Clinical classification of acute myocardial infarction: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
 
(16 intermediate revisions by 3 users not shown)
Line 1: Line 1:
{{Infobox_Disease |
#redirect:[[ST elevation myocardial infarction diagnostic criteria#Modern Classification as to the Type of MI]]
  Name          = Myocardial infarction|
  Image          = |
  Caption        = |
  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}}
__NOTOC__
'''Associate Editor-In-Chief:''' {{CZ}}
 
==Prior MI Classification Schemes==
 
There have been several prior classification schemes for characterizing MI:
 
1. '''Transmural''' (necrosis of full thickness of ventricle) vs. '''non transmural''' (necrosis of partial thickness of ventricle)
 
2. [[Q wave]] vs. '''non Q wave''': Based upon the development of electrocardiographic Q waves representing electrically inert tissue.
 
3. [[ST elevation MI]] ([[STEMI]]) and [[Non ST elevation myocardial infarction]] ([[NSTEMI]])
 
At one time it was thought that Transmural MI and Q wave MI were synonymous. However, not all Q wave MIs are transmural, and not all transmural MIs are associated with Q waves.
 
Likewise, not all ST elevation [[MI]]s go on to cause [[q wave]]s. Non ST elevation MIs can result in [[q wave]]s.
 
Thus, ST elevation MI should not be equated with transmural MI or q wave MI. Likewise, Non ST elevation MI should not be equated with non transmural MI or non q wave MI.  These 3 designations reflect three separate but overlapping characterization schemes.
 
==New MI Clinical Classification System==
A new clinical evidence based classification system has been introduced by '''Thygesen K, Alpert JS, White HD, et al.''' and jointly sponsored by the American College of Cardiology (ACC), American Heart Association (AHA), European Society of Cardiology (ESC), and the World Heart Federation (WHF).<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al''|title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284|doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref>
 
==Definitions==
 
Myocardial infarction can be characterized pathologically as '''acute''', '''healing''' or '''healed'''.
 
'''Acute''' phase of myocardial infarction is characterized by the presence of [[polymorphonuclear leukocytes]]. If the time interval between the onset of the infarction and death is quite brief, e.g. 6 hours, minimal or no polymorphonuclear leukocytes may be seen.
 
The presence of [[mononuclear cells]] and [[fibroblasts]], and the absence of polymorphonuclear leukocytes characterize '''healing infarction'''.
 
'''Healed infarction''' is characterized by scar tissue without cellular infiltration. The entire process leading to a healed infarction usually takes at least 5–6 weeks.
 
[[Reperfusion]] may alter the macroscopic and microscopic appearance of the necrotic zone by producing [[myocyte]]s with contraction bands and large quantities of extravasated [[erythrocyte]]s.
 
Myocardial infarctions can be classified temporally from clinical and other features, as well as according to the pathological appearance as:<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al''|title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284|doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref>
# Evolving phase of myocardial infarction: (>6 hours),
# Acute phase of myocardial infarction: (6 hours – 7 days),
# Healing phase of myocardial infarction: (7–28 days),
# Healed phase of myocardial infarction: (29 days and beyond).
 
It should be emphasized that the clinical and electrocardiographic timing of the onset of an acute myocardial infarction may not correspond precisely with the pathologic findings.  For example, the [[EKG]] may still demonstrate evolving [[ST segment]] / [[T wave]] changes and cardiac biomarkers may still be elevated (implying a recent infarct) at a time when pathologically the infarction is in the healing phase. <ref name="pmid10987628">{{cite journal |author=Alpert JS, Thygesen K, Antman E, Bassand JP |title=Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction |journal=J. Am. Coll. Cardiol. |volume=36 |issue=3 |pages=959–69 |year=2000 |month=September |pmid=10987628 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735109700008044}}</ref>
 
==Pathology of Myocardial Infarction==
 
Myocardial infarction is defined pathologically as myocardial cell death due to prolonged [[ischemia]]. Cell death is categorized pathologically as coagulation and/or contraction band [[necrosis]], which usually evolves through oncosis (early primary necrosis), but can result to a lesser degree from [[apoptosis]]. Careful analysis of histological sections by an experienced observer is essential to distinguish these entities.<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al''|title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284|doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref><ref name="pmid10987628">{{cite journal |author=Alpert JS, Thygesen K, Antman E, Bassand JP |title=Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction |journal=J. Am. Coll. Cardiol. |volume=36 |issue=3 |pages=959–69 |year=2000 |month=September |pmid=10987628 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735109700008044}}</ref>
 
After the onset of myocardial ischemia, cell death is not immediate but takes a brief period of time to develop (as little as 20 minutes or less in some animal models). It takes several hours before myocardial necrosis can be identified by macroscopic or microscopic postmortem examination. <ref name="pmid10987628">{{cite journal |author=Alpert JS, Thygesen K, Antman E, Bassand JP |title=Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction |journal=J. Am. Coll. Cardiol. |volume=36 |issue=3 |pages=959–69 |year=2000 |month=September |pmid=10987628 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735109700008044}}</ref>
 
Complete necrosis of all myocardial cells at risk requires at least 2–4 hours or longer depending on the presence of collateral circulation to the ischemic zone, whether the occlusion was persistent or intermittent, the sensitivity of the [[myocyte]]s to [[ischemia]], preconditioning, and/or, finally, individual demand for myocardial oxygen and nutrients. Myocardial infarctions are usually classified by the following:<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref> <ref name="pmid10987628">{{cite journal |author=Alpert JS, Thygesen K, Antman E, Bassand JP |title=Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction |journal=J. Am. Coll. Cardiol. |volume=36 |issue=3 |pages=959–69 |year=2000 |month=September |pmid=10987628 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735109700008044}}</ref>
 
A. '''Size''':
#'''Microscopic''': Focal necrosis,
#'''Small''': <10% of the [[left ventricle|left ventricular myocardium]],
#'''Moderate''': 10–30% of the [[left ventricle|left ventricular myocardium]], 
#'''Large''': >30% of the [[left ventricle|left ventricular myocardium]].
 
B. '''Location''': The pathological identification of the location of myocardial necrosis (anterior, posterior, lateral, inferior, apical) is made without reference to the coronary arterial tree
 
C. '''Clinical history'''.
 
==Clinical Presentation of Ischemia==
 
The term myocardial infarction indicates the presence of cell death of cardiac myocytes caused by ischemia, which is the result of a perfusion imbalance between myocardial oxygen supply and myocardial oxygen demand.
 
Ischemia in the clinical setting most often can be identified from the patient’s history and from the [[EKG]]. Possible ischemic symptoms include various combinations of chest, upper extremity, jaw, or epigastric discomfort with exertion or at rest.
 
The discomfort associated with acute myocardial infarction usually lasts at least 20 minutes. Often, the discomfort is diffuse, not localized, not positional, not affected by movement of the region, and it may be accompanied by [[dyspnea]], [[diaphoresis]], [[nausea]], or [[syncope]].
 
These symptoms are not specific to myocardial ischemia and can be misdiagnosed and thus attributed to gastrointestinal, neurological, pulmonary, or musculoskeletal disorders.
 
Myocardial infarction may occur with atypical symptoms, or even without symptoms, being detected only by [[EKG]], elevation of biomarkers, or cardiac imaging.<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref>
 
==Criteria for Diagnosis of Acute Myocardial Infarction==
The term myocardial infarction should be used when there is evidence of myocardial necrosis in a clinical setting consistent with myocardial ischemia. Under these conditions any one of the following criteria meets the diagnosis for acute myocardial infarction. <ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref>
 
#Detection of rise and/or fall of cardiac biomarkers (preferably Troponin) with at least one of the following
#:a. Symptoms of [[ischemia]]
#:b. [[EKG]] changes indicative of ischemia as new ([[ST segment]] / [[T wave]] changes or new left bundle branch block [[LBBB]])
#:c. Development of pathological [[Q wave]]s
#:d. Imaging evidence of new viable myocardium or wall motion abnormality
#[[Sudden cardiac death|Sudden unexpected cardiac death]], including cardiac arrest, often with symptoms suggestive of myocardial [[ischemia]], accompanied by presumably new [[ST segment]] elevation, or new [[LBBB]], and/or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, if death has occurred before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood
#In patients with normal baseline [[troponin]] values, a greater than 3 times increase above the 99th percentile of the upper limit of normal of cardiac biomarkers has been designated as the definition of [[PCI]] related myocardial infarction. A subtype related to documented stent thrombosis is recognized.
#For patients with [[CABG|CABG surgery]]; (In patients with normal baseline [[troponin]] values) increases of cardiac biomarkers greater than 5 times, (> 5 times the 99th percentile upper limit of normal) and either new [[Q wave|pathological Q waves]] or new [[LBBB]] or angiographically evidence of new graft or native vessel occlusion have been designated as defining [[CABG|CABG surgery]] related myocardial infarction.
#Pathological findings of acute myocardial infarction.
 
==Criteria for Prior Myocardial Infarction==
 
Any of the following criteria meets the diagnosis for prior myocardial infarction:<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref>
 
*Development of new pathological [[Q wave]]s with or without symptoms
*Imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract in the absence of a non ischemic cause.
*Pathological findings of healed or healing myocardial infarction.
 
==Classification==
 
Clinically the various types of myocardial infarction can be classified as follow: <ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref>
#Spontaneous '''myocardial infarction''' related to [[ischemia]] due to a primary coronary event, such as plaque erosion and/or rupture, fissuring, or dissection.
#'''Myocardial infarction''' secondary to [[ischemia]] due to an imbalance of O<sub>2</sub> supply and demand, as from coronary spasm or [[embolism]], [[anemia]], [[arrhythmias]], [[hypertension]], or [[hypotension]]
#[[Sudden cardiac death|Sudden unexpected cardiac death]], including [[cardiac arrest]], often with symptoms suggesting [[ischemia]] with new [[STEMI|ST segment elevation]]; new [[left bundle branch block]]; or pathologic or angiographic evidence of fresh [[thrombus|coronary thrombus]] (in the absence of reliable biomarker findings)
#
#:a. '''Myocardial infarction''' associated with [[PCI|Percutaneous Coronary Interventions]] ([[PCI]])
#:b. '''Myocardial infarction''' associated with documented in stent thrombosis.
#'''Myocardial infarction''' associated with [[Cardiac surgery|Coronary Artery Bypass Graft surgery]]
 
==Diagnostic Applications for Acute Myocardial Infarction==
 
===Differential Diagnosis for [[EKG]] in Acute Myocardial Infarction===
 
Conditions that confound the EKG diagnosis of myocardial infarction are the following: <ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref>;
 
*A QS complex in lead V<sub>1</sub> is normal.
*A [[Q wave]] <0.03 s and <1/4 of the [[R wave]] amplitude in lead III is normal if the frontal [[QRS axis]] is between 30 and 0°.
*The [[Q wave]] may be normal in aVL if the frontal [[QRS axis]] is between 60 and 90°. Small septal [[Q wave]]s are non pathological [[Q wave]]s if <0.03 s and <1/4 of the [[R wave]] amplitude in leads I, aVL, aVF, and V<sub>4</sub>-V<sub>5</sub>-V<sub>6</sub> 
*The following may be associated with Q/QS complexes in the absence of myocardial infarction:
:[[Wolff Parkinson White syndrome|Preexcitation syndromes]]
:[[Cardiomyopathy|Obstructive or dilated cardiomyopathy]]
:[[LBBB]]
:[[RBBB]]
:[[Left anterior fascicular block]]
:[[LVH]]
:[[RVH]]
:[[Myocarditis]]
:[[Cor pulmonale|Acute cor pulmonale]]
:[[Hyperkalemia]]
 
===Diseases That May be Confused with Acute MI===
#Benign early repolarization (e.g. high take-off)
#[[Pericarditis]]
#[[LBBB]]
#[[Pulmonary embolism]]
#[[Myocarditis]]
#[[Brugada syndrome]]
#[[Wolff-Parkinson-White Syndrome|Preexcitation syndromes]]
#[[Subarachnoid hemorrhage]]
#[[Cholecystitis]]
#Electrolyte imbalance ([[hyperkalemia]])
#[[Lead placement errors|Lead misplacements]]
#Different lead configurations (e.g. modified Mason-Likar lead configurations)
#Misevaluation of [[J point]] variations
 
==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.
 
* [[Pericardiocentesis]] when the needle comes into contact with the myocardium, there can be ST segment elevation reflecting local injury of the myocardium.
 
* [[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.
 
===Disease States that May Cause a False Negative Evaluation of the EKG in Acute MI===
#Prior myocardial infarction with [[Q wave]]s and/or persistent [[ST segment]] elevation.
#[[LBBB]]
#[[Paced rhythm]]
 
===[[EKG]] Manifestations of Acute Myocardial Injury or Ischemia===
 
[[EKG]] manifestations of acute myocardial injury or ischemia in absence of [[left ventricular hypertrophy]] and [[LBBB]] as follow<ref name="pmid15992631">{{cite journal |author=Wong CK, French JK, Aylward PE, ''et al'' |title=Patients with prolonged ischemic chest pain and presumed-new left bundle branch block have heterogeneous outcomes depending on the presence of ST-segment changes |journal=J. Am. Coll. Cardiol. |volume=46 |issue=1 |pages=29–38 |year=2005 |month=July |pmid=15992631 |doi=10.1016/j.jacc.2005.02.084 |url=}}</ref><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>
 
*'''[[ST segment]] elevation'''
 
In general, [[ST segment]] elevation reflects myocardial injury, which may be irreversible (unlike ischemia which may be reversible) and which is associated with a risk of necrosis. ST elevation is defined as new [[ST segment]] elevation at the [[J point]] in two contiguous leads with the cut off points ≥0.2 mV in men or ≥0.15 mV in women in V<sub>2</sub>-V<sub>3</sub> and ≥0.1 mV in other leads.
 
*'''[[ST segment]] depression''' and '''[[T wave]] changes'''
 
In general, [[ST segment]] depression represents reversible ischemia (less likely to result in irreversible necorsis). One exception is the presence of [[ST segment]] depression in the anterior precordial leads that can reflect posterior injury rather than anterior ischemia. Ischemia is defined as new horizontal or downsloping [[ST segment]] changes as ≥0.05 mV in two contiguous leads and/or [[T wave]] inversion ≥0.1 mV in two contiguous leads with prominent R wave or in situations which R wave amplitude / S wave amplitude ratio is >1.
 
Althought it is not observed in women, the [[J point]] elevation in men decreases with increasing age.<ref name="pmid11781962">{{cite journal |author=Macfarlane PW |title=Age, sex, and the ST amplitude in health and disease |journal=J Electrocardiol |volume=34 Suppl |issue= |pages=235–41 |year=2001 |pmid=11781962 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/ajelc034b0235}}</ref>
 
''The term of '''contiguous lead''' represents lead groups such as anterior leads (V<sub>1</sub>-V<sub>6</sub>), inferior leads (II, III, and aVF), or lateral/apical leads (I and aVL).''
 
===EKG Changes of Prior Myocardial Infarction===
 
#Any [[Q wave]] in V<sub>2</sub>-V<sub>3</sub> ≥0.02 sec or presence of QS complex in V<sub>2</sub> and V<sub>3</sub>.
#[[Q wave]] ≥0.03 sec and ≥0.1 mV deep or presence of QS complexes in leads I, II, aVL, aVF or V<sub>4</sub>-V<sub>5</sub>-V<sub>6</sub> in any two leads of a contiguous lead grouping (I, aVL, V<sub>6</sub>; V<sub>4</sub>-V<sub>5</sub>-V<sub>6</sub>, II, III and aVF). The same criteria are used for supplemental leads V<sub>7</sub>-V<sub>8</sub>-V<sub>9</sub>, and for the Cabrera frontal plane leads.
#R wave ≥0.04 sec in V<sub>1</sub>-V<sub>2</sub> and R/S >1 with a concordant positive [[T wave]] in the absence of a conduction defect.<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref>
 
==Evaluation of Biomarkers==
 
Myocardial cell death can be recognized by the appearance in the blood of different proteins released into the circulation from the damaged [[myocyte]]s: [[myoglobin]], cardiac [[troponin]] T ([[cTnT]]) and I ([[cTnI]]), [[CK]] ([[Creatine Kinase]]), [[LDH]] ([[Lactate Dehydrogenase]]), as well as many other enzyme markers of necrosis.<ref name="pmid10982533">{{cite journal |author=Jaffe AS, Ravkilde J, Roberts R, ''et al'' |title=It's time for a change to a troponin standard |journal=Circulation |volume=102 |issue=11 |pages=1216–20 |year=2000 |month=September |pmid=10982533 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10982533}}</ref>
 
Myocardial infarction is diagnosed when blood levels of sensitive and specific biomarkers such as cardiac troponins (T and I) or CK-MB are increased in the clinical setting of acute myocardial ischemia. <ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref>
 
Although elevations in these biomarkers reflect myocardial necrosis, they do not indicate its mechanism. Thus, an elevated value of cardiac troponin in the absence of clinical evidence of ischemia should prompt a search for other etiologies of myocardial necrosis. <ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref><ref name="pmid17384331">{{cite journal |author=Morrow DA, Cannon CP, Jesse RL, ''et al'' |title=National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical characteristics and utilization of biochemical markers in acute coronary syndromes |journal=Circulation |volume=115 |issue=13 |pages=e356–75 |year=2007 |month=April |pmid=17384331 |doi=10.1161/CIRCULATIONAHA.107.182882 |url=}}</ref><ref name="pmid16814641">{{cite journal |author=Jaffe AS, Babuin L, Apple FS |title=Biomarkers in acute cardiac disease: the present and the future |journal=J. Am. Coll. Cardiol. |volume=48 |issue=1 |pages=1–11 |year=2006 |month=July |pmid=16814641 |doi=10.1016/j.jacc.2006.02.056 |url=}}</ref><ref name="pmid17084246">{{cite journal |author=Jaffe AS |title=Chasing troponin: how low can you go if you can see the rise? |journal=J. Am. Coll. Cardiol. |volume=48 |issue=9 |pages=1763–4 |year=2006 |month=November |pmid=17084246 |doi=10.1016/j.jacc.2006.08.006 |url=}}</ref><ref name="pmid17384332">{{cite journal |author=Apple FS, Jesse RL, Newby LK, Wu AH, Christenson RH |title=National Academy of Clinical Biochemistry and IFCC Committee for Standardization of Markers of Cardiac Damage Laboratory Medicine Practice Guidelines: Analytical issues for biochemical markers of acute coronary syndromes |journal=Circulation |volume=115 |issue=13 |pages=e352–5 |year=2007 |month=April |pmid=17384332 |doi=10.1161/CIRCULATIONAHA.107.182881 |url=}}</ref><ref name="pmid16556688">{{cite journal |author=Macrae AR, Kavsak PA, Lustig V, ''et al'' |title=Assessing the requirement for the 6-hour interval between specimens in the American Heart Association Classification of Myocardial Infarction in Epidemiology and Clinical Research Studies |journal=Clin. Chem. |volume=52 |issue=5 |pages=812–8 |year=2006 |month=May |pmid=16556688 |doi=10.1373/clinchem.2005.059550 |url=}}</ref>
 
==Electrocardiographic Detection of Myocardial Infarction==
 
The acute or evolving changes in the [[ST segment]], [[T wave]] and [[Q wave]] when present, potentially allow the clinician to date the event, to gain insight into the location of the infarct related artery, and to estimate the amount of myocardium at risk.
 
Coronary artery dominance, size and distribution of arterial segments, collateral vessels, and location, extent, and severity of coronary stenoses can also impact [[EKG]] manifestations of myocardial ischemia. The [[EKG]] is notoriously inaccurate in localizing which artery is the culprit.
 
The [[EKG]] by itself is often insufficient to diagnose acute myocardial ischemia or infarction since [[ST segment]] changes may be observed in other conditions. Also [[Q wave]]s may occur due to myocardial fibrosis in the absence of coronary artery disease such as [[Chagas]] disease.<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |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><ref name="pmid12621138">{{cite journal |author=Zimetbaum PJ, Josephson ME |title=Use of the electrocardiogram in acute myocardial infarction |journal=N. Engl. J. Med. |volume=348 |issue=10 |pages=933–40 |year=2003 |month=March |pmid=12621138 |doi=10.1056/NEJMra022700 |url=}}</ref>
 
Also, the [[EKG]] is a useful clinical marker of tissue perfusion. Greater [[ST segment]] resolution on the static and the continuous [[EKG]] correlate with [[TIMI Flow Grade (TFG)|TIMI grade 3 flow]], [[TIMI Myocardial Perfusion Grade 3]], smaller infarct sizes, and improved survival.<ref name=" Gibson-2003">{{cite journal | author= Gibson CM | title= Has my patient achieved adequate myocardial reperfusion? | journal= Circulation | year=2003 | volume=108 | pages=504-07| id= PMID 12900495}}</ref>
 
==Echocardiography==
 
[[Echocardiography]] is a reliable real time imaging technique with moderate spatial and temporal resolution. Its strength is the assessment of myocardial thickness, thickening, and motion at rest. This can be aided by tissue Doppler imaging. <ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref><ref name="pmid15541235">{{cite journal |author=Korosoglou G, Labadze N, Hansen A, ''et al'' |title=Usefulness of real-time myocardial perfusion imaging in the evaluation of patients with first time chest pain |journal=Am. J. Cardiol. |volume=94 |issue=10 |pages=1225–31 |year=2004 |month=November |pmid=15541235 |doi=10.1016/j.amjcard.2004.07.104 |url=}}</ref>
 
==Radionuclide Imaging==
 
Several radionuclide tracers allow viable myocytes to be imaged directly, including thallium-201, technetium-99m MIBI, tetrofosmin, and [18F]2-fluorodeoxyglucose (FDG).<ref name="pmid8790039">{{cite journal |author=Medrano R, Lowry RW, Young JB, ''et al'' |title=Assessment of myocardial viability with 99mTc sestamibi in patients undergoing cardiac transplantation. A scintigraphic/pathological study |journal=Circulation |volume=94 |issue=5 |pages=1010–7 |year=1996 |month=September |pmid=8790039 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=8790039}}</ref><ref name="pmid9386154">{{cite journal |author=Dakik HA, Howell JF, Lawrie GM, ''et al'' |title=Assessment of myocardial viability with 99mTc-sestamibi tomography before coronary bypass graft surgery: correlation with histopathology and postoperative improvement in cardiac function |journal=Circulation |volume=96 |issue=9 |pages=2892–8 |year=1997 |month=November |pmid=9386154 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=9386154}}</ref><ref name="pmid11790695">{{cite journal |author=Klein C, Nekolla SG, Bengel FM, ''et al'' |title=Assessment of myocardial viability with contrast-enhanced magnetic resonance imaging: comparison with positron emission tomography |journal=Circulation |volume=105 |issue=2 |pages=162–7 |year=2002 |month=January |pmid=11790695 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=11790695}}</ref>
 
Radionuclide assessment of perfusion at the time of patient presentation can be performed with immediate tracer injection and imaging that can be delayed for up to several hours. The technique is interpreter dependent, although objective quantitative analysis is available. [[EKG]] gating provides simultaneous information and reliable assessment on myocardial motion, thickening, and global [[left ventricle|left ventricular]] function. <ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref><ref name="pmid12573373">{{cite journal |author=Wagner A, Mahrholdt H, Holly TA, ''et al'' |title=Contrast-enhanced MRI and routine single photon emission computed tomography (SPECT) perfusion imaging for detection of subendocardial myocardial infarcts: an imaging study |journal=Lancet |volume=361 |issue=9355 |pages=374–9 |year=2003 |month=February |pmid=12573373 |doi=10.1016/S0140-6736(03)12389-6 |url=}}</ref>
 
==Multi Slice Computed Tomography==
 
Infarcted myocardium is initially visible to computerized tomography as a focal area of decreased left ventricular enhancement, but later examination shows hyperenhancement as with late gadolinium imaging by MRI. Contrast enhanced CT may be performed and helpful for suspected embolism and aortic dissection, conditions with clinical features that overlap with those of acute myocardial infarction. <ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref>  <ref name="pmid15150010">{{cite journal |author=Gosalia A, Haramati LB, Sheth MP, Spindola-Franco H |title=CT detection of acute myocardial infarction |journal=AJR Am J Roentgenol |volume=182 |issue=6 |pages=1563–6 |year=2004 |month=June |pmid=15150010 |doi= |url=http://www.ajronline.org/cgi/pmidlookup?view=long&pmid=15150010}}</ref>
 
==Cardiac Magnetic Resonance Imaging==
 
Cardiac [[MRI]] (C-MRI) has high spatial resolution and moderate temporal resolution. Although not widely available and not commonly used in acute setting, it is a well validated standard for the assessment of myocardial function and has, in theory, similar capability to echocardiography in suspected acute myocardial infarction and can play an important role in its detection.
 
Paramagnetic contrast agents can be used to assess myocardial perfusion and the increase in extracellular space associated with the fibrosis of chronic phase of myocardial infarction.<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref><ref name="pmid12957440">{{cite journal |author=Lima JA |title=Myocardial viability assessment by contrast-enhanced magnetic resonance imaging |journal=J. Am. Coll. Cardiol. |volume=42 |issue=5 |pages=902–4 |year=2003 |month=September |pmid=12957440 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735109703008398}}</ref><ref name="pmid15944538">{{cite journal |author=Isbell DC, Kramer CM |title=Cardiovascular magnetic resonance: structure, function, perfusion, and viability |journal=J Nucl Cardiol |volume=12 |issue=3 |pages=324–36 |year=2005 |pmid=15944538 |doi= |url=}}</ref>
 
==Diagnosis of Recurrent Myocardial Infarction (re-MI)==
 
The [[EKG]] diagnosis of [[recurrent myocardial infarction]] ([[re-MI]], [[reinfarction]]) following the initial infarction may be confounded by the initial evolutionary [[EKG]] changes.
 
[[Reinfarction]] should be considered when [[ST segment]] elevation ≥0.1 mV reoccurs in a patient having a lesser degree of [[ST segment]] elevation or new pathognomonic [[Q wave]]s, in at least two contiguous leads, particularly when associated with ischemic symptoms for 20 min or longer.
 
In patients where recurrent myocardial infarction is suspected from clinical signs or symptoms following the initial infarction, an immediate measurement of the employed cardiac marker is recommended. A second sample should be obtained 3–6 h later.
 
Recurrent myocardial infarction is diagnosed if there is a >20% increase of the value in the second sample. Although CK-MB used to be a test of choice for detecting recurrent myocardial infarction, trials data supports troponin use for the same purpose <ref name="pmid15563477">{{cite journal |author=Apple FS, Murakami MM |title=Cardiac troponin and creatine kinase MB monitoring during in-hospital myocardial reinfarction |journal=Clin. Chem. |volume=51 |issue=2 |pages=460–3 |year=2005 |month=February |pmid=15563477 |doi=10.1373/clinchem.2004.042887 |url=}}</ref>.
 
The re-elevation of the [[ST segment]] can, however, also be seen in threatening myocardial rupture and should lead to additional diagnostic work-up. Periodical and frequent [[EKG]] recordings, continuous monitoring of [[ST segment]]s with bedside monitors or holter systems might be helpful for early diagnosis.
 
'''[[ST segment]] depression or [[LBBB]] on their own should not be considered valid criteria for myocardial infarction'''.<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref>
 
==Prior Myocardial Infarction==
 
The specificity of the [[EKG]] diagnosis for myocardial infarction is greatest when [[Q wave]]s occur in several leads or lead groups. [[ST segment]] deviations or [[T wave]]s alone are non-specific findings for myocardial necrosis. However, when these abnormalities occur in the same leads as the [[Q wave]]s, the likelihood of myocardial infarction is increased. For example, minor [[Q wave]]s ≥0.02 and <0.03 s that are ≥0.1 mV deep are suggestive of prior infarction if accompanied by inverted [[T wave]]s in the same lead group. <ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref><ref name="pmid832343">{{cite journal |author=Savage RM, Wagner GS, Ideker RE, Podolsky SA, Hackel DB |title=Correlation of postmortem anatomic findings with electrocardiographic changes in patients with myocardial infarction: retrospective study of patients with typical anterior and posterior infarcts |journal=Circulation |volume=55 |issue=2 |pages=279–85 |year=1977 |month=February |pmid=832343 |doi= |url=}}</ref><ref name="pmid5544988">{{cite journal |author=Horan LG, Flowers NC, Johnson JC |title=Significance of the diagnostic Q wave of myocardial infarction |journal=Circulation |volume=43 |issue=3 |pages=428–36 |year=1971 |month=March |pmid=5544988 |doi= |url=}}</ref><ref name=" Pahlm-1998">{{cite journal | author= Pahlm US, Chaitman BR, Rautaharju PM, Selvester RH, Wagner GS.| title= Comparison of the various electrocardiographic scoring codes for estimating anatomically documented sizes of single and multiple infarcts of the left ventricle.| journal= Am J Cardiol | year=1998 | volume=81 | pages=809-15| id= PMID 9555767}}</ref>
 
Other validated myocardial infarction coding algorithms, such as the Minnesota code, Novacode, and WHO MONICA, define [[Q wave]] depth on the basis of depth, width, and ratio of R wave amplitude, such as [[Q wave]] depth at least one-third or one-fifth of R wave amplitude, and have been used extensively in epidemiological studies and clinical trials. <ref name=" Pahlm-1998">{{cite journal | author= Pahlm US, Chaitman BR, Rautaharju PM, Selvester RH, Wagner GS.| title= Comparison of the various electrocardiographic scoring codes for estimating anatomically documented sizes of single and multiple infarcts of the left ventricle.| journal= Am J Cardiol | year=1998 | volume=81 | pages=809-15| id= PMID 9555767}}</ref><ref name="pmid10493844">{{cite journal |author=Porela P, Helenius H, Pulkki K, Voipio-Pulkki LM |title=Epidemiological classification of acute myocardial infarction: time for a change? |journal=Eur. Heart J. |volume=20 |issue=20 |pages=1459–64 |year=1999 |month=October |pmid=10493844 |doi=10.1053/euhj.1998.1529 |url=}}</ref><ref name="pmid9682893">{{cite journal |author=Rautaharju PM, Park LP, Chaitman BR, Rautaharju F, Zhang ZM |title=The Novacode criteria for classification of ECG abnormalities and their clinically significant progression and regression |journal=J Electrocardiol |volume=31 |issue=3 |pages=157–87 |year=1998 |month=July |pmid=9682893 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0022-0736(98)90132-7}}</ref>
 
==Diagnosis of Myocardial Infarction Associated with Coronary Revascularization Procedures==
 
The [[EKG]] abnormalities that occur during or after percutaneous coronary intervention ([[PCI]]) are similar to those seen during spontaneous myocardial infarction. Injury can be due to embolization, vasoconstriction, edema, or reperfusion injury that occur as part of either [[PCI]] or [[CABG]]. Multiple events that can lead to myocardial necrosis are taking place, often in combination, during both types of intervention. <ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref> <ref name=" Ricciardi-2003">{{cite journal | author= Ricciardi MJ, Davidson CJ, Gubermikoff G, Beohar N, Eckman LJ, Parker MA, Bonow RO.| title= Troponin I elevation and cardiac events after percutaneous coronary intervention | journal= Am Heart J. | year=2003 | volume=145 | pages=522-28 | id= PMID 12660677}}</ref> <ref name=" Noora-2005">{{cite journal | author= Noora J, Ricci C, Hastings D, Hills S, Cybulsky I. | title= Determination of troponin I release after CABG surgery | journal= J Card Surg | year=1998 | volume=20 | pages=129-35| id= PMID 15725136}}</ref>
 
In patients who have undergone [[CABG|CABG surgery]], new [[ST segment]] - [[T wave]] abnormalities are common but not necessarily diagnostic of myocardial ischemia.<ref name="pmid11024394">{{cite journal |author=Yokoyama Y, Chaitman BR, Hardison RM, ''et al'' |title=Association between new electrocardiographic abnormalities after coronary revascularization and five-year cardiac mortality in BARI randomized and registry patients |journal=Am. J. Cardiol. |volume=86 |issue=8 |pages=819–24 |year=2000 |month=October |pmid=11024394 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(00)01099-7}}</ref>
 
When new pathological [[Q wave]]s appear in territories other than those identified before [[CABG|CABG surgery]], myocardial infarction should be considered, particularly if associated with elevated biomarkers, new wall motion abnormalities, or hemodynamic instability.
 
===Diagnosis of Myocardial Infarction in Patients Undergoing [[PCI|Percutaneous Coronary Intervention]]===
 
During [[PCI]], myocardial necrosis may result from recognizable peri-procedural events, alone or in combination, such as side-branch occlusion, disruption of collateral flow, distal embolization, coronary artery dissection, slow flow or no-reflow phenomenon, and microvascular plugging. Embolization of intracoronary thrombus or atherosclerotic particulate debris cannot be entirely prevented despite current antithrombotic and antiplatelet adjunctive therapy or protection devices. Such events induce extensive inflammation of non-infarcted myocardium surrounding small islets of myocardium necrosis. <ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref> <ref name="pmid11827918">{{cite journal |author=Akkerhuis KM, Alexander JH, Tardiff BE, ''et al'' |title=Minor myocardial damage and prognosis: are spontaneous and percutaneous coronary intervention-related events different? |journal=Circulation |volume=105 |issue=5 |pages=554–6 |year=2002 |month=February |pmid=11827918 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=11827918}}</ref><ref name=" Herrman-2005">{{cite journal | author= Herrman J. | title= Peri-procedural myocardial injury: 2005 update | journal= Eur Heart J. | year=2005 | volume=26 | pages=2493–2519 | id= PMID 16176941}}</ref> <ref name=" Ricciardi-2003">{{cite journal | author= Ricciardi MJ, Davidson CJ, Gubermikoff G, Beohar N, Eckman LJ, Parker MA, Bonow RO.| title= Troponin I elevation and cardiac events after percutaneous coronary intervention | journal= Am Heart J. | year=2003 | volume=145 | pages=522-28 | id= PMID 12660677}}<ref name="pmid11387602">{{cite journal |author=Saadeddin SM, Habbab MA, Sobki SH, Ferns GA |title=Minor myocardial injury after elective uncomplicated successful PTCA with or without stenting: detection by cardiac troponins |journal=Catheter Cardiovasc Interv |volume=53 |issue=2 |pages=188–92 |year=2001 |month=June |pmid=11387602 |doi=10.1002/ccd.1146 |url=}}</ref><ref name="pmid11401931">{{cite journal |author=Ricciardi MJ, Wu E, Davidson CJ, ''et al'' |title=Visualization of discrete microinfarction after percutaneous coronary intervention associated with mild creatine kinase-MB elevation |journal=Circulation |volume=103 |issue=23 |pages=2780–3 |year=2001 |month=June |pmid=11401931 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=11401931}}</ref>
 
In the setting of [[PCI]], the balloon inflation during a procedure almost always results in cardiac ischemia whether or not accompanied by [[ST segment|ST]]-[[T wave|T]] changes. The occurrence of procedure-related cell necrosis can be detected by measurement of cardiac biomarkers before or immediately after the procedure, and again at 6–12 and 18–24 h.<ref name="pmid15204231">{{cite journal |author=Gustavsson CG, Hansen O, Frennby B |title=Troponin must be measured before and after PCI to diagnose procedure-related myocardial injury |journal=Scand. Cardiovasc. J. |volume=38 |issue=2 |pages=75–9 |year=2004 |month=May |pmid=15204231 |doi=10.1080/14017430410026755 |url=}}</ref>{{cite journal | author= Miller WL, Garratt KN, Burrit MF, Lennon RJ, Reeder GS, Jaffe AS.| title= Baseline troponin level: key to understanding the importance of post-PCI troponin elevations. | journal= Eur Heart J. | year=2006 | volume=27 | pages=1061–69 | id= PMID 16481332}}</ref> Elevations of biomarkers above the 99th percentile URL after [[PCI]], assuming a normal baseline [[troponin]] value, are indicative of post-procedural myocardial necrosis. There is currently no solid scientific basis for defining a biomarker threshold for the diagnosis of peri-procedural myocardial infarction. Pending further data, and by arbitrary convention, it is suggested to designate increases more than three times the 99th percentile URL as [[PCI]] related myocardial infarction ('''type 4a'''). <ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref> <ref name=" Herrman-2005">{{cite journal | author= Herrman J. | title= Peri-procedural myocardial injury: 2005 update | journal= Eur Heart J. | year=2005 | volume=26 | pages=2493–2519 | id= PMID 16176941}}</ref>
 
If cardiac [[troponin]] is elevated before the procedure and not stable for at least two samples 6 h apart, there are insufficient
data to recommend biomarker criteria for the diagnosis of peri-procedural myocardial infarction.<ref name=" Miller-2003">{{cite journal | author= Miller WL, Garratt KN, Burrit MF, Lennon RJ, Reeder GS, Jaffe AS.| title= Baseline troponin level: key to understanding the importance of post-PCI troponin elevations. | journal= Eur Heart J. | year=2006 | volume=27 | pages=1061–69 | id= PMID 16481332}}</ref>
 
If the values are stable or falling, criteria for reinfarction by further measurement of biomarkers together with the features of the [[EKG]] or imaging can be applied.
 
A separate subcategory of myocardial infarction ('''type 4b''') is related to stent thrombosis as documented by angiography and/or autopsy. Although iatrogenic, myocardial infarction '''type 4b''' with verified stent thrombosis must meet the criteria for spontaneous myocardial infarction as well.<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref> <ref name=" Herrman-2005">{{cite journal | author= Herrman J. | title= Peri-procedural myocardial injury: 2005 update | journal= Eur Heart J. | year=2005 | volume=26 | pages=2493–2519 | id= PMID 16176941}}</ref>
 
===Diagnosis of Myocardial Infarction in Patients Undergoing [[CABG|CABG surgery]]===
 
During [[CABG|CABG surgery]], numerous additional factors can lead to peri-procedural necrosis. These include direct myocardial trauma from sewing needles or manipulation of the heart, coronary dissection, global or regional ischemia related to inadequate cardiac protection, microvascular events related to reperfusion, myocardial damage induced by oxygen free radical generation, or failure to reperfuse areas of the myocardium that are not subtended by graftable vessels. <ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref> <ref name=" Kovacevic-2004">{{cite journal | author= Kovacevic R, Majkic-Singh N, Ignjatovic S, Otasevic P, Obrenovic R, Paris M, Vilotijevic B, Guermonprez JL.| title= Troponin T levels in detection of perioperative myocardial infarction after coronary artery bypass surgery | journal= Clin Lab.| year=2004 | volume=50 | pages=437-45 | id= PMID 15330513}}</ref> <ref name=" Noora-2005">{{cite journal | author= Noora J, Ricci C, Hastings D, Hills S, Cybulsky I. | title= Determination of troponin I release after CABG surgery | journal= J Card Surg | year=1998 | volume=20 | pages=129-35| id= PMID 15725136}}</ref> <ref name="pmid11588444">{{cite journal |author=Benoit MO, Paris M, Silleran J, Fiemeyer A, Moatti N |title=Cardiac troponin I: its contribution to the diagnosis of perioperative myocardial infarction and various complications of cardiac surgery |journal=Crit. Care Med. |volume=29 |issue=10 |pages=1880–6 |year=2001 |month=October |pmid=11588444 |doi= |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0090-3493&volume=29&issue=10&spage=1880}}</ref>
 
Any increase of cardiac biomarkers after [[CABG]] indicates myocyte necrosis, implying that an increasing magnitude of biomarker is likely to be related to an impaired outcome. This has been demonstrated in clinical studies employing CK-MB where elevations five, 10 and 20 times the upper limit of normal after [[CABG]] were associated with worsened prognosis. <ref name="pmid11723020">{{cite journal |author=Costa MA, Carere RG, Lichtenstein SV, ''et al'' |title=Incidence, predictors, and significance of abnormal cardiac enzyme rise in patients treated with bypass surgery in the arterial revascularization therapies study (ARTS) |journal=Circulation |volume=104 |issue=22 |pages=2689–93 |year=2001 |month=November |pmid=11723020 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=11723020}}</ref><ref name="pmid11583884">{{cite journal |author=Klatte K, Chaitman BR, Theroux P, ''et al'' |title=Increased mortality after coronary artery bypass graft surgery is associated with increased levels of postoperative creatine kinase-myocardial band isoenzyme release: results from the GUARDIAN trial |journal=J. Am. Coll. Cardiol. |volume=38 |issue=4 |pages=1070–7 |year=2001 |month=October |pmid=11583884 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(01)01481-4}}</ref><ref name="pmid12475456">{{cite journal |author=Brener SJ, Lytle BW, Schneider JP, Ellis SG, Topol EJ |title=Association between CK-MB elevation after percutaneous or surgical revascularization and three-year mortality |journal=J. Am. Coll. Cardiol. |volume=40 |issue=11 |pages=1961–7 |year=2002 |month=December |pmid=12475456 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S073510970202538X}}</ref>
 
Likewise, the increase of troponin levels after [[CABG]] indicates necrosis of myocardial cells, which predicts a poor outcome, in particular when elevated to the highest quartile or quintile of the troponin measurements.<ref name="pmid11985917">{{cite journal |author=Januzzi JL, Lewandrowski K, MacGillivray TE, ''et al'' |title=A comparison of cardiac troponin T and creatine kinase-MB for patient evaluation after cardiac surgery |journal=J. Am. Coll. Cardiol. |volume=39 |issue=9 |pages=1518–23 |year=2002 |month=May |pmid=11985917 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735109702017898}}</ref><ref name="pmid17000912">{{cite journal |author=Croal BL, Hillis GS, Gibson PH, ''et al'' |title=Relationship between postoperative cardiac troponin I levels and outcome of cardiac surgery |journal=Circulation |volume=114 |issue=14 |pages=1468–75 |year=2006 |month=October |pmid=17000912 |doi=10.1161/CIRCULATIONAHA.105.602370 |url=}}</ref>
 
Unlike the prognosis, scant literature exists concerning the use of biomarkers for defining myocardial infarction in the setting of [[CABG]]. Therefore, '''biomarkers cannot stand alone in diagnosing myocardial infarction (type 5)'''.<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref>
 
In view of the adverse impact on survival observed in patients with significant biomarker elevations, the most recent ACC/AHA/ESC/WHF Task Force suggests, by arbitrary convention, that biomarker values more than five times the 99th percentile of the normal reference range during the '''first 72 h following [[CABG]]''', when associated with the appearance of new pathological [[Q wave]]s or new [[LBBB]], or angiographically documented new graft or native coronary artery occlusion, or imaging evidence of new loss of viable myocardium, should be considered as diagnostic of a [[CABG]] related myocardial infarction (type 5 myocardial infarction).<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref> <ref name=" Kovacevic-2004">{{cite journal | author= Kovacevic R, Majkic-Singh N, Ignjatovic S, Otasevic P, Obrenovic R, Paris M, Vilotijevic B, Guermonprez JL.| title= Troponin T levels in detection of perioperative myocardial infarction after coronary artery bypass surgery | journal= Clin Lab.| year=2004 | volume=50 | pages=437-45 | id= PMID 15330513}}</ref>
 
==Application in the Setting of Myocardial Infarction==
 
 
===A. In acute phase===
 
Imaging techniques can be useful in the diagnosis of myocardial infarction because of the ability to detect wall motion abnormalities in the presence of elevated cardiac biomarkers. An important role of acute [[echocardiography]] (in Emergency Department for triage or bedside]] or radionuclide imaging is in patients with suspected myocardial infarction and/or presence of a non diagnostic [[EKG]].
<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref><ref name="pmid2316447">{{cite journal |author=Peels CH, Visser CA, Kupper AJ, Visser FC, Roos JP |title=Usefulness of two-dimensional echocardiography for immediate detection of myocardial ischemia in the emergency room |journal=Am. J. Cardiol. |volume=65 |issue=11 |pages=687–91 |year=1990 |month=March |pmid=2316447 |doi= |url=}}</ref><ref name="pmid1914101">{{cite journal |author=Sabia P, Abbott RD, Afrookteh A, Keller MW, Touchstone DA, Kaul S |title=Importance of two-dimensional echocardiographic assessment of left ventricular systolic function in patients presenting to the emergency room with cardiac-related symptoms |journal=Circulation |volume=84 |issue=4 |pages=1615–24 |year=1991 |month=October |pmid=1914101 |doi= |url=}}</ref><ref name="pmid7977092">{{cite journal |author=Saeian K, Rhyne TL, Sagar KB |title=Ultrasonic tissue characterization for diagnosis of acute myocardial infarction in the coronary care unit |journal=Am. J. Cardiol. |volume=74 |issue=12 |pages=1211–5 |year=1994 |month=December |pmid=7977092 |doi= |url=}}</ref><ref name="pmid8998090">{{cite journal |author=Tatum JL, Jesse RL, Kontos MC, ''et al'' |title=Comprehensive strategy for the evaluation and triage of the chest pain patient |journal=Ann Emerg Med |volume=29 |issue=1 |pages=116–25 |year=1997 |month=January |pmid=8998090 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0196-0644(97)70317-2}}</ref>
 
A normal [[echocardiogram]] or resting [[EKG]] gated scintigram has a 95–98% negative predictive value for excluding acute infarction.<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref>
 
===B. In the healing or healed phase===
 
Imaging techniques are useful in myocardial infarction for analysis of left ventricular function, both at rest and during dynamic exercise or pharmacological stress, to provide an assessment of remote inducible [[ischemia]]. Non-invasive imaging techniques can diagnose healing or healed infarction by demonstrating regional wall motion, thinning, or scar in the absence of other causes.
 
[[Echocardiography]] and radionuclide techniques, in conjunction with exercise or pharmacological stress, can identify ischemia and myocardial viability.
 
The high resolution of contrast enhanced [[MRI]] (CE MRI) means that areas of late enhancement correlate well with areas of fibrosis and thereby enable differentiation between transmural and subendocardial scarring. CE MRI is potentially valuable in assessing [[left ventricle|left ventricular]] function and areas of viable and potentially hibernating myocardium.<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref><ref name="pmid10556226">{{cite journal |author=Kim RJ, Fieno DS, Parrish TB, ''et al'' |title=Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function |journal=Circulation |volume=100 |issue=19 |pages=1992–2002 |year=1999 |month=November |pmid=10556226 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10556226}}</ref><ref name="pmid18246410">{{cite journal |author=Appelbaum E, Kirtane AJ, Clark A, ''et al'' |title=Association of TIMI Myocardial Perfusion Grade and ST-segment resolution with cardiovascular magnetic resonance measures of microvascular obstruction and infarct size following ST-segment elevation myocardial infarction |journal=J. Thromb. Thrombolysis |volume= |issue= |pages= |year=2008 |month=February |pmid=18246410 |doi=10.1007/s11239-008-0197-y |url=}}</ref>
 
==Impact on Clinical Trials in Which Myocardial Infarction is an Endpoint==
 
In the design of a new study, clinical trial investigators should specify which definition of myocardial infarction they expect will be altered by the new treatment under investigation. Factors that should be considered include:<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref><ref name="pmid15814567">{{cite journal |author=Salomaa V, Koukkunen H, Ketonen M, ''et al'' |title=A new definition for myocardial infarction: what difference does it make? |journal=Eur. Heart J. |volume=26 |issue=17 |pages=1719–25 |year=2005 |month=September |pmid=15814567 |doi=10.1093/eurheartj/ehi185 |url=}}</ref>
 
* Assessment of the incidence of spontaneous myocardial infarction ('''type 1''') and infarction related to myocardial oxygen supplies and demand ('''type 2''') in treated patients vs. control subjects.
 
* Assessment of the incidence of [[sudden cardiac death|sudden death]] related to myocardial infarction when applying the suggested criteria ('''type 3''').
 
* Assessment of the incidence of revascularization procedure related myocardial infarctions and biomarker elevations (for [[PCI]], '''type 4a''' and '''type 4b'''; and for [[CABG]], '''type 5''').
 
==Public Policy Implications of Redefinition of Myocardial Infarction==
 
Increasing the sensitivity of diagnostic criteria for myocardial infarction may result in more cases being identified and identify more patients who would be appropriate for secondary prevention measures.
 
Increasing the specificity of diagnostic criteria for myocardial infarction will result in more accurate diagnosis but will not exclude the presence of [[coronary artery disease]], patients who might benefit from secondary prevention. <ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref><ref name="pmid16908764">{{cite journal |author=Roger VL, Killian JM, Weston SA, ''et al'' |title=Redefinition of myocardial infarction: prospective evaluation in the community |journal=Circulation |volume=114 |issue=8 |pages=790–7 |year=2006 |month=August |pmid=16908764 |doi=10.1161/CIRCULATIONAHA.106.627505 |url=}}</ref>
 
In order to meet this challenge;
#Physicians must be adequately informed of the altered diagnostic criteria.
#Educational materials will need to be created, treatment guidelines must be appropriately adapted and freely delivered.
#Professional societies should take steps to facilitate the rapid dissemination of the revised definition to:
#:a. Physicians,
#:b. Other health care professionals,
#:c. Administrators,
#:d. The general public,
#:e. Insurers,
#:f. Regulatory authorities
 
==Global Impact of Redefinition of Myocardial Infarction==
 
Beyond the substantial impact on the identification, prevention, and treatment of cardiovascular disease throughout the world, the changes in the definition of acute myocardial infarction have critical consequences for less developed and developing countries. In many countries, the resources to apply the new definition may not be available in all hospitals. However, many developing countries already do have medical facilities capable of or currently employing the proposed definition of acute myocardial infarction. The new definition will also impact epidemiological data from developing countries related to prevalence and incidence of acute MI.<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref>
 
In less advantaged hospitals, the diagnosis of myocardial infarction may depend mostly on clinical signs and symptoms coupled with less sophisticated biomarker analyses. Some of these institutions may only have access to Creatin Kinase and its isoenzymes at the present time.
 
The redefinition arises from and is compatible with the latest scientific knowledge and with advances in technology, particularly with regard to the use of biomarkers, high quality [[electrocardiography]], and imaging techniques.
 
The definition can and should be used by developed countries immediately, and by developing countries as quickly as resources become available.<ref name="pmid17951284">{{cite journal |author=Thygesen K, Alpert JS, White HD, ''et al'' |title=Universal definition of myocardial infarction |journal=Circulation |volume=116 |issue=22 |pages=2634–53 |year=2007 |month=November |pmid=17951284 |doi=10.1161/CIRCULATIONAHA.107.187397 |url=}}</ref>
 
==Pathologic diagnosis of MI==
Images displayed in this section are courtesy of Professor Peter Anderson, and published with permission.
© PEIR, University of Alabama at Birmingham, Department of Pathology [http://peir.net/ PEIR]
 
[[Image:Image15001.jpg|left|thumb|400px|Acute Myocardial infarction]]
<br clear="left"/>
 
[[Image:Image15533.jpg|left|thumb|400px|Myocardial infarction, fibrosis. Right Coronary Artery's territory]]
<br clear="left"/>
 
 
[[Image:Image15973.jpg|left|thumb|400px|Acute Myocardial infarction; Posterior wall]]
<br clear="left"/>
 
[[Image:Image15380.jpg|left|thumb|400px|Acute Myocardial infarction with PMNs]]
<br clear="left"/>
 
[[Image:Image15383.jpg|left|thumb|400px|Acute Myocardial infarction, coagulative necrosis]]
<br clear="left"/>
 
[[Image:Image917.JPG|left|thumb|400px|Gross example of myocardial infarction that is several weeks or perhaps months of age ]]
<br clear="left"/>
 
[[Image:Image918.JPG|left|thumb|400px|The same heart. Another view.]]
<br clear="left"/>
 
[[Image:Image919.JPG|left|thumb|400px|The same heart. Multi sliced view]]
<br clear="left"/>
 
[[Image:Image916.JPG|left|thumb|400px|The same heart. Microscopic view. H&E, medium magnification view of healing infarct.]]
<br clear="left"/>
 
[[Image:Image903.JPG|left|thumb|400px|Gross example of acute infarction in fixed heart. Lesion is reflow necrosis stone heart also has old scar ]]
<br clear="left"/>
 
[[Image:Image905.JPG|left|thumb|400px|Gross example of acute infarction in fixed heart. Lesion is reflow necrosis stone heart also has old scar.]] Multisliced view.
<br clear="left"/>
 
[[Image:Image15637.jpg|left|thumb|400px|Myocardial infarction, subacute phase.]]
<br clear="left"/>
 
<div align="left">
<gallery heights="175" widths="175">
Image:Image15644.jpg|Myocardial infarction, subacute, granulation tissue.
Image:Image15645.jpg|Myocardial infarction, subendocardial ischemia with swollen myocytes
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:Image15646.jpg|Myocardial infarction, mural thrombus
Image:Image15882.jpg|Acute myocardial infarction, ischemic fibers demonstrated by aldehyde fuchsin stain
</gallery>
</div>
 
==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 dated resource of Cardiovascular Research]
 
{{STEMI}}
 
[[tr:Akut miyokard enfarktüsünün klinik sınıflaması]]
 
[[Category:Emergency medicine]]
[[Category:Cardiology]]
[[Category:Intensive care medicine]]
 
{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Latest revision as of 18:52, 10 August 2012

Redirect to:

Retrieved from "https://www.wikidoc.org/index.php?title=Clinical_classification_of_acute_myocardial_infarction&oldid=680905"