New concepts regarding events that lead to myocardial infarction.

In addition to new knowledge concerning the mechanisms whereby conventional risk factors act, other risk factors have been newly described, such as dietary antioxidants, lack of exercise, insulin resistance, excess iron stores, increased plasma angiotensin-converting enzyme, and left ventricular hypertrophy. An intact endothelium protects both by the formation of nitric oxide, which is a vasodilator and also an inhibitor of platelet aggregation and neutrophil adhesion, and by manufacturing tissue plasminogen activator. The acute thrombotic event occurs with a diurnal variation but may be precipitated by acute exertion, especially in untrained individuals, and reflects a balance between vasoconstrictory and vasodilatory stimuli from the vascular endothelium, as well as procoagulant versus anticoagulant effects of complex balancing systems. Increased risk of sudden cardiac death in the morning is thought to be a reflection of transient risk factors, such as a blood pressure increase, heart rate increase, and changes in coagulation factors, as well as changes in platelet aggregation. There is an apparent paradox between the acute effect of exercise in promoting sudden cardiac death and the chronic effect of exercise training in decreasing the risk of myocardial infarction. The explanation may be that chronic exercise training has an inhibitory effect on adrenergic discharge.