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Supports antiplatelet therapy in atherothrombotic disease; leaves open optimal regimens and duration in contemporary cohorts.
Atherosclerosis is a systemic disease that starts early in life, asymptomatically progressing though adulthood, until clinically manifested. In the last few years, experimental, clinical and pathological investigation has led us to a better knowledge of the pathophysiology of atherothrombotic disease. Atherothrombosis is the result of atherosclerosis progression, and its potentially life-threatening clinical consequences include coronary artery disease, cerebrovascular disease and peripheral artery disease. These events are mostly secondary to atherosclerotic plaque disruption and subsequent in situ thrombus formation which may be embolized and dragged by the arterial flow until occluding distal vessels. The demonstrated beneficial role of antiplatelet drugs in reducing the incidence of nonfatal events in many large clinical trials has demonstrated the major role of platelets in the atherothrombotic process in the arterial tree.
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Badimón et al. (2007) studied this question.
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