A new, precise definition of acute myocardial infarction
ABSTRACTSeveral international cardiovascular societies have revised their diagnostic criteria for acute myocardial infarction (MI) (J Am Coll Cardiol 2007; 50:2173–2188). The cornerstone of diagnosis remains a high level of clinical suspicion, serial electrocardiograms, and troponin levels. This article reviews the new definition and the appropriate clinical tools necessary to diagnose acute MI accurately.
KEY POINTS
- The clinical presentation of acute MI varies considerably from patient to patient. Therefore, one must consider the symptoms, serial electrocardiographic findings, and serial biomarker results in concert.
- Troponin I or T is now the preferred biomarker of myocardial necrosis. Still, troponin can be elevated in many conditions other than ischemic heart disease.
- Electrocardiographic signs of acute ischemia have been precisely defined, but electrocardiography can give false-positive or false-negative results in a number of conditions.
- MI is now categorized into five types depending on cause.
Acute myocardial infarction (MI) portends important and substantial consequences. Angioplasty or fibrinolytic therapy to open the blocked coronary artery is proven to improve the patient’s chances of surviving without consequent morbidity or death. But the diagnosis is not always straightforward. The presentation of acute MI can vary widely, and a number of other conditions—many of them equally serious emergencies—can mimic its symptoms, electrocardiographic signs, and biomarker patterns.
In an attempt to improve the accuracy of the diagnosis of MI, a multinational task force met in 1999 under the auspices of the European Society of Cardiology and the American College of Cardiology. The goal was to develop a simple, clinically oriented definition of MI that could be widely adopted. A document was created and published simultaneously in 2000 in the European Heart Journal and the Journal of the American College of Cardiology.1 These organizations updated their paper in 2007 with a new definition of acute MI to account for advances in diagnosis and management.2
In this article we will review the new definition and how to make the diagnosis of acute MI today. Specifically, the updated definition includes:
- Subtypes of acute MI
- Imaging tests supporting the diagnosis
- Biomarker thresholds after percutaneous coronary intervention or bypass grafting.
TROPONIN: BETTER THAN CK, BUT NOT PERFECT
The original 2000 paper1 and the 2007 update2 featured the use of the cardiac biomarker troponin, which is considerably more sensitive and specific for heart damage than total creatine kinase (CK) or its isoform, CK-MB.
The new, more-sensitive biomarker-based definition of MI resulted in more cases of MI being diagnosed, and this has attracted the attention and scrutiny of many, especially population scientists and interventional cardiologists.3 This change has caused some controversy, especially when dealing with small rises in troponin following percutaneous coronary intervention.
In addition, some confusion over terminology remains. For example, the phrase “troponin leak” is often used to describe cases in which serum troponin levels rise but there is no MI. However, most experts believe that a rise and fall in troponin is due to true myocardial cell death. Troponin I and T are such large molecules that they cannot “leak” from a cardiac cell unless there has been irreparable cellular damage—that is, cell death.
Creatine kinase still has a role
In some cases, CK and CK-MB may be helpful in determining the acuity of myocardial necrosis, but their use will vary by institution. These biomarkers typically rise 2 to 4 hours after the initial event and fall within 24 to 48 hours, whereas troponin levels stay elevated for days or weeks. Thus, the presence of troponin without CK and CK-MB in the right clinical context may indicate a past MI that is no longer acute.
INFARCTION: CELL DEATH DUE TO ISCHEMIA
MI is myocardial cell death due to prolonged ischemia. Under the microscope, it can be categorized as coagulation necrosis in which ghost-like cell structures remain after hypoxic insult (typical of most MIs) or contraction band necrosis with amorphous cells that cannot contract anymore, the latter often a hallmark of excessive catecholamine damage or reperfusion injury. Apoptosis occurs in the heart but is technically not considered necrosis and is thought not to be associated with elevated troponin levels.6,7
In experiments in animals, cell death can occur as little as 20 minutes after coronary artery occlusion, although completion of infarction is thought to take 2 to 4 hours. The time to infarct completion may be longer in patients with collateral circulation or when the culprit coronary artery has intermittent (“stuttering”) occlusion. Preconditioning of myocardial cells with intermittent ischemia can also influence the timing of myocardial necrosis by protecting against cell death to some extent. Alteration in myocardial demand can influence the time required for completion of infarction either favorably or unfavorably; hence, reducing myocardial demand is beneficial in acute MI.
Three pathologic phases of MI
MI can be categorized pathologically as acute, healing, or healed.
Acute MI. In the first 6 hours after coronary artery occlusion, coagulation necrosis can be seen with no cellular infiltration. After 6 hours, polymorphonuclear leukocytes infiltrate the infarcted area, and this may continue for up to 7 days if coronary perfusion does not increase or myocardial demand does not decrease.
Healing MI is characterized by mononuclear cells and fibroblasts and the absence of polymorphonuclear leukocytes. The entire healing process takes 5 to 6 weeks and can be altered by coronary reperfusion.
Healed MI refers to scar tissue without cellular infiltration.
