Atherosclerosis and thrombosis in the coronary arteries

Vascular injury, platelet deposition and thrombus formation are key events in the initiation and progression of atherosclerosis. Angiography in patients with unstable angina or myocardial infarction with subtotal coronary occlusion often reveals eccentric stenosis with irregular borders suggesting ruptured atherosclerotic plaques and thrombosis. We have studied the mechanism of thrombus formation on severely damaged vascular wall to observe that local factors such as the local blood flow characteristics, the degree and geometry of stenosis, and the composition of the exposed vascular component or even the presence of residual thrombus are significant modulators of the acute platelet response to injury. Additionally the vasomotor tone control of the area is a contributor to the thrombotic risk. Systemic factors are equally modulators of the thrombotic outcome in the eventual occurrence of plaque rupture, as such, a surge of epinephrine can stimulate platelets for deposition at areas of injury. Hyperlipidemia, diabetes, increase PAI-inhibitors have shown to have a predisposing role for thrombotic complications in atherosclerosis and its specific mechanisms of intervention are being investigated.