In patients with a myocardial infarction more than 1 year previously, treatment with ticagrelor significantly reduced the risk of cardiovascular death, myocardial infarction, or stroke and increased the risk of major bleeding. (Funded by AstraZeneca; PEGASUS-TIMI 54 ClinicalTrials.gov number, NCT01225562.).

Abstract-During the past decade, our understanding of the pathophysiology of coronary artery disease (CAD) has undergone a remarkable evolution. We review here how these advances have altered our concepts of and clinical approaches to both the chronic and acute phases of CAD. Previously considered a cholesterol storage disease, we currently view atherosclerosis as an inflammatory disorder. The appreciation of arterial remodeling (compensatory enlargement) has expanded attention beyond stenoses evident by angiography to encompass the biology of nonstenotic plaques. Revascularization effectively relieves ischemia, but we now recognize the need to attend to nonobstructive lesions as well. Aggressive management of modifiable risk factors reduces cardiovascular events and should accompany appropriate revascularization. We now recognize that disruption of plaques that may not produce critical stenoses causes many acute coronary syndromes (ACS). The disrupted plaque represents a "solid-state" stimulus to thrombosis. Alterations in circulating prothrombotic or antifibrinolytic mediators in the "fluid phase" of the blood can also predispose toward ACS. Recent results have established the multiplicity of "high-risk" plaques and the widespread nature of inflammation in patients prone to develop ACS. These findings challenge our traditional view of coronary atherosclerosis as a segmental or localized disease. Thus, treatment of ACS should involve 2 overlapping phases: first, addressing the culprit lesion, and second, aiming at rapid "stabilization" of other plaques that may produce recurrent events. The concept of "interventional cardiology" must expand beyond mechanical revascularization to embrace preventive interventions that forestall future events. Key Words: atherogenesis Ⅲ inflammation Ⅲ ischemia Ⅲ plaque Ⅲ acute coronary syndromes D uring the past decade, our understanding of the pathophysiology of coronary artery disease (CAD) has undergone a remarkable evolution. As patients with CAD generally present with either chronic or acute manifestations, this discussion will consider in turn these distinct modes of presentation. The Pathophysiology of Chronic CAD Lesion FormationPreviously considered a cholesterol storage disease, we currently understand atherogenesis as a complex interaction of risk factors including cells of the artery wall and the blood and molecular messages that they exchange. A useful organizing theme, which emerged first from laboratory studies and has now gained currency in the clinic, accords inflammation a major role in all stages of atherogenesis. 1 Inflammation also participates in the local, myocardial, and systemic complications of atherosclerosis.When the arterial endothelium encounters certain bacterial products or risk factors as diverse as dyslipidemia, vasoconstrictor hormones inculpated in hypertension, the products of glycoxidation associated with hyperglycemia, or proinflammatory cytokines derived from excess adipose tissue, these cells augment the expression of adhesion molecules tha...

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In patients 75 years of age or younger who have myocardial infarction with ST-segment elevation and who receive aspirin and a standard fibrinolytic regimen, the addition of clopidogrel improves the patency rate of the infarct-related artery and reduces ischemic complications.

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