What an interventional cardiologist should know about the pathophysiology of acute myocardial infarction.

Basic knowledge of the sequence of cellular events that change the relative benign disease coronary atherosclerosis into a life-threatening acute coronary syndrome is of great importance for the interventional cardiologist in order to understand and choose the correct pharmacological and interventional management in patients with acute myocardial infarction. Plaque disruption, or fissuring, with superimposed thrombosis frequently complicates the course of coronary atherosclerosis. Small ruptures often remain clinically silent, whereas more extensive plaque rupture may lead to the development of unstable angina, acute myocardial infarction, and sudden cardiac death. The risk of plaque disruption depends more on plaque composition than on plaque size and stenosis severity. Major determinants of a plaque's vulnerability to rupture are: the size and consistency of the lipid-rich atheromatous core, the thickness of the fibrous cap covering the core, and inflammation and repair within the cap. The elevation of fibrinogen and C-reactive protein in patients with unstable angina may be markers of ongoing plaque inflammation. Both plaque vulnerability and rupture triggers are important for plaque disruption. The resultant thrombotic response, which is important for the clinical presentation and outcome, is in part determined by the reactivity of the circulating platelets and the balance between the fibrinolytic and coagulation systems. New ways of identification and treatment of the dangerous vulnerable plaques responsible for infarction and death and optimization of anti-thrombotic treatment are highly warranted in order to prevent and treat life-threatening coronary thrombosis.