Myocardial Infarction Redefined

Myocardial infarction (MI) can be defined from a number of different perspectives related to clinical, electrocardiographic (ECG), biochemical and pathologic characteristics. The term MI also has social and psychological implications, both as an indicator of a major health problem and as a measure of disease prevalence in population statistics and outcomes of clinical trials.

In the distant past, a general consensus existed for the clinical entity designated as MI. In studies of disease
prevalence by the World Health Organization (WHO), MI was defined by a combination of two of three characteristics: typical symptoms (i.e., chest discomfort), enzyme rise and a typical ECG pattern involving the development of Q waves. However, current clinical practice, health care delivery systems, as well as epidemiologic studies and clinical trials, all require a more precise definition of MI.

It is accepted that the term MI reflects a loss of cardiac myocytes (necrosis) caused by prolonged ischemia. Ischemia is the result of a perfusion-dependent imbalance between supply and demand. Ischemia in a clinical setting can be identified from the patient’s history and from the ECG. Possible ischemic symptoms include chest, epigastric, arm, wrist or jaw discomfort with exertion or at rest. The discomfort associated with acute MI usually lasts at least 20 min, but may be shorter in duration. The discomfort may develop in the central or left chest and then radiate to the arm, jaw, back or shoulder.

The presence or absence and the amount of myocardial damage resulting from prolonged ischemia can be assessed by a number of different means, including pathologic examination, measurement of myocardial proteins in the blood, ECG recordings (ST-T segment wave changes, Q waves), imaging modalities such as myocardial perfusion imaging, echocardiography and contrast ventriculography.

Myocardial necrosis results in and can be recognized by the appearance in the blood of different proteins released into the circulation due to the damaged myocytes: myoglobin, cardiac troponins T and I, creatine kinase, lactate dehydrogenase, as well as many others (Fig. 2). Myocardial infarction is diagnosed when blood levels of sensitive and specific biomarkers, such as cardiac troponin and the MB fraction of creatine kinase (CK-MB), are increased in the clinical setting of acute ischemia. These biomarkers reflect myocardial damage but do not indicate its mechanism. Thus, an elevated value in the absence of clinical evidence of ischemia should prompt a search for other causes of cardiac damage, such as myocarditis.