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Previous Volume 353:2373-2383 December 1, 2005 Number 22 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Atherosclerosis, the major cause of ischemic coronary artery disease and cerebrovascular disease, is a chronic inflammatory disorder in which immune mechanisms interact with metabolic risk factors to initiate, propagate, and activate vascular lesions.¹ Arterial thrombosis, an acute complication that develops on the surface of a ruptured atheromatous plaque or as a consequence of endothelial erosion,¹ may cause myocardial infarction or ischemic stroke. Platelets are key cellular components of arterial occlusive thrombi and may participate in the development and progression of atheromatous plaques.² Platelets are also vital components of hemostasis, the physiologic process that arrests hemorrhage after tissue trauma and vascular . . . [Full Text of this Article]

Pharmacokinetics

Mechanism of Action

Functional Consequences of the Expression and Inhibition of Cyclooxygenase

Clinical Pharmacology of the Inhibition of Platelet Cyclooxygenase

Drug Interactions

Aspirin Resistance

Efficacy and Safety of Low-Dose Aspirin in the Prevention and Treatment of Atherothrombosis in High-Risk Patients

Efficacy and Safety of Low-Dose Aspirin in Low-Risk Subjects

Future Directions

Source Information

From the Department of Pharmacology, University of Rome La Sapienza, Rome (C.P.); the Spanish Center for Pharmacoepidemiologic Research, Madrid (L.A.G.R.); the Department of Medicine, Catholic University School of Medicine, Rome (R.L.); and the Clinical Trial Service Unit and Epidemiological Studies Unit, University of Oxford, Oxford, United Kingdom (C.B.).

Address reprint requests to Dr. Patrono at University of Rome La Sapienza, Ospedale Sant'Andrea, Via di Grottarossa 1035, 00189 Rome, Italy, or at cpatrono@unich.it.

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