[Mechanisms of acute coronary syndrome].

The pathogenesis of coronary artery disease is characterized by an increased vasoconstriction, activation of platelet vessel wall interactions as well as the invasion of monocytes into the subintima with deposition of lipids as well as proliferation and migration of vascular smooth muscle cells. In the acute coronary syndromes plaque rupture as well as activation of platelets and coagulation as well as coronary vasoconstriction play an important role. Clinically these mechanisms lead to unstable angina and myocardial infarction. For the understanding of acute coronary syndromes, the mechanisms operative in the healthy blood vessel wall are important. Healthy coronary arteries are in a constant state of vasodilatation, platelets as well as the coagulation cascade are inactivated and vascular smooth muscle cells of the media are quiescent. Endothelial mediators such as nitric oxide, prostacyclin and tissue plasminogen activators and other mediators play an important role in this regard. The continuous release of nitric oxide and prostacyclin keeps the coronary circulation in a state of vasodilatation and inhibits platelet vessel wall interaction. Other mediators of the endothelium also inhibit coagulation and migration and proliferation of vascular smooth muscle cells. On the other hand in patients with cardiovascular risk factors and possibly also in those with genetic disposition as well as with aging, these mechanisms are impaired and in turn increased vasoconstrictor responses of coronary arteries, activation of platelet vessel wall interaction, invasion of monocytes into the subintima with lipid storage and proliferation/-migration of vascular smooth muscle cells occur. A cause oriented therapy of coronary artery disease and of acute coronary syndromes in particular must be based on these pathophysiological mechanisms.