New insights into the pathophysiology of acute coronary occlusion

The clinical features of acute coronary syndromes arise from rupture of an unstable atherosclerotic plaque with associated thrombosis and vasoconstric tion. The extent of the thrombotic response determines whether plaque ruptu re ultimately leads to full thickness infarction, partial thickness infarct ion or unstable angina. Recent advances in the biology of the coronary plaque have highlighted the importance of complex interactions between endothelial cells, smooth muscle cells, platelets and inflammatory cells in both the pathogenesis of plaque thrombosis and its subsequent healing. Therapeutic strategies based on con trol of inflammation and infection, such as the use of antibiotic therapy d irected against Chlamydia pneumoniae, show promise. There is also considera ble interest in the use of newer antiplatelet agents such as triflusal and the glycoprotein IIb/IIIa inhibitors in the treatment of unstable angina an d myocardial infarction. As our knowledge of the pathogenic processes underlying the acute coronary syndrome increases, it becomes clear that plaque instability may persist fo r a significant period following initial presentation, and that long-term t herapies may be required for full plaque passivation.