Platelets and atherothrombosis: An essential role for inflammation in vascular disease — A review

Atherothrombosis is the common link between clinical manifestations of arterial vascular disease including ischemic stroke and acute coronary syndromes, such as unstable angina and acute myocardial infarction. Our understanding of the common pathologic mechanisms underlying these conditions has significantly increased during the past ten years, yet atherothrombosis as the “root cause” of a large proportion of cardiovascular and cerebrovascular diseases is largely underappreciated. Although the classical risk factors of dyslipidemia, smoking, diabetes, hypertension, obesity, and sedentary lifestyle are widely recognized as being associated with a heightened risk of vascular disease, inflammation of the vascular system during the past decade has become increasingly regarded as the principal underlying mechanism in the development of clinical atherothrombotic disease. In addition, platelet-derived inflammatory mediators play an essential role in the pathogenesis of cardiovascular disease, being involved at all stages of plaque development until their eventual rupture and subsequent formation of a platelet-rich thrombus. Mounting evidence supports the role of both localized and systemic inflammation in these events. Platelets are central to vascular inflammatory processes. Thus, inflammation can stimulate local thrombosis and thrombosis can amplify inflammation. Consequently, antiplatelet therapy for the prevention of serious vascular events may provide a double benefit via an anti-inflammatory action of the antiplatelet agent in modifying plaque formation and stability and antiplatelet activity that inhibits platelet aggregation and thrombus formation from occurring following plaque rupture.