[Amyloidosis]]
-[[Fabry disease]]
-[[Homocystinuria]]
-[[Mucopolysaccharidoses]] or [[Hurler disease]]
-[[Pseudoxanthoma elasticum]]
-[[Thiamine deficiency]] has been associated with ST elevation and myonecrosis <ref name="pmid16020883">{{cite journal |author=Kawano H, Koide Y, Toda G, Yano K |title=ST-segment elevation of electrocardiogram in a patient with Shoshin beriberi |journal=Intern. Med. |volume=44 |issue=6 |pages=578–85 |year=2005 |month=June |pmid=16020883 |doi= |url=http://joi.jlc.jst.go.jp/JST.JSTAGE/internalmedicine/44.578?from=PubMed}}</ref><ref>Hundley JM, Ashburn LL, Sebrell WH. The electrocardiogram in chronic thiamine deficiency in rats. Am J Physiol 144: 404–414, 1954. </ref><ref name="pmid7197132">{{cite journal |author=Read DH, Harrington DD |title=Experimentally induced thiamine deficiency in beagle dogs: clinical observations |journal=Am. J. Vet. Res. |volume=42 |issue=6 |pages=984–91 |year=1981 |month=June |pmid=7197132 |doi= |url=}}</ref>
-|-
-|-bgcolor="LightSteelBlue"
-| '''Obstetric/Gynecologic'''
-|bgcolor="Beige"| Spontaneous coronary [[dissection]] in the setting of [[pregnancy]]
-|-
-|-bgcolor="LightSteelBlue"
-| '''Oncologic'''
-|bgcolor="Beige"| [[Radiation therapy]] can accelerate atherosclerosis particularly in the distribution of the left anterior descending artery;
-|-
-|-bgcolor="LightSteelBlue"
-| '''Opthalmologic'''
-|bgcolor="Beige"| No underlying causes
-|-
-|-bgcolor="LightSteelBlue"
-| '''Overdose / Toxicity'''
-|bgcolor="Beige"| [[Cocaine]] ingestion which may result in direct myocyte injury due to an adrendergic surge, vasoconstriction of the microvasculature or plaque rupture and thrombus formation;
-[[Marijuana]] ingestion has been identified as a [[trigger of MI]].
-|-
-|-bgcolor="LightSteelBlue"
-| '''Psychiatric'''
-|bgcolor="Beige"| Anger, [[anxiety]], [[bereavement]], work-related stress, earthquakes, bombings and other psychosocial stressors have been identified as [[triggers of MI]], and it is not clear if the mechanism is plaque rupture or hyperadrenergic tone;
-[[Stress cardiomyopathy]] or [[Broken heart syndrome]] causes ST segment elevation most often in the anterior precordium and is thought to be due to direct [[myocyte]] injury from a hyperadrenergic stimulation emanating from the central nervous system.
-|-
-|-bgcolor="LightSteelBlue"
-| '''Pulmonary'''
-|bgcolor="Beige"| A recent [[upper respiratory tract infection]]s has been associated with a 4.9 fold rise in the risk of [[trigger of MI|MI]]
-|-
-|-bgcolor="LightSteelBlue"
-| '''Renal / Electrolyte'''
-|bgcolor="Beige"| [[Homocystinuria]]
-|-
-|-bgcolor="LightSteelBlue"
-| '''Rheum / Immune / Allergy'''
-|bgcolor="Beige"| Takayasus
-|-
-|-bgcolor="LightSteelBlue"
-| '''Sexual'''
-|bgcolor="Beige"| Sexual activity has been identified as a [[trigger of MI]]
-|-
-|-bgcolor="LightSteelBlue"
-| '''Trauma'''
-|bgcolor="Beige"| Both penetrating and non-penetrating trauma to the heart or [[myocardial contusion]], [[commotio cordis]] can be associated with ST elevation and myonecrosis.
-|-
-|-bgcolor="LightSteelBlue"
-| '''Urologic'''
-|bgcolor="Beige"| No underlying causes
-|-
-|-bgcolor="LightSteelBlue"
-| '''Miscellaneous'''
-|bgcolor="Beige"| [[Hypotension]] particularly if it is prolonged
-|-
-|}
 ==Physical Exertion and MI==
@@ Line 200: / Line 33: @@
 <ref name="pmid8232457">{{cite journal |author=Willich SN, Lewis M, Löwel H, Arntz HR, Schubert F, Schröder R |title=Physical exertion as a trigger of acute myocardial infarction. Triggers and Mechanisms of Myocardial Infarction Study Group |journal=N. Engl. J. Med. |volume=329 |issue=23 |pages=1684–90 |year=1993 |month=December |pmid=8232457 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=8232457&promo=ONFLNS19}}</ref><ref name="pmid9603539">{{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 |volume=97 |issue=18 |pages=1837–47 |year=1998 |month=May |pmid=9603539 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=9603539}}</ref><ref name="pmid8232456">{{cite journal |author=Mittleman MA, Maclure M, Tofler GH, Sherwood JB, Goldberg RJ, Muller JE |title=Triggering of acute myocardial infarction by heavy physical exertion. Protection against triggering by regular exertion. Determinants of Myocardial Infarction Onset Study Investigators |journal=N. Engl. J. Med. |volume=329 |issue=23 |pages=1677–83 |year=1993 |month=December |pmid=8232456 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=8232456&promo=ONFLNS19}}</ref>
 <ref name="pmid10707914">{{cite journal |author=Hallqvist J, Möller J, Ahlbom A, Diderichsen F, Reuterwall C, de Faire U |title=Does heavy physical exertion trigger myocardial infarction? A case-crossover analysis nested in a population-based case-referent study |journal=Am. J. Epidemiol. |volume=151 |issue=5 |pages=459–67 |year=2000 |month=March |pmid=10707914 |doi= |url=http://aje.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=10707914}}</ref>
-<ref name="pmid10568645">{{cite journal |author=Giri S, Thompson PD, Kiernan FJ, ''et al'' |title=Clinical and angiographic characteristics of exertion-related acute myocardial infarction |journal=JAMA |volume=282 |issue=18 |pages=1731–6 |year=1999 |month=November |pmid=10568645 |doi= |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=10568645}}</ref><ref name="pmid11070099">{{cite journal |author=Albert CM, Mittleman MA, Chae CU, Lee IM, Hennekens CH, Manson JE |title=Triggering of sudden death from cardiac causes by vigorous exertion |journal=N. Engl. J. Med. |volume=343 |issue=19 |pages=1355–61 |year=2000 |month=November |pmid=11070099 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=11070099&promo=ONFLNS19}}</ref><ref name="pmid16551711">{{cite journal |author=Whang W, Manson JE, Hu FB, ''et al'' |title=Physical exertion, exercise, and sudden cardiac death in women |journal=JAMA |volume=295 |issue=12 |pages=1399–403 |year=2006 |month=March |pmid=16551711 |doi=10.1001/jama.295.12.1399 |url=}}</ref><ref name="pmid6472399">{{cite journal |author=Siscovick DS, Weiss NS, Fletcher RH, Lasky T |title=The incidence of primary cardiac arrest during vigorous exercise |journal=N. Engl. J. Med. |volume=311 |issue=14 |pages=874–7 |year=1984 |month=October |pmid=6472399 |doi= |url=}}</ref> The ONSET study demonstrated that intense exertion (defined as >/= 6 metabloic equivalents of METS) within the previous hour was associated with a 5.9 fold rise in the risk of MI
+<ref name="pmid10568645">{{cite journal |author=Giri S, Thompson PD, Kiernan FJ, ''et al'' |title=Clinical and angiographic characteristics of exertion-related acute myocardial infarction |journal=JAMA |volume=282 |issue=18 |pages=1731–6 |year=1999 |month=November |pmid=10568645 |doi= |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=10568645}}</ref><ref name="pmid11070099">{{cite journal |author=Albert CM, Mittleman MA, Chae CU, Lee IM, Hennekens CH, Manson JE |title=Triggering of sudden death from cardiac causes by vigorous exertion |journal=N. Engl. J. Med. |volume=343 |issue=19 |pages=1355–61 |year=2000 |month=November |pmid=11070099 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=11070099&promo=ONFLNS19}}</ref><ref name="pmid16551711">{{cite journal |author=Whang W, Manson JE, Hu FB, ''et al'' |title=Physical exertion, exercise, and sudden cardiac death in women |journal=JAMA |volume=295 |issue=12 |pages=1399–403 |year=2006 |month=March |pmid=16551711 |doi=10.1001/jama.295.12.1399 |url=}}</ref><ref name="pmid6472399">{{cite journal |author=Siscovick DS, Weiss NS, Fletcher RH, Lasky T |title=The incidence of primary cardiac arrest during vigorous exercise |journal=N. Engl. J. Med. |volume=311 |issue=14 |pages=874–7 |year=1984 |month=October |pmid=6472399 |doi= |url=}}</ref> The ONSET study demonstrated that intense exertion (defined as >/= 6 metabolic equivalents of METS) within the previous hour was associated with a 5.9 fold rise in the risk of MI
 <ref name="pmid8232456">{{cite journal |author=Mittleman MA, Maclure M, Tofler GH, Sherwood JB, Goldberg RJ, Muller JE |title=Triggering of acute myocardial infarction by heavy physical exertion. Protection against triggering by regular exertion. Determinants of Myocardial Infarction Onset Study Investigators |journal=N. Engl. J. Med. |volume=329 |issue=23 |pages=1677–83 |year=1993 |month=December |pmid=8232456 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=8232456&promo=ONFLNS19}}</ref>.
-'''Studies Linking Physical Exertion to MI'''
+Studies linking physical exertion to MI:
-:* The ONSET Study: Relative risk = 5.9 <ref name="pmid8232456">{{cite journal |author=Mittleman MA, Maclure M, Tofler GH, Sherwood JB, Goldberg RJ, Muller JE |title=Triggering of acute myocardial infarction by heavy physical exertion. Protection against triggering by regular exertion. Determinants of Myocardial Infarction Onset Study Investigators |journal=N. Engl. J. Med. |volume=329 |issue=23 |pages=1677–83 |year=1993 |month=December |pmid=8232456 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=8232456&promo=ONFLNS19}}</ref>
+* The ONSET Study: Relative risk = 5.9 <ref name="pmid8232456">{{cite journal |author=Mittleman MA, Maclure M, Tofler GH, Sherwood JB, Goldberg RJ, Muller JE |title=Triggering of acute myocardial infarction by heavy physical exertion. Protection against triggering by regular exertion. Determinants of Myocardial Infarction Onset Study Investigators |journal=N. Engl. J. Med. |volume=329 |issue=23 |pages=1677–83 |year=1993 |month=December |pmid=8232456 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=8232456&promo=ONFLNS19}}</ref>
-:* The Stockholm Heart Epidemiology Program (SHEEP): Relative risk = 6.1 <ref name="pmid10707914">{{cite journal |author=Hallqvist J, Möller J, Ahlbom A, Diderichsen F, Reuterwall C, de Faire U |title=Does heavy physical exertion trigger myocardial infarction? A case-crossover analysis nested in a population-based case-referent study |journal=Am. J. Epidemiol. |volume=151 |issue=5 |pages=459–67 |year=2000 |month=March |pmid=10707914 |doi= |url=http://aje.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=10707914}}</ref>
+* The Stockholm Heart Epidemiology Program (SHEEP): Relative risk = 6.1 <ref name="pmid10707914">{{cite journal |author=Hallqvist J, Möller J, Ahlbom A, Diderichsen F, Reuterwall C, de Faire U |title=Does heavy physical exertion trigger myocardial infarction? A case-crossover analysis nested in a population-based case-referent study |journal=Am. J. Epidemiol. |volume=151 |issue=5 |pages=459–67 |year=2000 |month=March |pmid=10707914 |doi= |url=http://aje.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=10707914}}</ref>
-:* The Triggers and Mechanisms of Myocardial Infarction (TRIMM) study: Relative risk = 2.1 <ref name="pmid8232457">{{cite journal |author=Willich SN, Lewis M, Löwel H, Arntz HR, Schubert F, Schröder R |title=Physical exertion as a trigger of acute myocardial infarction. Triggers and Mechanisms of Myocardial Infarction Study Group |journal=N. Engl. J. Med. |volume=329 |issue=23 |pages=1684–90 |year=1993 |month=December |pmid=8232457 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=8232457&promo=ONFLNS19}}</ref>
+* The Triggers and Mechanisms of Myocardial Infarction (TRIMM) study: Relative risk = 2.1 <ref name="pmid8232457">{{cite journal |author=Willich SN, Lewis M, Löwel H, Arntz HR, Schubert F, Schröder R |title=Physical exertion as a trigger of acute myocardial infarction. Triggers and Mechanisms of Myocardial Infarction Study Group |journal=N. Engl. J. Med. |volume=329 |issue=23 |pages=1684–90 |year=1993 |month=December |pmid=8232457 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=8232457&promo=ONFLNS19}}</ref>
-Blizzards have often been cited as a trigger of MI, and the physical exertion of snow shoveling has frequently been cited as a contributor.
+Blizzards have often been cited as a trigger of MI, and the physical exertion of snow shoveling has frequently been cited as a contributor. <ref name="pmid85066">{{cite journal |author=Glass RI, Zack MM |title=Increase in deaths from ischaemic heart-disease after blizzards |journal=Lancet |volume=1 |issue=8114 |pages=485–7 |year=1979 |month=March |pmid=85066 |doi= |url=}}</ref>
-<ref name="pmid85066">{{cite journal |author=Glass RI, Zack MM |title=Increase in deaths from ischaemic heart-disease after blizzards |journal=Lancet |volume=1 |issue=8114 |pages=485–7 |year=1979 |month=March |pmid=85066 |doi= |url=}}</ref>
 <ref name="pmid8623739">{{cite journal |author=Franklin BA, Bonzheim K, Gordon S, Timmis GC |title=Snow shoveling: a trigger for acute myocardial infarction and sudden coronary death |journal=Am. J. Cardiol. |volume=77 |issue=10 |pages=855–8 |year=1996 |month=April |pmid=8623739 |doi=10.1016/S0002-9149(97)89181-3 |url=}}</ref>
-'''Impact of a Sedentary Lifestyle'''
+Impact of a sedentary lifestyle:
 The relative risk of MI quoted above increases dramatically among those individuals who lead a sedentary lifestyle. For those in poor physical condition, the relative risk was 107 fold higher in the ONSET study.  In contrast, among those individuals who reported that they engaged in physical activity 5 days a week or more, the risk was only doubled.
-'''Mechanism'''
+Mechanism:
 It has been hypothesized that exertion increases blood pressure, pulse and oscillatory shear which in turn may increase the risk of plaque rupture.
 ==Physical Exertion and Sudden Death==
-While the above discussion pertains to documented ''nonfatal MI'', approximately a quarter of MI patients may die of ''[[sudden death]]'' or ''fatal MI'' before reaching the hospital. In a cohort of 21,481 male physicians in the United States who by self report who had no prior history of [[coronary artery disease]], there was a 16.9 fold rise in the risk of [[sudden cardiac death]] within 30 minutes of intense exertion (>/= 6 METS).
+While the above discussion pertains to documented nonfatal MI, approximately a quarter of MI patients may die of [[sudden death]] or fatal MI before reaching the hospital. In a cohort of 21,481 male physicians in the United States who by self report who had no prior history of [[coronary artery disease]], there was a 16.9 fold rise in the risk of [[sudden cardiac death]] within 30 minutes of intense exertion (>/= 6 METS)
-<ref name="pmid11070099">{{cite journal |author=Albert CM, Mittleman MA, Chae CU, Lee IM, Hennekens CH, Manson JE |title=Triggering of sudden death from cardiac causes by vigorous exertion |journal=N. Engl. J. Med. |volume=343 |issue=19 |pages=1355–61 |year=2000 |month=November |pmid=11070099 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=11070099&promo=ONFLNS19}}</ref>
+<ref name="pmid11070099">{{cite journal |author=Albert CM, Mittleman MA, Chae CU, Lee IM, Hennekens CH, Manson JE |title=Triggering of sudden death from cardiac causes by vigorous exertion |journal=N. Engl. J. Med. |volume=343 |issue=19 |pages=1355–61 |year=2000 |month=November |pmid=11070099 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=11070099&promo=ONFLNS19}}</ref>.
 Similar to what has been reported with respect to the onset of MI, there was no increase in the risk of sudden death with heavy exertion among those nurses who exercised more than 2 hours per week.
 ==Psychological Stress==
 Psychological stress associated with anger <ref name="pmid7671353">{{cite journal |author=Mittleman MA, Maclure M, Sherwood JB, ''et al'' |title=Triggering of acute myocardial infarction onset by episodes of anger. Determinants of Myocardial Infarction Onset Study Investigators |journal=Circulation |volume=92 |issue=7 |pages=1720–5 |year=1995 |month=October |pmid=7671353 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7671353}}</ref>, work related stressful events <ref name="pmid15598722">{{cite journal |author=Möller J, Theorell T, de Faire U, Ahlbom A, Hallqvist J |title=Work related stressful life events and the risk of myocardial infarction. Case-control and case-crossover analyses within the Stockholm heart epidemiology programme (SHEEP) |journal=J Epidemiol Community Health |volume=59 |issue=1 |pages=23–30 |year=2005 |month=January |pmid=15598722 |pmc=1763356 |doi=10.1136/jech.2003.019349 |url=}}</ref>, wartime bombing <ref name="pmid12459401">{{cite journal |author=Johnston SC, Sorel ME, Sidney S |title=Effects of the September 11th attacks on urgent and emergent medical evaluations in a Northern California managed care plan |journal=Am. J. Med. |volume=113 |issue=7 |pages=556–62 |year=2002 |month=November |pmid=12459401 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002934302013219}}</ref> <ref name="pmid16128473">{{cite journal |author=Vukovic DS, Krotin ME, Babic MM, Zivanovic BM |title=Anxiety level and responses to stress caused by air raids among patients with ischemic heart disease |journal=Prehosp Disaster Med |volume=20 |issue=4 |pages=249–52 |year=2005 |pmid=16128473 |doi= |url=}}</ref>
 , earthquakes <ref name="pmid6131167">{{cite journal |author=Trichopoulos D, Katsouyanni K, Zavitsanos X, Tzonou A, Dalla-Vorgia P |title=Psychological stress and fatal heart attack: the Athens (1981) earthquake natural experiment |journal=Lancet |volume=1 |issue=8322 |pages=441–4 |year=1983 |month=February |pmid=6131167 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(83)91439-3}}</ref> and other natural disasters has been associated with an increased risk of onset of myocardial infarction.
 ====Anger====
 Intense anger (fist / teeth clenched) has been associated with a risk in the risk of MI in the 2 hours following the episode in the following studies:
+* ONSET: 2.3 fold rise<ref name="pmid7671353">{{cite journal |author=Mittleman MA, Maclure M, Sherwood JB, ''et al'' |title=Triggering of acute myocardial infarction onset by episodes of anger. Determinants of Myocardial Infarction Onset Study Investigators |journal=Circulation |volume=92 |issue=7 |pages=1720–5 |year=1995 |month=October |pmid=7671353 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7671353}}</ref>
-ONSET: 2.3 fold rise
+* SHEEP: 9 fold rise<ref name="pmid10593637">{{cite journal |author=Möller J, Hallqvist J, Diderichsen F, Theorell T, Reuterwall C, Ahlbom A |title=Do episodes of anger trigger myocardial infarction? A case-crossover analysis in the Stockholm Heart Epidemiology Program (SHEEP) |journal=Psychosom Med |volume=61 |issue=6 |pages=842–9 |year=1999 |pmid=10593637 |doi= |url=http://www.psychosomaticmedicine.org/cgi/pmidlookup?view=long&pmid=10593637}}</ref>
-<ref name="pmid7671353">{{cite journal |author=Mittleman MA, Maclure M, Sherwood JB, ''et al'' |title=Triggering of acute myocardial infarction onset by episodes of anger. Determinants of Myocardial Infarction Onset Study Investigators |journal=Circulation |volume=92 |issue=7 |pages=1720–5 |year=1995 |month=October |pmid=7671353 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7671353}}</ref>
+*Kotton et al: 14 fold rise<ref name="pmid15596741">{{cite journal |author=Koton S, Tanne D, Bornstein NM, Green MS |title=Triggering risk factors for ischemic stroke: a case-crossover study |journal=Neurology |volume=63 |issue=11 |pages=2006–10 |year=2004 |month=December |pmid=15596741 |doi= |url=http://www.neurology.org/cgi/pmidlookup?view=long&pmid=15596741}}</ref>
-SHEEP: 9 fold rise
-<ref name="pmid10593637">{{cite journal |author=Möller J, Hallqvist J, Diderichsen F, Theorell T, Reuterwall C, Ahlbom A |title=Do episodes of anger trigger myocardial infarction? A case-crossover analysis in the Stockholm Heart Epidemiology Program (SHEEP) |journal=Psychosom Med |volume=61 |issue=6 |pages=842–9 |year=1999 |pmid=10593637 |doi= |url=http://www.psychosomaticmedicine.org/cgi/pmidlookup?view=long&pmid=10593637}}</ref>
-Kotton et al: 14 fold rise
-<ref name="pmid15596741">{{cite journal |author=Koton S, Tanne D, Bornstein NM, Green MS |title=Triggering risk factors for ischemic stroke: a case-crossover study |journal=Neurology |volume=63 |issue=11 |pages=2006–10 |year=2004 |month=December |pmid=15596741 |doi= |url=http://www.neurology.org/cgi/pmidlookup?view=long&pmid=15596741}}</ref>
 The psychosocial stressors that precipitated the anger were as follows:
+*Argument with family members (25%)
-#Argument with family members (25%)
+*Conflicts at work (22%)
-#Conflicts at work (22%)
+*Legal problems (8%)
-#Legal problems (8%)
 ====Anxiety====
-If a patient is in the >75th percentile for anxiety, this increases the relative risk of MI 1.6 fold for the 2 hours following the period of anxiety.
+If a patient is in the >75th percentile for [[anxiety]], this increases the relative risk of MI 1.6 fold for the 2 hours following the period of anxiety.<ref name="pmid7671353">{{cite journal |author=Mittleman MA, Maclure M, Sherwood JB, ''et al'' |title=Triggering of acute myocardial infarction onset by episodes of anger. Determinants of Myocardial Infarction Onset Study Investigators |journal=Circulation |volume=92 |issue=7 |pages=1720–5 |year=1995 |month=October |pmid=7671353 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7671353}}</ref>
-<ref name="pmid7671353">{{cite journal |author=Mittleman MA, Maclure M, Sherwood JB, ''et al'' |title=Triggering of acute myocardial infarction onset by episodes of anger. Determinants of Myocardial Infarction Onset Study Investigators |journal=Circulation |volume=92 |issue=7 |pages=1720–5 |year=1995 |month=October |pmid=7671353 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7671353}}</ref>
 ====Bereavement and the Broken Heart Syndrome====
+[[Stress cardiomyopathy]] which is also known as Left Ventricular Apical Ballooning Syndrome, Takotsubo cardiomyopathy, or Ampulla-shaped cardiomyopathy is a cardiac syndrome characterized by a reversible transient apical ventricular dysfunction. Since the [[cardiomyopathy]] is often triggered by emotional stress, such as the death of a loved one, the condition is sometimes also referred to as the Broken Heart Syndrome. In 2006, the syndrome was renamed Stress Cardiomyopathy, and was classified as an acquired cardiomyopathy. <ref name="pmid16567565">{{cite journal |author=Maron BJ, Towbin JA, Thiene G, ''et al'' |title=Contemporary definitions and classification of the cardiomyopathies: an American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention |journal=Circulation |volume=113 |issue=14 |pages=1807–16 |year=2006 |pmid=16567565 |doi=10.1161/CIRCULATIONAHA.106.174287}}</ref>
-[[Stress cardiomyopathy]] which is also known as '''Left Ventricular Apical Ballooning Syndrome''', '''Takotsubo cardiomyopathy''', or '''Ampulla-Shaped Cardiomyopathy''' is a cardiac syndrome characterized by a reversible transient apical ventricular dysfunction. Since the [[cardiomyopathy]] is often triggered by emotional stress, such as the death of a loved one, the condition is sometimes also referred to as the '''Broken Heart Syndrome'''. In 2006, the syndrome was renamed '''Stress Cardiomyopathy''', and was classified as an acquired cardiomyopathy. <ref name="pmid16567565">{{cite journal |author=Maron BJ, Towbin JA, Thiene G, ''et al'' |title=Contemporary definitions and classification of the cardiomyopathies: an American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention |journal=Circulation |volume=113 |issue=14 |pages=1807–16 |year=2006 |pmid=16567565 |doi=10.1161/CIRCULATIONAHA.106.174287}}</ref>
+The typical presentation of someone with takotsubo cardiomyopathy is a sudden onset of [[congestive heart failure]] or chest pain associated with [[electrocardiogram|EKG]] changes suggestive of an [[left ventricle|anterior wall]] [[myocardial infarction|acute MI]].  During the course of evaluation of the patient, a bulging out of the left ventricular apex with a hypercontractile base of the left ventricle is often noted.  It is the hallmark bulging out of the apex of the heart with preserved function of the base that earned the syndrome its name "tako tsubo", or octopus trap in Japan, where it was first described.  Evaluation of individuals with takotsubo cardiomyopathy typically include a [[coronary angiogram]], which does not reveal any significant blockages that would cause the [[left ventricle|left ventricular]] dysfunction.  Provided that the individual survives their initial presentation, the left ventricular function improves within days to weeks<ref name="pmid17483198">{{cite journal |author=Akashi YJ, Barbaro G, Sakurai T, Nakazawa K, Miyake F |title=Cardiac autonomic imbalance in patients with reversible ventricular dysfunction takotsubo cardiomyopathy |journal=QJM |volume=100 |issue=6 |pages=335–43 |year=2007 |pmid=17483198 |doi=10.1093/qjmed/hcm028}}</ref>.
+Takotsubo cardiomyopathy is more commonly seen in post-menopausal women<ref name=Azzarelli-2006>{{cite journal | author=Azzarelli S, Galassi AR, Amico F, Giacoppo M, Argentino V, Tomasello SD, Tamburino C, Fiscella A. | title=Clinical features of transient left ventricular apical ballooning | journal=Am J Cardiol. | year=2006 | volume=98 | issue=9 | pages=1273-6 | id=PMID 17056345}}</ref>.  Often there is a history of a recent severe emotional or physical stress.<ref name=Azzarelli-2006 />
-The typical presentation of someone with takotsubo cardiomyopathy is a sudden onset of [[congestive heart failure]] or chest pain associated with [[electrocardiogram|EKG]] changes suggestive of an [[left ventricle|anterior wall]] [[myocardial infarction|acute MI]].  During the course of evaluation of the patient, a bulging out of the left ventricular apex with a hypercontractile base of the left ventricle is often noted.  It is the hallmark bulging out of the apex of the heart with preserved function of the base that earned the syndrome its name "tako tsubo", or octopus trap in Japan, where it was first described.  Evaluation of individuals with takotsubo cardiomyopathy typically include a [[coronary angiogram]], which does not reveal any significant blockages that would cause the [[left ventricle|left ventricular]] dysfunction.  Provided that the individual survives their initial presentation, the left ventricular function improves within days to weeks.<ref name="pmid17483198">{{cite journal |author=Akashi YJ, Barbaro G, Sakurai T, Nakazawa K, Miyake F |title=Cardiac autonomic imbalance in patients with reversible ventricular dysfunction takotsubo cardiomyopathy |journal=QJM |volume=100 |issue=6 |pages=335–43 |year=2007 |pmid=17483198 |doi=10.1093/qjmed/hcm028}}</ref>
-Takotsubo cardiomyopathy is more commonly seen in post-menopausal women.<ref name=Azzarelli-2006>{{cite journal | author=Azzarelli S, Galassi AR, Amico F, Giacoppo M, Argentino V, Tomasello SD, Tamburino C, Fiscella A. | title=Clinical features of transient left ventricular apical ballooning | journal=Am J Cardiol. | year=2006 | volume=98 | issue=9 | pages=1273-6 | id=PMID 17056345}}</ref>  Often there is a history of a recent severe emotional or physical stress.<ref name=Azzarelli-2006 />
 ===Work Related Stress===
 ====Deadlines====
-An agressive timeline or deadline at work has been associated with a rise in the risk of MI:
+An aggressive timeline or deadline at work has been associated with a rise in the risk of MI:
+*The SHEEP study: 6 fold rise
-The SHEEP study: 6 fold rise
+*The ONSET study: 2.3 fold rise
-The ONSET study: 2.3 fold rise
 ====Firing an Employee====
 The stress of firing an employee has been associated with a rise in the risk of MI:
+*The ONSET study: 2.2 fold rise
-The ONSET study: 2.2 fold rise
 ===Natural Disasters===
@@ Line 278: / Line 93: @@
 <ref name="pmid8651102">{{cite journal |author=Leor J, Kloner RA |title=The Northridge earthquake as a trigger for acute myocardial infarction |journal=Am. J. Cardiol. |volume=77 |issue=14 |pages=1230–2 |year=1996 |month=June |pmid=8651102 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914996001695}}</ref>
 <ref name="pmid8552142">{{cite journal |author=Leor J, Poole WK, Kloner RA |title=Sudden cardiac death triggered by an earthquake |journal=N. Engl. J. Med. |volume=334 |issue=7 |pages=413–9 |year=1996 |month=February |pmid=8552142 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=8552142&promo=ONFLNS19}}</ref>
-It is notable that the association of earthquakes with MI is variable depending upon the time of day that the earthquake occurs. The LA eathquake occurred just after 4 A.M., just when platelet aggregation may be at a peak (see below). However, the earthquake that struck San Francisco Bay in 1989 at 5 P.M. was not associated with an increased risk of MI.
+It is notable that the association of earthquakes with MI is variable depending upon the time of day that the earthquake occurs. The LA earthquake occurred just after 4 A.M., just when platelet aggregation may be at a peak (see below). However, the earthquake that struck San Francisco Bay in 1989 at 5 P.M. was not associated with an increased risk of MI.
 <ref name="pmid10220631">{{cite journal |author=Brown DL |title=Disparate effects of the 1989 Loma Prieta and 1994 Northridge earthquakes on hospital admissions for acute myocardial infarction: importance of superimposition of triggers |journal=Am. Heart J. |volume=137 |issue=5 |pages=830–6 |year=1999 |month=May |pmid=10220631 |doi= |url=}}</ref>
@@ Line 293: / Line 108: @@
 The stress of sporting events has been associated with an increased risk of MI in a population. An example that has been cited is the 50% increase in the risk of MI or stroke among Dutch men associated with the loss of Holland to France in the 1996 European football finals. It is notable that no such rise in risk was observed among Dutch women or the French.
 <ref name="pmid11124170">{{cite journal |author=Witte DR, Bots ML, Hoes AW, Grobbee DE |title=Cardiovascular mortality in Dutch men during 1996 European football championship: longitudinal population study |journal=BMJ |volume=321 |issue=7276 |pages=1552–4 |year=2000 |pmid=11124170 |pmc=27557 |doi= |url=http://bmj.com/cgi/pmidlookup?view=long&pmid=11124170}}</ref>
-<ref name="pmid11403063">{{cite journal |author=Toubiana L, Hanslik T, Letrilliart L |title=French cardiovascular mortality did not increase during 1996 European football championship |journal=BMJ |volume=322 |issue=7297 |pages=1306 |year=2001 |month=May |pmid=11403063 |pmc=1120392 |doi= |url=}}</ref>
+<ref name="pmid11403063">{{cite journal |author=Toubiana L, Hanslik T, Letrilliart L |title=French cardiovascular mortality did not increase during 1996 European football championship |journal=BMJ |volume=322 |issue=7297 |pages=1306 |year=2001 |month=May |pmid=11403063 |pmc=1120392 |doi= |url=}}</ref> The World Cup of soccer has been associated with a doubling of MI incidence. <ref>N Engl J Med 2008; 358:475-483.</ref>
 ==Sexual Activity==
-The association of sexual activity with the onset of MI may represent components of physical exertion as well as psychologic stress. In both the SHEEP and the ONSET studies, recent sexual activity increased the risk of MI by 2.5 fold.
+The association of sexual activity with the onset of MI may represent components of physical exertion as well as psychologic stress. In both the SHEEP and the ONSET studies, recent sexual activity increased the risk of MI by 2.5 fold
-<ref name="pmid8618365">{{cite journal |author=Muller JE, Mittleman MA, Maclure M, Sherwood JB, Tofler GH |title=Triggering myocardial infarction by sexual activity. Low absolute risk and prevention by regular physical exertion. Determinants of Myocardial Infarction Onset Study Investigators |journal=JAMA |volume=275 |issue=18 |pages=1405–9 |year=1996 |month=May |pmid=8618365 |doi= |url=}}</ref><ref name="pmid11559674">{{cite journal |author=Möller J, Ahlbom A, Hulting J, ''et al'' |title=Sexual activity as a trigger of myocardial infarction. A case-crossover analysis in the Stockholm Heart Epidemiology Programme (SHEEP) |journal=Heart |volume=86 |issue=4 |pages=387–90 |year=2001 |month=October |pmid=11559674 |pmc=1729949 |doi= |url=http://heart.bmj.com/cgi/pmidlookup?view=long&pmid=11559674}}</ref>
+<ref name="pmid8618365">{{cite journal |author=Muller JE, Mittleman MA, Maclure M, Sherwood JB, Tofler GH |title=Triggering myocardial infarction by sexual activity. Low absolute risk and prevention by regular physical exertion. Determinants of Myocardial Infarction Onset Study Investigators |journal=JAMA |volume=275 |issue=18 |pages=1405–9 |year=1996 |month=May |pmid=8618365 |doi= |url=}}</ref><ref name="pmid11559674">{{cite journal |author=Möller J, Ahlbom A, Hulting J, ''et al'' |title=Sexual activity as a trigger of myocardial infarction. A case-crossover analysis in the Stockholm Heart Epidemiology Programme (SHEEP) |journal=Heart |volume=86 |issue=4 |pages=387–90 |year=2001 |month=October |pmid=11559674 |pmc=1729949 |doi= |url=http://heart.bmj.com/cgi/pmidlookup?view=long&pmid=11559674}}</ref>.
-Again, to place this relative risk into clinical context, it should be noted that only 3% of MI patients had had sexual intercourse within the past 2 hours prior to the onset of MI. It should also be noted that the increase in risk of MI with sexual activity did not differ between patients with and without a history of coronary artery disease.
+Again, to place this [[relative risk]] into clinical context, it should be noted that only 3% of MI patients had had sexual intercourse within the past 2 hours prior to the onset of MI. It should also be noted that the increase in risk of MI with sexual activity did not differ between patients with and without a history of coronary artery disease.
 The risk of MI with sexual intercourse is a frequent concern among patients who have coronary artery disease. Again, the data above indicates that recent sexual activity doubles the risk of an MI, and this may on the surface appear to be disconcerting to both a patient and healthcare professional. But again, to place this relative risk into context, the absolute risk must be taken into account. The average risk of an MI in a patient at average risk has been estimated to be about 1 chance in a million during any given hour during middle age. Sexual activity increases that risk to 2 in a million per hour for the 2 hours after sexual intercourse.  If the annual risk of MI is about 1%, weekly sexual intercourse will increase this annual risk to just 1.01%.
@@ Line 307: / Line 122: @@
 ==Air Pollution / Fine Particulate Matter==
-Exposure to high levels of ambeint air pollution (exposure to fine particulate matter in the past 2 - 24 hours) has been associated with a transient elevation in the risk of myocardial infarction <ref name="pmid11401937">{{cite journal |author=Peters A, Dockery DW, Muller JE, Mittleman MA |title=Increased particulate air pollution and the triggering of myocardial infarction |journal=Circulation |volume=103 |issue=23 |pages=2810–5 |year=2001 |month=June |pmid=11401937 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=11401937}}</ref>.  There is a rise in CRP and plasma viscosity following exposure to fine particulate matter and it has been speculated that the pulmonary inflammation that follows such exposure may trigger a systemic state of hypercoagulability <ref name="pmid9174559">{{cite journal |author=Peters A, Döring A, Wichmann HE, Koenig W |title=Increased plasma viscosity during an air pollution episode: a link to mortality? |journal=Lancet |volume=349 |issue=9065 |pages=1582–7 |year=1997 |month=May |pmid=9174559 |doi=10.1016/S0140-6736(97)01211-7 |url=}}</ref><ref name="pmid11440492">{{cite journal |author=Peters A, Fröhlich M, Döring A, ''et al'' |title=Particulate air pollution is associated with an acute phase response in men; results from the MONICA-Augsburg Study |journal=Eur. Heart J. |volume=22 |issue=14 |pages=1198–204 |year=2001 |month=July |pmid=11440492 |doi=10.1053/euhj.2000.2483 |url=}}</ref>.  Exposure to fine particulate matter has also been associated with changes in autonomic tone manifested by sinus tachycardia <ref name="pmid9927345">{{cite journal |author=Pope CA3rd, Dockery DW, Kanner RE, Villegas GM, Schwartz J |title=Oxygen saturation, pulse rate, and particulate air pollution: A daily time-series panel study |journal=Am. J. Respir. Crit. Care Med. |volume=159 |issue=2 |pages=365–72 |year=1999 |month=February |pmid=9927345 |doi= |url=http://ajrccm.atsjournals.org/cgi/pmidlookup?view=long&pmid=9927345}}</ref> <ref name="pmid10568625">{{cite journal |author=Peters A, Perz S, Döring A, Stieber J, Koenig W, Wichmann HE |title=Increases in heart rate during an air pollution episode |journal=Am. J. Epidemiol. |volume=150 |issue=10 |pages=1094–8 |year=1999 |month=November |pmid=10568625 |doi= |url=http://aje.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=10568625}}</ref>, as well as a reduction in heart rate variability <ref name="pmid10378998">{{cite journal |author=Liao D, Creason J, Shy C, Williams R, Watts R, Zweidinger R |title=Daily variation of particulate air pollution and poor cardiac autonomic control in the elderly |journal=Environ. Health Perspect. |volume=107 |issue=7 |pages=521–5 |year=1999 |month=July |pmid=10378998 |pmc=1566669 |doi= |url=}}</ref> <ref name="pmid10539820">{{cite journal |author=Pope CA, Verrier RL, Lovett EG, ''et al'' |title=Heart rate variability associated with particulate air pollution |journal=Am. Heart J. |volume=138 |issue=5 Pt 1 |pages=890–9 |year=1999 |month=November |pmid=10539820 |doi= |url=}}</ref> <ref name="pmid10725286">{{cite journal |author=Gold DR, Litonjua A, Schwartz J, ''et al'' |title=Ambient pollution and heart rate variability |journal=Circulation |volume=101 |issue=11 |pages=1267–73 |year=2000 |month=March |pmid=10725286 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10725286}}</ref>. Finally, ventricular arrhythmias as manifested by firing of AICDs has been associated with exposure to fine particulate matter <ref name="pmid10615837">{{cite journal |author=Peters A, Liu E, Verrier RL, ''et al'' |title=Air pollution and incidence of cardiac arrhythmia |journal=Epidemiology |volume=11 |issue=1 |pages=11–7 |year=2000 |month=January |pmid=10615837 |doi= |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=1044-3983&volume=11&issue=1&spage=11}}</ref>.
+Exposure to high levels of ambeint air pollution (exposure to fine particulate matter in the past 2 - 24 hours) has been associated with a transient elevation in the risk of myocardial infarction <ref name="pmid11401937">{{cite journal |author=Peters A, Dockery DW, Muller JE, Mittleman MA |title=Increased particulate air pollution and the triggering of myocardial infarction |journal=Circulation |volume=103 |issue=23 |pages=2810–5 |year=2001 |month=June |pmid=11401937 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=11401937}}</ref>.  There is a rise in [[CRP]] and plasma viscosity following exposure to fine particulate matter and it has been speculated that the pulmonary inflammation that follows such exposure may trigger a systemic state of hypercoagulability <ref name="pmid9174559">{{cite journal |author=Peters A, Döring A, Wichmann HE, Koenig W |title=Increased plasma viscosity during an air pollution episode: a link to mortality? |journal=Lancet |volume=349 |issue=9065 |pages=1582–7 |year=1997 |month=May |pmid=9174559 |doi=10.1016/S0140-6736(97)01211-7 |url=}}</ref><ref name="pmid11440492">{{cite journal |author=Peters A, Fröhlich M, Döring A, ''et al'' |title=Particulate air pollution is associated with an acute phase response in men; results from the MONICA-Augsburg Study |journal=Eur. Heart J. |volume=22 |issue=14 |pages=1198–204 |year=2001 |month=July |pmid=11440492 |doi=10.1053/euhj.2000.2483 |url=}}</ref>.  Exposure to fine particulate matter has also been associated with changes in autonomic tone manifested by [[sinus tachycardia]] <ref name="pmid9927345">{{cite journal |author=Pope CA3rd, Dockery DW, Kanner RE, Villegas GM, Schwartz J |title=Oxygen saturation, pulse rate, and particulate air pollution: A daily time-series panel study |journal=Am. J. Respir. Crit. Care Med. |volume=159 |issue=2 |pages=365–72 |year=1999 |month=February |pmid=9927345 |doi= |url=http://ajrccm.atsjournals.org/cgi/pmidlookup?view=long&pmid=9927345}}</ref> <ref name="pmid10568625">{{cite journal |author=Peters A, Perz S, Döring A, Stieber J, Koenig W, Wichmann HE |title=Increases in heart rate during an air pollution episode |journal=Am. J. Epidemiol. |volume=150 |issue=10 |pages=1094–8 |year=1999 |month=November |pmid=10568625 |doi= |url=http://aje.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=10568625}}</ref>, as well as a reduction in heart rate variability <ref name="pmid10378998">{{cite journal |author=Liao D, Creason J, Shy C, Williams R, Watts R, Zweidinger R |title=Daily variation of particulate air pollution and poor cardiac autonomic control in the elderly |journal=Environ. Health Perspect. |volume=107 |issue=7 |pages=521–5 |year=1999 |month=July |pmid=10378998 |pmc=1566669 |doi= |url=}}</ref> <ref name="pmid10539820">{{cite journal |author=Pope CA, Verrier RL, Lovett EG, ''et al'' |title=Heart rate variability associated with particulate air pollution |journal=Am. Heart J. |volume=138 |issue=5 Pt 1 |pages=890–9 |year=1999 |month=November |pmid=10539820 |doi= |url=}}</ref> <ref name="pmid10725286">{{cite journal |author=Gold DR, Litonjua A, Schwartz J, ''et al'' |title=Ambient pollution and heart rate variability |journal=Circulation |volume=101 |issue=11 |pages=1267–73 |year=2000 |month=March |pmid=10725286 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10725286}}</ref>. Finally, [[ventricular arrhythmia]]s as manifested by firing of AICDs has been associated with exposure to fine particulate matter <ref name="pmid10615837">{{cite journal |author=Peters A, Liu E, Verrier RL, ''et al'' |title=Air pollution and incidence of cardiac arrhythmia |journal=Epidemiology |volume=11 |issue=1 |pages=11–7 |year=2000 |month=January |pmid=10615837 |doi= |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=1044-3983&volume=11&issue=1&spage=11}}</ref>.
 ==Antecedent Infection==
-Acute severe infection, such as [[pneumonia]], can trigger myocardial infarction <ref name="pmid15602021">{{cite journal |author=Smeeth L, Thomas SL, Hall AJ, Hubbard R, Farrington P, Vallance P |title=Risk of myocardial infarction and stroke after acute infection or vaccination |journal=N. Engl. J. Med. |volume=351 |issue=25 |pages=2611–8 |year=2004 |month=December |pmid=15602021 |doi=10.1056/NEJMoa041747 |url=}}</ref>. 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 | id=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 | id=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 | id=PMID 15928286}}</ref>
+Acute severe infection, such as [[pneumonia]], can trigger myocardial infarction <ref name="pmid15602021">{{cite journal |author=Smeeth L, Thomas SL, Hall AJ, Hubbard R, Farrington P, Vallance P |title=Risk of myocardial infarction and stroke after acute infection or vaccination |journal=N. Engl. J. Med. |volume=351 |issue=25 |pages=2611–8 |year=2004 |month=December |pmid=15602021 |doi=10.1056/NEJMoa041747 |url=}}</ref>. 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 | id=PMID 1733381}}</ref>. While this intracellular organism has been demonstrated in atherosclerotic [[plaque]]s, 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 | id=PMID 1733381}}</ref>.Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of [[heart attack]]s 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 | id=PMID 15928286}}</ref>
 ==A Heavy Meal==
@@ Line 321: / Line 136: @@
 ==Cocaine==
-Ingestion of cocaine has been associated with STEMI <ref name="pmid10351966">{{cite journal |author=Mittleman MA, Mintzer D, Maclure M, Tofler GH, Sherwood JB, Muller JE |title=Triggering of myocardial infarction by cocaine |journal=Circulation |volume=99 |issue=21 |pages=2737–41 |year=1999 |month=June |pmid=10351966 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10351966}}</ref>.
+Ingestion of [[cocaine]] has been associated with STEMI <ref name="pmid10351966">{{cite journal |author=Mittleman MA, Mintzer D, Maclure M, Tofler GH, Sherwood JB, Muller JE |title=Triggering of myocardial infarction by cocaine |journal=Circulation |volume=99 |issue=21 |pages=2737–41 |year=1999 |month=June |pmid=10351966 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10351966}}</ref>.
 ==Marijuana==
-Marijuana use has been associated with a 4.8 fold rise in the risk of MI.
+[[Marijuana]] use has been associated with a 4.8 fold rise in the risk of MI.
 <ref name="pmid11401936">{{cite journal |author=Mittleman MA, Lewis RA, Maclure M, Sherwood JB, Muller JE |title=Triggering myocardial infarction by marijuana |journal=Circulation |volume=103 |issue=23 |pages=2805–9 |year=2001 |month=June |pmid=11401936 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=11401936}}</ref>
-==Circadian Variation in Onset of STEMI==
+==Circadian Variation in the Onset of STEMI==
 Most MIs occur in the early morning hours when cortisol and adrenaline rise and platelets are more activated. This diurnal variation is obliterated with [[aspirin]] therapy, pointing to the putative role of platelets in the initiation of MI.
 <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 |month=November |pmid=2865677 |doi= |url=}}</ref>
@@ Line 340: / Line 155: @@
 When a creful history is obtained, approximately half (48%) of MI patients will report a trigger
 <ref name="pmid2193495">{{cite journal |author=Tofler GH, Stone PH, Maclure M, ''et al'' |title=Analysis of possible triggers of acute myocardial infarction (the MILIS study) |journal=Am. J. Cardiol. |volume=66 |issue=1 |pages=22–7 |year=1990 |month=July |pmid=2193495 |doi= |url=}}</ref>.
-It is notable that 13% of patients will report that there were of 2 or more triggers. The following triggers were most commonly associated with the onset of MI in the Multicenter Investigation of Limitation of Infarct Size (MILIS) study <ref name="pmid2193495">{{cite journal |author=Tofler GH, Stone PH, Maclure M, ''et al'' |title=Analysis of possible triggers of acute myocardial infarction (the MILIS study) |journal=Am. J. Cardiol. |volume=66 |issue=1 |pages=22–7 |year=1990 |month=July |pmid=2193495 |doi= |url=}}</ref>.:
+It is notable that 13% of patients will report that there were of 2 or more triggers. The following triggers were most commonly associated with the onset of MI in the Multicenter Investigation of Limitation of Infarct Size (MILIS) study <ref name="pmid2193495">{{cite journal |author=Tofler GH, Stone PH, Maclure M, ''et al'' |title=Analysis of possible triggers of acute myocardial infarction (the MILIS study) |journal=Am. J. Cardiol. |volume=66 |issue=1 |pages=22–7 |year=1990 |month=July |pmid=2193495 |doi= |url=}}</ref>:
 #Emotional upset (18%)
 #Moderate physical activity (14%)
@@ Line 348: / Line 162: @@
 #Overeating (7%)
-==Sources==
+==STEMI Triggers in Popular Culture==
-*The 2004 ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction <ref name="pmid15339869">{{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, Alpert JS, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK |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=Circulation |volume=110 |issue=9 |pages=e82–292 |year=2004 |month=August |pmid=15339869 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=15339869}}</ref>
+[[Image:russert.jpg|thumbnail|left|200px|The sudden death of Tim Russert has prompted interest in the triggers of an MI]]
+Following the sudden death of Tim Russert of NBC's Meet the Press on June 13th 2008, many laypeople and physicians alike have asked "what are the triggers of a sudden heart attack"? Barbara Walters speculated that Tim Russert may have died from "the stress of the job". Others were concerned about a recent weight gain and lack of sleep. This chapter reviews the literature pertaining to triggers of acute MI.
-*The 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction <ref name="pmid18071078">{{cite journal |author=Antman EM, Hand M, Armstrong PW, ''et al'' |title=2007 Focused Update of the ACC/AHA 2004 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: developed in collaboration With the Canadian Cardiovascular Society endorsed by the American Academy of Family Physicians: 2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee |journal=Circulation |volume=117 |issue=2 |pages=296–329 |year=2008 |month=January |pmid=18071078 |doi=10.1161/CIRCULATIONAHA.107.188209 |url=}}</ref>
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 ==References==
 {{reflist|2}}
-==External links==
-* [http://www.themdtv.org The MD TV: Comments on Hot Topics, State of the Art Presentations in Cardiovascular Medicine, Expert Reviews on Cardiovascular Research]
-* [http://www.clinicaltrialresults.org Clinical Trial Results: An up to date resource of Cardiovascular Research]
-* [http://hp2010.nhlbihin.net/atpiii/calculator.asp?usertype=pub Risk Assessment Tool for Estimating Your 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]]
-* [http://www.nlm.nih.gov/medlineplus/heartattack.html Heart Attack] - overview of resources from [[MedlinePlus]].
-* [http://ww2.heartandstroke.ca/Page.asp?PageID=1975&ArticleID=5288 Heart Attack Warning Signals] from the Heart and Stroke Foundation of Canada
-* [http://www.regionalpci-stemi.org/index.html Regional PCI for STEMI Resource Center] - Evidence based online resource center for the development of regional PCI networks for acute STEMI
-* [http://www.stemisystems.org/ STEMI Systems] - Articles, profiles, and reviews of the latest publications involved in STEMI care. Quarterly newsletter.
-* [http://d2b.acc.org/ American College of Cardiology (ACC) Door to Balloon (D2B) Initiative.]
-*[http://www.americanheart.org/heartattack American Heart Association's Heart Attack web site] - Information and resources for preventing, recognizing and treating heart attack.
-{{STEMI}}
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+[[Category:Disease]]
 [[Category:Cardiology]]
+[[Category:Ischemic heart diseases]]
+[[Category:Intensive care medicine]]
 [[Category:Emergency medicine]]
+[[Category:Mature chapter]]