Post percutaneous coronary intervention antiplatelet therapy: Current perceptions, prospects and perplexity

Dual antiplatelet therapy (DAT) has become standard care for patients undergoing percutaneous coronary intervention (PCI). Following balloon injury and stent placement, the intima at the site is distressed, resulting in the activation of coagulation cascade and platelets. In the case of bare metal stents (BMS), it takes six to eight weeks for the stent surface to be covered with neointima. However, in the case of a drug-eluting stent (DES), the process of healing is delayed and neointima may not form for months or even years. To prevent the formation of platelet thrombi, dual antiplatelet therapy is given as a combination of aspirin and clopidogrel for three months in a case of BMS and for a minimum of one year in a case of DES. A prolonged duration of therapy is often required for a subset of patients who are highly prone to thrombus formation. During most non-cardiac surgeries, dual antiplatelet therapy should be continued if bleeding can be directly controlled and excessive bleeding will have no adverse effect on the outcome of surgery. Prasugrel, another thienopyridine, is more potent and faster acting than clopidogrel, and is therefore of great value in cases of acute coronary syndrome during PCI, particularly in diabetics. Triple drug therapy, by adding cilastozol, is reserved for some selected thrombotic lesions. Ticagrelor and cangrelor are two new antiplatelet agents undergoing various clinical trials. (Cardiol J 2011; 18, 6: 712–717

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Inflammation and Atherosclerosis—Revisited:

Atherogenesis has been traditionally viewed as a metabolic disease representing arterial obstruction by fatty deposits in its wall. Today, it is believed that atherogenesis involves highly specific biochemical and molecular responses with constant interactions between various cellular players. Despite the presence of inflammatory reaction in each and every step of atherosclerosis from its inception to terminal manifestation, the cause–effect relationship of these 2 processes remains unclear. In this article, we have attempted to review the role of inflammation in the development of atherosclerosis and in its major complication—coronary heart disease