ST elevation myocardial infarction electrocardiogram: Difference between revisions

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{{Infobox_Disease |
__NOTOC__
  Name          = Myocardial infarction electrocardiogram|
{{ST elevation myocardial infarction}}
  Image          = ST elevation measurements.png |
{{CMG}}; {{AE}} {{CZ}}
  Caption        = Illustration of ST segment elevation with measurement of the magnitude of ST elevation 60 milliseconds after the J point.|
  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}}
{{CMG}}


'''Associate Editors-In-Chief:''' {{CZ}}
==Overview==
A primary purpose of the [[electrocardiogram]] is to detect [[ischemia]] or acute coronary injury in broad, symptomatic [[emergency department]] populations. Common EKG findings in STEMI include ST segment elevation, new LBBB pattern and hyperacute T waves.


{{Editor Join}}
==Electrocardiogram==
The characteristic ECG changes consistent with STEMI are:<ref name="O'GaraKushner2013">{{cite journal|last1=O'Gara|first1=Patrick T.|last2=Kushner|first2=Frederick G.|last3=Ascheim|first3=Deborah D.|last4=Casey|first4=Donald E.|last5=Chung|first5=Mina K.|last6=de Lemos|first6=James A.|last7=Ettinger|first7=Steven M.|last8=Fang|first8=James C.|last9=Fesmire|first9=Francis M.|last10=Franklin|first10=Barry A.|last11=Granger|first11=Christopher B.|last12=Krumholz|first12=Harlan M.|last13=Linderbaum|first13=Jane A.|last14=Morrow|first14=David A.|last15=Newby|first15=L. Kristin|last16=Ornato|first16=Joseph P.|last17=Ou|first17=Narith|last18=Radford|first18=Martha J.|last19=Tamis-Holland|first19=Jacqueline E.|last20=Tommaso|first20=Carl L.|last21=Tracy|first21=Cynthia M.|last22=Woo|first22=Y. Joseph|last23=Zhao|first23=David X.|title=2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction|journal=Journal of the American College of Cardiology|volume=61|issue=4|year=2013|pages=e78–e140|issn=07351097|doi=10.1016/j.jacc.2012.11.019}}</ref>
* [[ST elevation]] in at least 2 contiguous leads of 2 mm (0.2 mV) in men or 1.5 mm (0.15 mV) in women in leads V2–V3 and/or of 1 mm (0.1mV) in other contiguous chest leads or the limb leads
* [[ST depression]] in at least two precordial leads V1-V4 (suggestive of posterior MI)
* [[ST depression]] in several leads plus ST elevation in lead aVR (suggestive of occlusion of the left main or proximal LAD artery)
* New [[left bundle branch block]] ([[LBBB]])


==Overview==
[[The 12 lead ECG]] is used to classify patients into one of three groups:
A primary purpose of the [[electrocardiogram]] is to detect [[ischemia]] or acute coronary injury in broad, symptomatic [[emergency department]] populations. [[The 12 lead ECG]] is used to classify patients into one of three groups:
*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]]),  
*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]]),  
*Those with ST segment depression or T wave inversion (suspicious for ischemia), and  
*Those with ST segment depression or T wave inversion (suspicious for ischemia), and  
*Those with a so-called non-diagnostic or normal ECG.<ref name="ECC_2005_ACS">"2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - Part 8: Stabilization of the Patient With Acute Coronary Syndromes." ''Circulation'' 2005; '''112''': IV-89 - IV-110.</ref>  
*Those with a so-called non-diagnostic or normal ECG.<ref name="ECC_2005_ACS">"2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - Part 8: Stabilization of the Patient With Acute Coronary Syndromes." ''Circulation'' 2005; '''112''': IV-89 - IV-110.</ref>  
A normal ECG does not rule out the presence of acute myocardial infarction. Sometimes the earliest presentation of acute myocardial infarction is instead the hyperacute [[T wave]].<ref name="pmid11992348">{{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= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735675702921935}}</ref> In clinical practice, hyperacute T waves are rarely seen, because they exists for only 2-30 minutes after the onset of infarction.<ref name="ACS_Clin_NA">Smith SW, Whitwam W. "Acute Coronary Syndromes." ''Emerg Med Clin N Am'' 2006; '''24(1)''': 53-89. PMID 16308113</ref> Hyperacute T waves need to be distinguished from the peaked T waves associated with [[hyperkalemia]].<ref name="ECG_Noncardiac">"The clinical value of the ECG in noncardiac conditions." ''Chest'' 2004; '''125(4)''': 1561-76. PMID 15078775</ref>  
A normal ECG does not rule out the presence of acute myocardial infarction. Sometimes the earliest presentation of acute myocardial infarction is instead the presence of a hyperacute [[T wave]].<ref name="pmid11992348">{{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= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735675702921935}}</ref> In clinical practice, hyperacute T waves are rarely seen, because they exists for only 2-30 minutes after the onset of infarction.<ref name="ACS_Clin_NA">Smith SW, Whitwam W. "Acute Coronary Syndromes." ''Emerg Med Clin N Am'' 2006; '''24(1)''': 53-89. PMID 16308113</ref> Hyperacute T waves need to be distinguished from the peaked T waves associated with [[hyperkalemia]].<ref name="ECG_Noncardiac">"The clinical value of the ECG in noncardiac conditions." ''Chest'' 2004; '''125(4)''': 1561-76. PMID 15078775</ref>
 
==Definition of ST Elevation==
The current guidelines for the ECG diagnosis of acute myocardial infarction require at least 1 mm (0.1 mV) of ST segment elevation in 2 or more anatomically contiguous leads.<ref name="ECC_2005_ACS"/> 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="pmid16308113">{{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 |url=}}</ref>
 
==Differential Diagnosis of Causes of ST Segment Elevation in the Absence of Myonecrosis==
'''ST Segment Elevation Does Not Always Signify a Myocardial Infarction.''' ST segment elevation should alert the clinician to the possibility of myocardial injury, however, there are a [[ST elevation myocardial infarction electrocardiogram|variety of conditions that cause ST segment elevation]] which are not associated with myonecrosis.  Indeed, 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="pmid14645641">{{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]], benign [[early repolarization]], [[pericarditis]], [[hyperkalemia]], and ventricular aneurysm.<ref name="pmid10645842">{{cite journal |author=Brady WJ, Chan TC, Pollack M |title=Electrocardiographic manifestations: patterns that confound the EKG diagnosis of acute myocardial infarction-left bundle branch block, ventricular paced rhythm, and left ventricular hypertrophy |journal=J Emerg Med |volume=18 |issue=1 |pages=71–8 |year=2000 |month=January |pmid=10645842 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0736-4679(99)00178-X}}</ref><ref name="pmid11282670">{{cite journal |author=Brady WJ, Perron AD, Chan T |title=Electrocardiographic ST-segment elevation: correct identification of acute myocardial infarction (AMI) and non-AMI syndromes by emergency physicians |journal=Acad Emerg Med |volume=8 |issue=4 |pages=349–60 |year=2001 |month=April |pmid=11282670 |doi= |url=}}</ref><ref name="pmid14645641">{{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>
 
[[Left bundle branch block]] and [[artificial pacemaker|pacing]] can interfere with the electrocardiographic diagnosis of acute myocadial infarction. 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="pmid8559200">{{cite journal |author=Sgarbossa EB, Pinski SL, Barbagelata A, ''et al'' |title=Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. GUSTO-1 (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries) Investigators |journal=N. Engl. J. Med. |volume=334 |issue=8 |pages=481–7 |year=1996 |month=February |pmid=8559200 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=8559200&promo=ONFLNS19}}</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="pmid11581081">{{cite journal |author=Brady WJ, Syverud SA, Beagle C, ''et al'' |title=Electrocardiographic ST-segment elevation: the diagnosis of acute myocardial infarction by morphologic analysis of the ST segment |journal=Acad Emerg Med |volume=8 |issue=10 |pages=961–7 |year=2001 |month=October |pmid=11581081 |doi= |url=}}</ref>
 
Acute epicardial artery occlusion by [[thrombus]] is certainly one cause of ST segment elevation, but other causes of ST segment elevation which are not associated with myonecrosis include the following: (listed in alphabetical order) <ref name="pmid14645641">{{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><ref name="pmid15014192">{{cite journal |author=Ako J, Honda Y, Fitzgerald PJ |title=Conditions associated with ST-segment elevation |journal=N. Engl. J. Med. |volume=350 |issue=11 |pages=1152–5; author reply 1152–5 |year=2004 |month=March |pmid=15014192 |doi=10.1056/NEJM200403113501118 |url=}}</ref>
 
* [[Aneurysm]] of the ventricle can result in persistent ST segment elevation that can be exacerbated with tachycardia.
 
* [[Arrhythmogenic right ventricular cardiomyopathy]]
 
* Balloon inflation in a coronary artery during percutaneous coronary intervention
 
* [[Brugada syndrome]]
 
* [[Cardioversion|Transthoracic cardioversion]]
 
* [[Coronary artery]] rupture during percutaneous coronary intervention
 
* [[Early repolarization]] is a normal variant that can result in ST segment elevation. It is more common in males of younger age. The ST elevation is exacerbated by [[bradycardia]].
 
* [[Hyperkalemia]] known as the "dialyzable current of njury" hyperkalemia may cause hyperacute ECG changes due to changes in membrane polarity
 
* [[Left bundle branch block]] is associated with ST segment elevation in those leads that are discordant to the QRS. Stated differently, if the QRS is predominantly of a negative deflection, it is normal to observe ST segment elevation in the same leads. The presence of ST elevation in leads where the QRS deflection is upright (concordance) may be a marker of myocardial injury.
 
* [[Myopericarditis]] can cause injury to the subepicardial myocytes and ST segment elevation.


* [[Myocarditis]] can cause injury to the subepicardial myocytes and ST segment elevation.
===ST Elevation===
The electrocardiographic definition of ST elevation MI requires the following: at least 1 mm (0.1 mV) of ST segment elevation in 2 or more anatomically contiguous leads.<ref name="ECC_2005_ACS"/> While these criteria are sensitive, they are not specific as thrombotic coronary occlusion is not the most common cause of ST segment elevation in [[chest pain]] patients.<ref name="pmid16308113">{{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 |url=}}</ref>


* [[Pericardiocentesis]] when the needle comes into contact with the myocardium, there can be ST segment elevation reflecting local injury of the myocardium.
===ST Depression===
 
ST depression in the anterior leads might either represent reciprocal changes on EKG<ref name="pmid2522957">{{cite journal| author=Norell MS, Lyons JP, Gardener JE, Layton CA, Balcon R| title=Significance of "reciprocal" ST segment depression: left ventriculographic observations during left anterior descending coronary angioplasty. | journal=J Am Coll Cardiol | year= 1989 | volume= 13 | issue= 6 | pages= 1270-4 | pmid=2522957 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2522957  }} </ref> or might be pathologically caused by either anterior ischemia in the context of a patent artery<ref name="pmid11994554">{{cite journal| author=Gibson CM, Chen M, Angeja BG, Murphy SA, Marble SJ, Barron HV et al.| title=Precordial ST-segment depression in inferior myocardial infarction is associated with slow flow in the non-culprit left anterior descending artery. | journal=J Thromb Thrombolysis | year= 2002 | volume= 13 | issue= 1 | pages= 9-12 | pmid=11994554 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11994554  }} </ref> or posterior infarct due to the complete occlusion of a coronary artery.<ref name="pmid20723851">{{cite journal| author=Pride YB, Tung P, Mohanavelu S, Zorkun C, Wiviott SD, Antman EM et al.| title=Angiographic and clinical outcomes among patients with acute coronary syndromes presenting with isolated anterior ST-segment depression: a TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel-Thrombolysis In Myocardial Infarction 38) substudy. | journal=JACC Cardiovasc Interv | year= 2010 | volume= 3 | issue= 8 | pages= 806-11 | pmid=20723851 | doi=10.1016/j.jcin.2010.05.012 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20723851  }} </ref>
* [[Pericarditis]] can cause injury to the subepicardial myocytes and ST elevation.
 
* [[Pulmonary Embolism]]
 
* [[Prinzmetal's angina]] is associated with ST segment elevation due to transient epicardial coronary artery spasm either in the absence or presence of atherosclerosis. If the condition persists long enough, myonecrosis can be observed.
 
* [[Stroke]] [[Intracranial hemorrhage]] can in some cases cause ST segment elevation due to direct [[myocyte]] injury from a hyperadrenergic stimulation emanating from the central nervous system.
 
==Differential Diagnosis of Causes 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


Shown below is a table depicting the interpretation of ST elevation and ST depression by the involved contiguous leads.


{| Class=wikitable
|-
|-
|-bgcolor="LightSteelBlue"
| style="height: 30px; line-height: 30px; background: #4479BA; border: 0px; font-size: 100%; text-shadow: 0 -1px 0 rgba(0, 0, 0, 0.5);" align=center ; colspan="3"| {{fontcolor|#FFF|'''ST elevation'''}}
| '''Chemical / poisoning'''
|bgcolor="Beige"| [[Carbon monoxide poisoning]]
|-
|-
|-bgcolor="LightSteelBlue"
| '''Leads''' || '''Interpretation'''|| '''Involved artery'''
| '''Dermatologic'''
|bgcolor="Beige"| No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
| V1-V2 || Septal [[MI]], or <br> [[Right ventricular MI]]<ref name="pmid11275929">{{cite journal| author=Tsuka Y, Sugiura T, Hatada K, Nakamura S, Yuasa F, Iwasaka T| title=Clinical significance of ST-segment elevation in lead V1 in patients with acute inferior wall Q-wave myocardial infarction. | journal=Am Heart J | year= 2001 | volume= 141 | issue= 4 | pages= 615-20 | pmid=11275929 | doi=10.1067/mhj.2001.113996 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11275929  }} </ref> ||[[LAD]] <br> [[RCA]]
| '''Drug Side Effect'''
|bgcolor="Beige"| [[Oral contraceptive pills]], particularly among women who smoke
 
[[Anabolic steroids]]
|-
|-
|-bgcolor="LightSteelBlue"
| V3-V4 || [[Anterior MI]] || [[LAD]]
| '''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"
| V5-V6 <br> I-aVL || [[Lateral MI]] || [[Left circumflex artery]]
| '''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"
| II-III-aVF|| [[Inferior MI]] || [[RCA]] in 85% of the cases<br> [[Left circumflex artery]] in 15% of the cases
| '''Genetic'''
|bgcolor="Beige"| [[Familial hypercholesterolemia]]
|-
|-
|-bgcolor="LightSteelBlue"
|V1-V2- V4R|| [[Right ventricular MI]]<ref name="pmid6821897">{{cite journal| author=Klein HO, Tordjman T, Ninio R, Sareli P, Oren V, Lang R et al.| title=The early recognition of right ventricular infarction: diagnostic accuracy of the electrocardiographic V4R lead. | journal=Circulation | year= 1983 | volume= 67 | issue= 3 | pages= 558-65 | pmid=6821897 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6821897  }} </ref>|| [[RCA]]
| '''Hematologic'''
|bgcolor="Beige"| [[Disseminated intravascular coagulation]] ([[DIC]])
 
[[Hypercoagulable states]]
 
[[Polycythemia vera]]
 
[[Thrombocytosis]]
|-
|-
|-bgcolor="LightSteelBlue"
| style="height: 30px; line-height: 30px; background: #4479BA; border: 0px; font-size: 100%; text-shadow: 0 -1px 0 rgba(0, 0, 0, 0.5);" align=center ; colspan="3"| {{fontcolor|#FFF|'''ST depression'''}}
| '''Iatrogenic'''
|bgcolor="Beige"| [[Epinephrine]] overdose
 
Sudden withdrawal of [[Beta blockers]] or [[nitrates]]
|-
|-
|-bgcolor="LightSteelBlue"
| '''Leads''' || '''Interpretation'''|| '''Involved artery'''
| '''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"
| V1-V2-V3 || Anterior [[ischemia]]<ref name="pmid11994554">{{cite journal| author=Gibson CM, Chen M, Angeja BG, Murphy SA, Marble SJ, Barron HV et al.| title=Precordial ST-segment depression in inferior myocardial infarction is associated with slow flow in the non-culprit left anterior descending artery. | journal=J Thromb Thrombolysis | year= 2002 | volume= 13 | issue= 1 | pages= 9-12 | pmid=11994554 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11994554  }} </ref>, or <br> [[Posterior MI]] <ref name="pmid20723851">{{cite journal| author=Pride YB, Tung P, Mohanavelu S, Zorkun C, Wiviott SD, Antman EM et al.| title=Angiographic and clinical outcomes among patients with acute coronary syndromes presenting with isolated anterior ST-segment depression: a TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel-Thrombolysis In Myocardial Infarction 38) substudy. | journal=JACC Cardiovasc Interv | year= 2010 | volume= 3 | issue= 8 | pages= 806-11 | pmid=20723851 | doi=10.1016/j.jcin.2010.05.012 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20723851  }} </ref>, or <br> Reciprocal changes<ref name="pmid2522957">{{cite journal| author=Norell MS, Lyons JP, Gardener JE, Layton CA, Balcon R| title=Significance of "reciprocal" ST segment depression: left ventriculographic observations during left anterior descending coronary angioplasty. | journal=J Am Coll Cardiol | year= 1989 | volume= 13 | issue= 6 | pages= 1270-4 | pmid=2522957 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2522957  }} </ref>|| [[LAD]] <br> [[RCA]] or [[left circumflex artery]] <br>-
| '''Musculoskeletal / Ortho'''
|bgcolor="Beige"| No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|}
| '''Neurologic'''
 
|bgcolor="Beige"| No underlying causes
==EKG Examples==
|-
Shown below is an [[EKG]] of STEMI demonstrating the evolution of an infarct on the EKG. [[ST elevation]], [[Q wave]] formation, [[T wave inversion]], normalization with a persistent Q wave.
|-bgcolor="LightSteelBlue"
 
| '''Nutritional / Metabolic'''
[[Image:STEMI evolution.png|center|500px]]
|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>;
Copyleft image obtained courtesy of ECGpedia, http://en.ecgpedia.org/wiki/File:AMI_evolutie.png


[[Amyloidosis]]
----


[[Fabry disease]]
Shown below is an  EKG demonstrating [[ST elevation]] in lead [[Electrocardiogram#Precordial|V1]] and aVr; reversal of [[Electrocardiogram#Precordial|V6]] depicting STEMI.


[[Homocystinuria]]
[[Image:ST elevation in V1 and aVr.jpg|center|500px]]


[[Mucopolysaccharidoses]] or [[Hurler disease]]
Copyleft image obtained courtesy of ECGpedia,http://en.ecgpedia.org/wiki/Main_Page


[[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>
Shown below is an [[EKG]] demonstrating [[ST elevation]] in the right  [[precordial lead]]s depicting STEMI
|-
[[Image:STEMI 1 RV.jpg|center|500px]]
|-bgcolor="LightSteelBlue"
Copyleft image obtained courtesy of, http://en.ecgpedia.org/wiki/Main_Page
| '''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]].
Shown below is an EKG demonstrating clear [[ST elevation]] in the right [[precordial lead]]s depicting STEMI. A [[coronary angiography]] revealed a proximal right coronary artery occlusion.
|-
|-bgcolor="LightSteelBlue"
[[Image:STEMI 20 a.jpg|center|500px]]
| '''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.
Copyleft image obtained courtesy of, http://en.ecgpedia.org/wiki/Main_Page
|-
|-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
|-
|}


==Limitations of the 12 lead ECG==
'''For more EKG examples of ST elevation myocardial infarction click [[ST elevation myocardial infarction EKG examples|here]]'''
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 [[electrocardiogram|ECG]] may not accurately represent the entire picture. It is therefore desirable to obtain serial 12 lead [[ECG]]s, particularly if the first [[electrocardiogram|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="pmid8998085">{{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= |url=http://linkinghub.elsevier.com/retrieve/pii/S0196064497000279}}</ref> It should also be appreciated that the standard 12 lead [[electrocardiogram|ECG]] does not directly examine the [[right ventricle]], and does a relatively poor job of 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]]. The use of non-standard [[electrocardiogram|ECG]] leads like right-sided lead 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 [[electrocardiogram|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="pmid17015790">{{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=}}</ref>


==Localization of the infarct using the 12 lead ECG==
----
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.


As the myocardial infarction evolves, there may be loss of R wave height and development of pathological Q waves. T wave inversion may persist for months or even permanently following acute myocardial infarction.<ref name="pmid1934778">{{cite journal |author=Namba Y, Bando M, Takeda K, Iwata M, Mannen T |title=[Marchiafava-Bignami disease with symptoms of the motor impersistence and unilateral hemispatial neglect] |language=Japanese |journal=Rinsho Shinkeigaku |volume=31 |issue=6 |pages=632–5 |year=1991 |month=June |pmid=1934778 |doi= |url=}}</ref> Typically, however, the T wave recovers, leaving a pathological Q wave as the only remaining evidence that an acute myocardial infarction has occurred.
==Limitations of the 12 lead ECG==
While clinicians are widely familar with the 12 lead ECG, there are limitations to its sensitivity and specificity in detecting myocardial injury due to thrombotic vessel occlusion. A single static [[electrocardiogram|ECG]] represents a brief sample in time.  In STEMI, the culprit artery is often opening and closing or "winking and blinking" due to cyclic flow variations with the clot dissolving and reforming again. Furthermore, patients with acute coronary syndromes often have rapidly changing supply versus demand characteristics.  As a clinical example, one of the authors (CM Gibson) once saw a patient with 6 hours of chest pain who had non-specific ECG changes. 15 minutes later the patient complained of worsening chest pain, and at that time the ECG showed ST elevation.  Had the second ECG with ST elevation been instead the first ECG that was reviewed, it would have been concluded that the patient was infarcting for over 6 hours, when instead, the artery was occluded for 15 minutes at most during the recent episode of chest pain. Because a single [[electrocardiogram|ECG]] may not accurately represent evolving myocardial injury, it is standard practice to obtain serial 12 lead [[ECG]]s, particularly if the first [[electrocardiogram|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="pmid8998085">{{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= |url=http://linkinghub.elsevier.com/retrieve/pii/S0196064497000279}}</ref>  
While the standard 12 lead ECG is well designed to detect anterior ischemia, by virtue of the fact that it samples only electrical vectors from the front left chest wall, the 12 lead ECG may miss right ventricular and posterior infarctions. In particular, acute myocardial infarction in the distribution of the [[circumflex artery]] is likely to produce a nondiagnostic [[ECG]] or ST segment depression in the anterior precordial leads. The use of non-standard [[electrocardiogram|ECG]] leads like right-sided lead V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. Newer technologies such as the 80 lead ECG have demonstrated greater sensitivity in detecting RV and posterior infarcts compared with the 12 lead ECG.  The failure to identify patients with ST elevation MI delays care and has a negative effect on the quality of patient care.<ref name="pmid17015790">{{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=}}</ref>


[[Image:Coronary arteries related myocardial area.png|thumb|center|450px]]
==Localization of the Culprit Artery Based Upon the 12 lead ECG==
While the ECG leads that are involved with ST elevation and depression are often used to predict the potential location of the culprit artery, the sensitivity and specificity of these techniques are often poor.  New technologies such as [[80 lead ECGs]] may prove to be more useful in this regard. Identification of the potential culprit artery can be important in guiding patient management.  In particular, the ECG should be used to identify patients with a right ventricular infarct where nitrate administration is contraindicated.  The 12 lead ECG can also be used to identify the most appropriate artery to perform angiography on first when performing primary angioplasty.


{| class="wikitable"
[[Image:Coronary arteries related myocardial area.png|thumb|none|450px|Coronary arteries related myocardial area]]
|-
|+'''Evolution of the EKG during acute myocardial infarction'''
|-
!
!Figure
!change
|-
!minutes
|[[image:STEMI evolution a.png|60px]]
[[image:STEMI evolution b.png|60px]]
| hyperacute [[T wave]]s (peaked [[T wave]]s)
ST-elevation
|-
!hours
|[[image:STEMI evolution c.png|60px]]
[[image:STEMI evolution d.png|60px]]
| ST-elevation, with terminal negative [[T wave]]
negative [[T wave]] (these can last for months)
|-
!days
| [[image:STEMI evolution e.png|60px]]
| [[Pathologic_Q_Waves|Pathologic Q Waves]]
|-
|}


{| class=wikitable border="1" cellspacing="0" cellpadding="5" align="left"
{| style="width:80%; height:100px" border="1"
! Wall Affected
! Wall Affected
! Leads Showing ST Segment Elevation
! Leads Showing ST Segment Elevation
Line 302: Line 141:
| I, aVL
| I, aVL
| [[Right coronary artery|Right Coronary Artery (RCA)]]
| [[Right coronary artery|Right Coronary Artery (RCA)]]
|-
|}
==Evolution of ST Segment Elevation==
As the myocardial infarction evolves, there may be loss of R wave height and development of pathological Q waves. T wave inversion may persist for months or even permanently following acute myocardial infarction.<ref name="pmid1934778">{{cite journal |author=Namba Y, Bando M, Takeda K, Iwata M, Mannen T |title=[Marchiafava-Bignami disease with symptoms of the motor impersistence and unilateral hemispatial neglect] |language=Japanese |journal=Rinsho Shinkeigaku |volume=31 |issue=6 |pages=632–5 |year=1991 |month=June |pmid=1934778 |doi= |url=}}</ref> Typically, however, the T wave recovers, leaving a pathological Q wave as the only remaining evidence that an acute myocardial infarction has occurred.  Understanding the typical time course of ST changes in acute MI is critical in distinguishing STEMI from pericarditis and other conditions.
{| class="wikitable"
|-
|+'''Evolution of the EKG during acute myocardial infarction'''
|-
!
!Figure
!change
|-
!minutes
|[[image:STEMI evolution a.png|60px]]
[[image:STEMI evolution b.png|60px]]
| hyperacute [[T wave]]s (peaked [[T wave]]s)
ST-elevation
|-
!hours
|[[image:STEMI evolution c.png|60px]]
[[image:STEMI evolution d.png|60px]]
| ST-elevation, with terminal negative [[T wave]]
negative [[T wave]] (these can last for months)
|-
!days
| [[image:STEMI evolution e.png|60px]]
| [[Pathologic_Q_Waves|Pathologic Q Waves]]
|-
|-
|}
|}


===Measurement of the Magnitude of ST Elevation: 60 Milliseconds after the J point===
===Measurement of the Magnitude of ST Elevation: 60 Milliseconds after the J point===
The optimal time after the J point to measure ST elevation is debated. This example shows the technique of measuring the magnitude of ST elevation 60 milliseconds or 1.5 small boxes after the J point.
The optimal time after the J point to measure ST elevation is debated. This example shows the technique of measuring the magnitude of ST elevation 60 milliseconds or 1.5 small boxes after the J point.
[[Image:ST elevation measurements.png|center|thumb|In this diagram ST elevation is measured 60ms or 80ms after the J point.]]


===Distinguishing Early Repolarization and Other Normal Variants from Pathologic ST Elevation===
===Distinguishing Early Repolarization and Other Normal Variants from Pathologic ST Elevation===
[[Image:Normal_ST_elevation.png|center|frame|'''Examples of Early Repolarization and Normal Variant of ST Elevation''']]
Early repolarization is an electrocardiographic pattern that can mimic the changes of ST elevation myocardial infarction.  It is often seen in younger males. As the example below shows, there is often a notch (shown in red) where the QRS and ST segments join.


==EKG Examples==
[[Image:Normal_ST_elevation.png|center|500px|'''Examples of Early Repolarization and Normal Variant of ST Elevation''']]
Copyleft image obtained courtesy of ECGpedia, http://en.ecgpedia.org/wiki/Main_Page


<div align="left">
===Diagnosing STEMI in the Setting of Left Bundle Branch Block===
<gallery heights="175" widths="175">
Ordinarily in the setting of [[left bundle branch block]], the [[T waves]] are inverted in the lateral leads (they are 'discordant'). If they become upright, they are called 'concordant', and concordant [[T waves]] can be observed in ST elevation MI.  The EKG below was obtained in a patient with a new [[left bundle branch block]] ([[LBBB]]) and a totally occluded [[left anterior descending artery]].
Image:STEMI evolution.png|The evolution of an infarct on the ECG. ST elevation, Q wave formation, T wave inversion, normalization with a persistent Q wave
[[Image:LBBB with pseudonormalization of T waves.jpg|500px|center]]
Image:Pathologic_ST_elevation.png|Pathologic ST elevation
</gallery>
</div>


==2013 Revised and 2004 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction (DO NOT EDIT)<ref name="pmid23247303">{{cite journal |author=O'Gara PT, Kushner FG, Ascheim DD, ''et al.'' |title=2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: Executive Summary: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines |journal=Circulation |volume= |issue= |pages= |year=2012 |month=December |pmid=23247303 |doi=10.1161/CIR.0b013e3182742c84 |url=}}</ref>==


<div align="left">
===Electrocardiogram (DO NOT EDIT)<ref name="pmid23247303">{{cite journal |author=O'Gara PT, Kushner FG, Ascheim DD, ''et al.'' |title=2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: Executive Summary: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines |journal=Circulation |volume= |issue= |pages= |year=2012 |month=December |pmid=23247303 |doi=10.1161/CIR.0b013e3182742c84 |url=}}</ref><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>===
<gallery heights="175" widths="175">
Image:ECG 001.jpg|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.
Image:STEMI 1.jpg|Acute inferior myocardial infarction with RV involvement.
</gallery>
</div>


{|class="wikitable"
|-
| colspan="1" style="text-align:center; background:LightGreen"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''1.''' Performance of a 12-lead electrocardiogram ([[ECG]]) by emergency medical services personnel at the site of first medical contact (FMC) is recommended in patients with symptoms consistent with [[STEMI]]<ref name="pmid18199862">{{cite journal |author=Le May MR, So DY, Dionne R, ''et al.'' |title=A citywide protocol for primary PCI in ST-segment elevation myocardial infarction |journal=N. Engl. J. Med. |volume=358 |issue=3 |pages=231–40 |year=2008 |month=January |pmid=18199862 |doi=10.1056/NEJMoa073102 |url=}}</ref><ref name="pmid20650431">{{cite journal |author=Dieker HJ, Liem SS, El Aidi H, ''et al.'' |title=Pre-hospital triage for primary angioplasty: direct referral to the intervention center versus interhospital transport |journal=JACC Cardiovasc Interv |volume=3 |issue=7 |pages=705–11 |year=2010 |month=July |pmid=20650431 |doi=10.1016/j.jcin.2010.04.010 |url=}}</ref><ref name="pmid19130984">{{cite journal |author=Diercks DB, Kontos MC, Chen AY, ''et al.'' |title=Utilization and impact of pre-hospital electrocardiograms for patients with acute ST-segment elevation myocardial infarction: data from the NCDR (National Cardiovascular Data Registry) ACTION (Acute Coronary Treatment and Intervention Outcomes Network) Registry |journal=J. Am. Coll. Cardiol. |volume=53 |issue=2 |pages=161–6 |year=2009 |month=January |pmid=19130984 |doi=10.1016/j.jacc.2008.09.030 |url=}}</ref><ref name="pmid19463447">{{cite journal |author=Rokos IC, French WJ, Koenig WJ, ''et al.'' |title=Integration of pre-hospital electrocardiograms and ST-elevation myocardial infarction receiving center (SRC) networks: impact on Door-to-Balloon times across 10 independent regions |journal=JACC Cardiovasc Interv |volume=2 |issue=4 |pages=339–46 |year=2009 |month=April |pmid=19463447 |doi=10.1016/j.jcin.2008.11.013 |url=}}</ref><ref name="pmid21138933">{{cite journal |author=Sørensen JT, Terkelsen CJ, Nørgaard BL, ''et al.'' |title=Urban and rural implementation of pre-hospital diagnosis and direct referral for primary percutaneous coronary intervention in patients with acute ST-elevation myocardial infarction |journal=Eur. Heart J. |volume=32 |issue=4 |pages=430–6 |year=2011 |month=February |pmid=21138933 |doi=10.1093/eurheartj/ehq437 |url=}}</ref> ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''2.''' A 12-lead ECG should be performed and shown to an experienced emergency physician within 10 minutes of ED arrival on all patients with [[chest discomfort]] (or anginal equivalent) or other symptoms suggestive of STEMI.''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''3.''' If the initial ECG is not diagnostic of STEMI but the patient remains symptomatic, and there is a high clinical suspicion for STEMI, serial ECGs at 5- to 10- minute intervals or continuous 12-lead ST-segment monitoring should be performed to detect the potential development of ST elevation.''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''4.''' In patients with inferior STEMI, right-sided ECG leads should be obtained to screen for ST elevation suggestive of RV infarction.''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>
|}


<div align="left">
==Sources==
<gallery heights="175" widths="175">
* 2013 Revised ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction<ref name="pmid23247303">{{cite journal|author=O'Gara PT, Kushner FG, Ascheim DD, ''et al.'' |title=2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: Executive Summary: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines |journal=Circulation |volume= |issue=|pages= |year=2012 |month=December |pmid=23247303 |doi=10.1161/CIR.0b013e3182742c84 |url=}}</ref>
Image:STEMI 1 RV.jpg|Same case. Right precordial leads.
Image:STEMI 2.jpg|Acute inferior MI
</gallery>
</div>


* 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>


<div align="left">
==Related Chapters==
<gallery heights="175" widths="175">
* [[STEMI case examples]]
Image:STEMI 3.jpg|Acute inferoposterior MI: ST elevation in II, III, AVF (in III > II). ST depression in I, AVL, V2. Tall R in V2, otherwise normal QRS morphology.
Image:STEMI 4.jpg|Acute inferior MI
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:STEMI 5.jpg|Acute posterolateral MI
Image:STEMI 6.jpg|Acute inferolateral MI: ST depression in V1, V4, tall R in V2. ST elevation in II, III, AVF, V5 and V6.
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:STEMI 7.jpg|Acute anterior MI. Loss of R waves throughout the anterior wall (V1-V6). QS complexes in V3-V5. ST elevation in V1-V5 with terminal negative T waves.
Image:STEMI 8.jpg|Sinus bradycardia with first degree AV block and inferior-posterior-lateral myocardial infarction.
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:STEMI 9.jpg|Sinus bradycardia with inferior-lateral myocardial infarction.
Image:STEMI 10.jpg|Acute anterior MI. LAD artery occlusion
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:STEMI 11.jpg|Sinus rhythm with anteroseptal myocardial infarction.
Image:STEMI 12.jpg|Sinus rhythm with [[left bundle branch block]], comparison with an old EKG is mandatory to evaluate whether the [[LBBB]] is new (a sign of myocardial infarction) or old.
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:STEMI 13.jpg|Inferior-posterior myocardial infarction with complete AV block and ventricular excape rhythm with [[RBBB]] pattern and left axis, followed by sinus rhythm.
Image:STEMI 14.jpg|Acute anterior myocardial infarction and left anterior hemiblock. [http://www.ganseman.com/ecgbibnl.htm#_top000 Image courtesy of Dr Jose Ganseman]
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:STEMI 15.jpg|Old anterior myocardial infarction and bifascicular block ([[RBBB]] and [[LAHB]]) [http://www.ganseman.com/ecgbibnl.htm#_top000 Image courtesy of Dr Jose Ganseman]
Image:STEMI 16.jpg|Acute MI with proximal LAD occlusion
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:STEMI 17.jpg|A 2 days old anterior infarction with Q waves in V1-V4 with persisting ST elevation, a sign of left ventricular aneurysm formation.
Image:STEMI 18.jpg|A 2 weeks old anterior infarction with Q waves in V2-V4 and persisting ST elevation, a sign of left ventricular aneurysm formation.
</gallery>
</div>
 
<div align="left">
<gallery heights="175" widths="175">
Image:STEMI 19.jpg|ECG on admission: A large anterior wall infarction
Image:STEMI 19 a.jpg|Detail for conduction times.
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:STEMI 19 b.jpg|The heart rate increases and there are two extra systoles short after each other. Then, a chaotic rhythm develops: [[ventricular fibrillation]].
Image:STEMI 20.jpg|Atrial fibrillation and inferior-posterior myocardial infarction.
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">>
Image:STEMI 20 a.jpg|Same patient's 2. EKG; This EKG shows clear ST elevation in the right precordial leads. A coronary angiography revealed a proximal right coronary artery occlusion.
Image:STEMI 21.jpg|Inferior-posterior-lateral myocardial infarction with a nodal escape rhythm
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:STEMI 22.jpg|Patient with [[RBBB]] and inferior MI. Note to left axis deviation.
Image:STEMI 23.jpg|Lead V4R in the same patient with [[RBBB]] and inferior MI clearly shows ST elevation.
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:STEMI 24.jpg|The same patient before acute MI developed. Horizontal axis.
Image:STEMI 25.jpg|Acute myocardial infarction in in a patient with a pacemaker and [[LBBB]]. Concordant ST elevation in V5-V6 are clearly visible. There is discordant ST segment elevation > 5 mm in lead V3.
</gallery>
</div>
 
<div align="left">
<gallery heights="175" widths="175">
Image:STEMI 25 a.jpg|The same patient as in the first example 2 months before the myocardial infarction. Normal [[LBBB]] pattern.
Image:STEMI 26.jpg|Acute MI in a patient with [[LBBB]]
</gallery>
</div>
 
<div align="left">
<gallery heights="175" widths="175">
Image:STEMI 27.jpg|Atrial fibrillation with inferior-posterior-lateral myocardial infarction and incomplete right bundle branch block. Lead I shows ST depression, suggestive of right coronary artery involvement.
Image:STEMI 28.png|Typical negative T waves post anterior myocardial infarction. This patient also shows QTc prolongation. Whether this has an effect on prognosis is debated. <ref name="pmid18019666">{{cite journal |author=Novotný T, Sisáková M, Floriánová A, ''et al'' |title=[QT dynamicity in risk stratification in patients after myocardial infarction] |language=Czech |journal=Vnitr Lek |volume=53 |issue=9 |pages=964–7 |year=2007 |month=September |pmid=18019666 |doi= |url=}}</ref><ref name="pmid15851335">{{cite journal |author=Jensen BT, Abildstrom SZ, Larroude CE, ''et al'' |title=QT dynamics in risk stratification after myocardial infarction |journal=Heart Rhythm |volume=2 |issue=4 |pages=357–64 |year=2005 |month=April |pmid=15851335 |doi=10.1016/j.hrthm.2004.12.028 |url=}}</ref><ref name="pmid12716101">{{cite journal |author=Chevalier P, Burri H, Adeleine P, ''et al'' |title=QT dynamicity and sudden death after myocardial infarction: results of a long-term follow-up study |journal=J. Cardiovasc. Electrophysiol. |volume=14 |issue=3 |pages=227–33 |year=2003 |month=March |pmid=12716101 |doi= |url=http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1045-3873&date=2003&volume=14&issue=3&spage=227}}</ref>
</gallery>
</div>


==References==
==References==
{{reflist|2}}
{{reflist|2}}


==See Also==
{{WikiDoc Help Menu}}
 
{{WikiDoc Sources}}
* [[STEMI case examples]]
 
==Additional Resources==
 
* Tanel RE. ECGs in the ED. Pediatr Emerg Care. 2008 Jan; 24 (1): 62-3. PMID 18212616
 
==External links==
 
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Latest revision as of 00:17, 30 July 2020

Acute Coronary Syndrome Main Page

ST Elevation Myocardial Infarction Microchapters

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ST elevation myocardial infarction electrocardiogram On the Web

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

A primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad, symptomatic emergency department populations. Common EKG findings in STEMI include ST segment elevation, new LBBB pattern and hyperacute T waves.

Electrocardiogram

The characteristic ECG changes consistent with STEMI are:[1]

  • ST elevation in at least 2 contiguous leads of 2 mm (0.2 mV) in men or 1.5 mm (0.15 mV) in women in leads V2–V3 and/or of 1 mm (0.1mV) in other contiguous chest leads or the limb leads
  • ST depression in at least two precordial leads V1-V4 (suggestive of posterior MI)
  • ST depression in several leads plus ST elevation in lead aVR (suggestive of occlusion of the left main or proximal LAD artery)
  • New left bundle branch block (LBBB)

The 12 lead ECG is used to classify patients into one of three groups:

  • Those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with thrombolytics or primary PCI),
  • Those with ST segment depression or T wave inversion (suspicious for ischemia), and
  • Those with a so-called non-diagnostic or normal ECG.[2]

A normal ECG does not rule out the presence of acute myocardial infarction. Sometimes the earliest presentation of acute myocardial infarction is instead the presence of a hyperacute T wave.[3] In clinical practice, hyperacute T waves are rarely seen, because they exists for only 2-30 minutes after the onset of infarction.[4] Hyperacute T waves need to be distinguished from the peaked T waves associated with hyperkalemia.[5]

ST Elevation

The electrocardiographic definition of ST elevation MI requires the following: at least 1 mm (0.1 mV) of ST segment elevation in 2 or more anatomically contiguous leads.[2] While these criteria are sensitive, they are not specific as thrombotic coronary occlusion is not the most common cause of ST segment elevation in chest pain patients.[6]

ST Depression

ST depression in the anterior leads might either represent reciprocal changes on EKG[7] or might be pathologically caused by either anterior ischemia in the context of a patent artery[8] or posterior infarct due to the complete occlusion of a coronary artery.[9]

Shown below is a table depicting the interpretation of ST elevation and ST depression by the involved contiguous leads.

ST elevation
Leads Interpretation Involved artery
V1-V2 Septal MI, or
Right ventricular MI[10]		 LAD
RCA
V3-V4 Anterior MI LAD
V5-V6
I-aVL		 Lateral MI Left circumflex artery
II-III-aVF Inferior MI RCA in 85% of the cases
Left circumflex artery in 15% of the cases
V1-V2- V4R Right ventricular MI[11] RCA
ST depression
Leads Interpretation Involved artery
V1-V2-V3 Anterior ischemia[8], or
Posterior MI [9], or
Reciprocal changes[7]		 LAD
RCA or left circumflex artery
-

EKG Examples

Shown below is an EKG of STEMI demonstrating the evolution of an infarct on the EKG. ST elevation, Q wave formation, T wave inversion, normalization with a persistent Q wave.

Copyleft image obtained courtesy of ECGpedia, http://en.ecgpedia.org/wiki/File:AMI_evolutie.png

Shown below is an EKG demonstrating ST elevation in lead V1 and aVr; reversal of V6 depicting STEMI.

Copyleft image obtained courtesy of ECGpedia,http://en.ecgpedia.org/wiki/Main_Page

Shown below is an EKG demonstrating ST elevation in the right precordial leads depicting STEMI

Copyleft image obtained courtesy of, http://en.ecgpedia.org/wiki/Main_Page

Shown below is an EKG demonstrating clear ST elevation in the right precordial leads depicting STEMI. A coronary angiography revealed a proximal right coronary artery occlusion.

Copyleft image obtained courtesy of, http://en.ecgpedia.org/wiki/Main_Page

For more EKG examples of ST elevation myocardial infarction click here

Limitations of the 12 lead ECG

While clinicians are widely familar with the 12 lead ECG, there are limitations to its sensitivity and specificity in detecting myocardial injury due to thrombotic vessel occlusion. A single static ECG represents a brief sample in time. In STEMI, the culprit artery is often opening and closing or "winking and blinking" due to cyclic flow variations with the clot dissolving and reforming again. Furthermore, patients with acute coronary syndromes often have rapidly changing supply versus demand characteristics. As a clinical example, one of the authors (CM Gibson) once saw a patient with 6 hours of chest pain who had non-specific ECG changes. 15 minutes later the patient complained of worsening chest pain, and at that time the ECG showed ST elevation. Had the second ECG with ST elevation been instead the first ECG that was reviewed, it would have been concluded that the patient was infarcting for over 6 hours, when instead, the artery was occluded for 15 minutes at most during the recent episode of chest pain. Because a single ECG may not accurately represent evolving myocardial injury, it is standard practice to obtain serial 12 lead ECGs, particularly if the first ECG is obtained during a pain-free episode. Alternatively, many emergency departments and chest pain centers use computers capable of continuous ST segment monitoring.[12] While the standard 12 lead ECG is well designed to detect anterior ischemia, by virtue of the fact that it samples only electrical vectors from the front left chest wall, the 12 lead ECG may miss right ventricular and posterior infarctions. In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG or ST segment depression in the anterior precordial leads. The use of non-standard ECG leads like right-sided lead V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. Newer technologies such as the 80 lead ECG have demonstrated greater sensitivity in detecting RV and posterior infarcts compared with the 12 lead ECG. The failure to identify patients with ST elevation MI delays care and has a negative effect on the quality of patient care.[13]

Localization of the Culprit Artery Based Upon the 12 lead ECG

While the ECG leads that are involved with ST elevation and depression are often used to predict the potential location of the culprit artery, the sensitivity and specificity of these techniques are often poor. New technologies such as 80 lead ECGs may prove to be more useful in this regard. Identification of the potential culprit artery can be important in guiding patient management. In particular, the ECG should be used to identify patients with a right ventricular infarct where nitrate administration is contraindicated. The 12 lead ECG can also be used to identify the most appropriate artery to perform angiography on first when performing primary angioplasty.

Coronary arteries related myocardial area
Wall Affected Leads Showing ST Segment Elevation Leads Showing Reciprocal ST Segment Depression Suspected Culprit Artery
Septal V1, V2 None Left Anterior Descending (LAD)
Anterior V3, V4 None Left Anterior Descending (LAD)
Anteroseptal V1, V2, V3, V4 None Left Anterior Descending (LAD)
Anterolateral V3, V4, V5, V6, I, aVL II, III, aVF Left Anterior Descending (LAD), Circumflex (LCX), or Obtuse Marginal
Extensive anterior (Sometimes called Anteroseptal with Lateral extension) V1,V2,V3, V4, V5, V6, I, aVL II, III, aVF Left main coronary artery (LCA)
Inferior II, III, aVF I, aVL Right Coronary Artery (RCA) or Circumflex (LCX)
Lateral I, aVL, V5, V6 II, III, aVF Circumflex (LCX) or Obtuse Marginal
Posterior (Usually associated with Inferior or Lateral but can be isolated) V7, V8, V9 V1,V2,V3, V4 Posterior Descending (PDA) (branch of the RCA or Circumflex (LCX))
Right ventricular (Usually associated with Inferior) II, III, aVF, V1, V4R I, aVL Right Coronary Artery (RCA)

Evolution of ST Segment Elevation

As the myocardial infarction evolves, there may be loss of R wave height and development of pathological Q waves. T wave inversion may persist for months or even permanently following acute myocardial infarction.[14] Typically, however, the T wave recovers, leaving a pathological Q wave as the only remaining evidence that an acute myocardial infarction has occurred. Understanding the typical time course of ST changes in acute MI is critical in distinguishing STEMI from pericarditis and other conditions.

Evolution of the EKG during acute myocardial infarction
Figure change
minutes

hyperacute T waves (peaked T waves)

ST-elevation

hours

ST-elevation, with terminal negative T wave

negative T wave (these can last for months)

days Pathologic Q Waves

Measurement of the Magnitude of ST Elevation: 60 Milliseconds after the J point

The optimal time after the J point to measure ST elevation is debated. This example shows the technique of measuring the magnitude of ST elevation 60 milliseconds or 1.5 small boxes after the J point.

Distinguishing Early Repolarization and Other Normal Variants from Pathologic ST Elevation

Early repolarization is an electrocardiographic pattern that can mimic the changes of ST elevation myocardial infarction. It is often seen in younger males. As the example below shows, there is often a notch (shown in red) where the QRS and ST segments join.

Examples of Early Repolarization and Normal Variant of ST Elevation
Examples of Early Repolarization and Normal Variant of ST Elevation

Copyleft image obtained courtesy of ECGpedia, http://en.ecgpedia.org/wiki/Main_Page

Diagnosing STEMI in the Setting of Left Bundle Branch Block

Ordinarily in the setting of left bundle branch block, the T waves are inverted in the lateral leads (they are 'discordant'). If they become upright, they are called 'concordant', and concordant T waves can be observed in ST elevation MI. The EKG below was obtained in a patient with a new left bundle branch block (LBBB) and a totally occluded left anterior descending artery.

2013 Revised and 2004 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction (DO NOT EDIT)[15]

Electrocardiogram (DO NOT EDIT)[15][16]

Class I
"1. Performance of a 12-lead electrocardiogram (ECG) by emergency medical services personnel at the site of first medical contact (FMC) is recommended in patients with symptoms consistent with STEMI[17][18][19][20][21] (Level of Evidence: B)"
"2. A 12-lead ECG should be performed and shown to an experienced emergency physician within 10 minutes of ED arrival on all patients with chest discomfort (or anginal equivalent) or other symptoms suggestive of STEMI.(Level of Evidence: C)"
"3. If the initial ECG is not diagnostic of STEMI but the patient remains symptomatic, and there is a high clinical suspicion for STEMI, serial ECGs at 5- to 10- minute intervals or continuous 12-lead ST-segment monitoring should be performed to detect the potential development of ST elevation.(Level of Evidence: C)"
"4. In patients with inferior STEMI, right-sided ECG leads should be obtained to screen for ST elevation suggestive of RV infarction.(Level of Evidence: B)"

Sources

  • 2013 Revised ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction[15]
  • The 2004 ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction [16]

Related Chapters

References

  1. ↑ O'Gara, Patrick T.; Kushner, Frederick G.; Ascheim, Deborah D.; Casey, Donald E.; Chung, Mina K.; de Lemos, James A.; Ettinger, Steven M.; Fang, James C.; Fesmire, Francis M.; Franklin, Barry A.; Granger, Christopher B.; Krumholz, Harlan M.; Linderbaum, Jane A.; Morrow, David A.; Newby, L. Kristin; Ornato, Joseph P.; Ou, Narith; Radford, Martha J.; Tamis-Holland, Jacqueline E.; Tommaso, Carl L.; Tracy, Cynthia M.; Woo, Y. Joseph; Zhao, David X. (2013). "2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction". Journal of the American College of Cardiology. 61 (4): e78–e140. doi:10.1016/j.jacc.2012.11.019. ISSN 0735-1097.
  2. ↑ 2.0 2.1 "2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - Part 8: Stabilization of the Patient With Acute Coronary Syndromes." Circulation 2005; 112: IV-89 - IV-110.
  3. ↑ Somers MP, Brady WJ, Perron AD, Mattu A (2002). "The prominant T wave: electrocardiographic differential diagnosis". Am J Emerg Med. 20 (3): 243–51. PMID 11992348. Unknown parameter |month= ignored (help)
  4. ↑ Smith SW, Whitwam W. "Acute Coronary Syndromes." Emerg Med Clin N Am 2006; 24(1): 53-89. PMID 16308113
  5. ↑ "The clinical value of the ECG in noncardiac conditions." Chest 2004; 125(4): 1561-76. PMID 15078775
  6. ↑ Smith SW, Whitwam W (2006). "Acute coronary syndromes". Emerg. Med. Clin. North Am. 24 (1): 53–89, vi. doi:10.1016/j.emc.2005.08.008. PMID 16308113. Unknown parameter |month= ignored (help)
  7. ↑ 7.0 7.1 Norell MS, Lyons JP, Gardener JE, Layton CA, Balcon R (1989). "Significance of "reciprocal" ST segment depression: left ventriculographic observations during left anterior descending coronary angioplasty". J Am Coll Cardiol. 13 (6): 1270–4. PMID 2522957.
  8. ↑ 8.0 8.1 Gibson CM, Chen M, Angeja BG, Murphy SA, Marble SJ, Barron HV; et al. (2002). "Precordial ST-segment depression in inferior myocardial infarction is associated with slow flow in the non-culprit left anterior descending artery". J Thromb Thrombolysis. 13 (1): 9–12. PMID 11994554.
  9. ↑ 9.0 9.1 Pride YB, Tung P, Mohanavelu S, Zorkun C, Wiviott SD, Antman EM; et al. (2010). "Angiographic and clinical outcomes among patients with acute coronary syndromes presenting with isolated anterior ST-segment depression: a TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel-Thrombolysis In Myocardial Infarction 38) substudy". JACC Cardiovasc Interv. 3 (8): 806–11. doi:10.1016/j.jcin.2010.05.012. PMID 20723851.
  10. ↑ Tsuka Y, Sugiura T, Hatada K, Nakamura S, Yuasa F, Iwasaka T (2001). "Clinical significance of ST-segment elevation in lead V1 in patients with acute inferior wall Q-wave myocardial infarction". Am Heart J. 141 (4): 615–20. doi:10.1067/mhj.2001.113996. PMID 11275929.
  11. ↑ Klein HO, Tordjman T, Ninio R, Sareli P, Oren V, Lang R; et al. (1983). "The early recognition of right ventricular infarction: diagnostic accuracy of the electrocardiographic V4R lead". Circulation. 67 (3): 558–65. PMID 6821897.
  12. ↑ Selker HP, Zalenski RJ, Antman EM; et al. (1997). "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". Ann Emerg Med. 29 (1): 1–12. PMID 8998085. Unknown parameter |month= ignored (help)
  13. ↑ Masoudi FA, Magid DJ, Vinson DR; et al. (2006). "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". Circulation. 114 (15): 1565–71. doi:10.1161/CIRCULATIONAHA.106.623652. PMID 17015790. Unknown parameter |month= ignored (help)
  14. ↑ Namba Y, Bando M, Takeda K, Iwata M, Mannen T (1991). "[Marchiafava-Bignami disease with symptoms of the motor impersistence and unilateral hemispatial neglect]". Rinsho Shinkeigaku (in Japanese). 31 (6): 632–5. PMID 1934778. Unknown parameter |month= ignored (help)
  15. ↑ 15.0 15.1 15.2 O'Gara PT, Kushner FG, Ascheim DD; et al. (2012). "2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: Executive Summary: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". Circulation. doi:10.1161/CIR.0b013e3182742c84. PMID 23247303. Unknown parameter |month= ignored (help)
  16. ↑ 16.0 16.1 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 (2004). "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)". Circulation. 110 (9): e82–292. PMID 15339869. Unknown parameter |month= ignored (help)
  17. ↑ Le May MR, So DY, Dionne R; et al. (2008). "A citywide protocol for primary PCI in ST-segment elevation myocardial infarction". N. Engl. J. Med. 358 (3): 231–40. doi:10.1056/NEJMoa073102. PMID 18199862. Unknown parameter |month= ignored (help)
  18. ↑ Dieker HJ, Liem SS, El Aidi H; et al. (2010). "Pre-hospital triage for primary angioplasty: direct referral to the intervention center versus interhospital transport". JACC Cardiovasc Interv. 3 (7): 705–11. doi:10.1016/j.jcin.2010.04.010. PMID 20650431. Unknown parameter |month= ignored (help)
  19. ↑ Diercks DB, Kontos MC, Chen AY; et al. (2009). "Utilization and impact of pre-hospital electrocardiograms for patients with acute ST-segment elevation myocardial infarction: data from the NCDR (National Cardiovascular Data Registry) ACTION (Acute Coronary Treatment and Intervention Outcomes Network) Registry". J. Am. Coll. Cardiol. 53 (2): 161–6. doi:10.1016/j.jacc.2008.09.030. PMID 19130984. Unknown parameter |month= ignored (help)
  20. ↑ Rokos IC, French WJ, Koenig WJ; et al. (2009). "Integration of pre-hospital electrocardiograms and ST-elevation myocardial infarction receiving center (SRC) networks: impact on Door-to-Balloon times across 10 independent regions". JACC Cardiovasc Interv. 2 (4): 339–46. doi:10.1016/j.jcin.2008.11.013. PMID 19463447. Unknown parameter |month= ignored (help)
  21. ↑ Sørensen JT, Terkelsen CJ, Nørgaard BL; et al. (2011). "Urban and rural implementation of pre-hospital diagnosis and direct referral for primary percutaneous coronary intervention in patients with acute ST-elevation myocardial infarction". Eur. Heart J. 32 (4): 430–6. doi:10.1093/eurheartj/ehq437. PMID 21138933. Unknown parameter |month= ignored (help)


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