Diagnosis of myocardial infarction

A diagnosis of myocardial infarction is created by integrating the history of the presenting illness and physical examination with electrocardiogram findings and cardiac markers (blood tests for heart muscle cell damage).

[5] According to the WHO criteria as revised in 2000,[6] a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI.

[8][9]: 1444 If heart failure ensues, elevated jugular venous pressure and hepatojugular reflux, or swelling of the legs due to peripheral edema may be found on inspection.

Mistakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the quality of patient care.

Now, the markers most widely used in detection of MI are MB subtype of the enzyme creatine kinase and cardiac troponins T and I as they are more specific for myocardial injury.

The cardiac troponins T and I which are released within 4–6 hours of an attack of MI and remain elevated for up to 2 weeks, have nearly complete tissue specificity and are now the preferred markers for assessing myocardial damage.

[16] Note that only the cardiac troponins are used clinically for myocardial infarction as creatine kinase adds little value in diagnosing MI while adding to system cost.

Because these enzyme levels are not elevated immediately following a heart attack, patients presenting with chest pain are generally treated with the assumption that a myocardial infarction has occurred and then evaluated for a more precise diagnosis.

[citation needed] Under the microscope, myocardial infarction presents as a circumscribed area of ischemic, coagulative necrosis (cell death).

[24] The interstitium at the margin of the infarcted area is initially infiltrated with neutrophils, then with lymphocytes and macrophages, who phagocytose ("eat") the myocyte debris.

The necrotic area is surrounded and progressively invaded by granulation tissue, which will replace the infarct with a fibrous (collagenous) scar (which are typical steps in wound healing).