Cellular death releases myocardial enzymes that can be used to diagnose the severity of the infarct. Enzymes such as lactate dehydrogenase, creatine phosphokinase, and serum aspartate aminotransferase levels are elevated at certain times after an infarct has occurred and may also give some indication of the severity of the damage. The time between the onset of ischemia and muscle cell death is about 15 to 20 minutes in most cases. Almost always the infarction occurs in the left ventricle and left ventricular function may be significantly diminished. The larger the affected area of the myocardium the greater the loss of contractility.
All myocardial infarctions have a central area of necrosis that is surrounded by an area of injury.
Myocardial tissue does not regenerate after injury so the necrotic tissue is replaced by scar tissue that may inhibit contractility. If a large area of tissue is involved the heart as a pump may be compromised and the symptoms of congestive heart failure or cardiogenic shock will be seen. Complications of myocardial infarction include various disturbances in the normal heart rhythm, congestive heart failure, cardiogenic shock, thromboembolisms, pericarditis, and myocardial rupture. Ninety percent of patients will have some disturbance of rhythm following myocardial infarction. This is a result of local changes that effect automaticity and conduction of the heart muscle.