If no cause is found that is amenable to special treatment, no established guidelines are available. Some clinicians, however, prefer an alternative antiplate-let agent such as clopidogrel, ticlopidine, dipyridamole or a combination with aspirin. Atherosclerosis is a disease that develops over several decades. Risk factors such as smoking, hypertension, hy-perlipidemia and diabetes can lead to the development of arterial fatty streaks and fibrous plaques in individuals. Clinical disease may stay clinically silent during several years, by which time atherosclerotic plaques may have developed.
Initial symptoms develop in the vascular bed in which the atherosclerotic process is most advanced.
However, symptoms in one vascular bed usually indicate widespread disease with a high risk of further is-chemic events elsewhere. Cracking, rupture and fissue of atherosclerotic lesions act as stimuli for platelet activation and resultant thrombosis. This process is called athe-rothrombosis. Platelets to not adhere to intact endothelium, but re-quire sites of vascular injury such as atherosclerotic plaques. The resultant exposure of thrombogenic suben-dothelial vessel wall constituents such as collagen, laminin, fibronectin and von Willebrand factor leads to platelet adhesion and activation at these sites.