[Acute coronary syndromes: physiopathology and therapeutic aspects]

This article discusses recent developments in the field of acute coronary syndromes including pathophysiological mechanisms as well as therapeutic strategies. A plaque disruption is caused by different stimuli in a plaque prone to rupture, i.e. a plaque with a lipid-rich core and high local concentration of inflammatory cells (T-cells, monocytes/macrophages, mast cells). These cells are capable of producing matrix degradation products and can reduce stability of a plaque. Thrombus formation, based on platelet activation and aggregation as well as fibrin formation, is the main consequence of plaque disruption. Depending on the degree of thrombus formation occlusion is followed clinically by unstable angina (subtotal occlusion) or by acute myocardial infarction (total occlusion). Accompanying vasoconstriction may further aggravate the situation. Principles of therapy are thrombus dissolution as well as prevention of new thrombus formation: main goals of thrombolytic therapy in acute myocardial infarction are a prompt (less than 3 hours), complete, and sustained (prevention of early thrombotic reocclusion) reperfusion.