Low-dose aspirin for the prevention of atherothrombosis

Carlo Patrono, Raffaele Landolfi, Luis A. García Rodríguez, Colin Baigent

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Abstract

n engl j med 353;22www.nejm.orgdecember 1, 2005The new england journal of medicine2373review articledrug therapyLow-Dose Aspirin for the Prevention of AtherothrombosisCarlo Patrono, M.D., Luis A. García Rodríguez, M.D., Raffaele Landolfi, M.D., and Colin Baigent, B.M., B.Ch.From the Department of Pharmacology,University of Rome La Sapienza, Rome(C.P.); the Spanish Center for Pharmaco-epidemiologic Research, Madrid (L.A.G.R.);the Department of Medicine, Catholic Uni-versity School of Medicine, Rome (R.L.);and the Clinical Trial Service Unit and Epi-demiological Studies Unit, University ofOxford, Oxford, United Kingdom (C.B.).Address reprint requests to Dr. Patrono atUniversity of Rome La Sapienza, OspedaleSant’Andrea, Via di Grottarossa 1035,00189 Rome, Italy, or at cpatrono@unich.it.N Engl J Med 2005;353:2373-83.Copyright © 2005 Massachusetts Medical Society.therosclerosis, the major cause of ischemic coronary arterydisease and cerebrovascular disease, is a chronic inflammatory disorder inwhich immune mechanisms interact with metabolic risk factors to initiate,propagate, and activate vascular lesions.1 Arterial thrombosis, an acute complicationthat develops on the surface of a ruptured atheromatous plaque or as a consequence ofendothelial erosion,1 may cause myocardial infarction or ischemic stroke. Platelets arekey cellular components of arterial occlusive thrombi and may participate in the devel-opment and progression of atheromatous plaques.2 Platelets are also vital componentsof hemostasis, the physiologic process that arrests hemorrhage after tissue trauma andvascular injury. Although the adhesion and activation of platelets can be viewed as arepair-oriented response to sudden fissuring or rupture of an atheromatous plaque,uncontrolled progression of such a process through a series of self-sustaining amplifi-cation loops may lead to the intraluminal formation of thrombus, vascular occlusion,and transient ischemia or infarction. The ability of platelets to participate in both nor-mal hemostasis and atherothrombosis depends on their adhesive properties and theircapacity to become activated very quickly in response to various stimuli.2Currently available antiplatelet drugs interfere with certain steps in the activationprocess by selectively blocking key platelet enzymes or receptors, reducing the risk ofarterial thrombosis through mechanisms that cannot be dissociated from an increasedrisk of bleeding complications.3 In particular, randomized trials indicate that low-doseaspirin can prevent arterial thrombosis under various circumstances, including firstvascular events among low-risk, healthy subjects and recurrent vascular events amongpatients with known acute or chronic occlusive vascular disease.3The aim of this review is to integrate our current understanding of the molecularmechanism of action of aspirin with the results of clinical trials and epidemiologicstudies of aspirin as an antiplatelet agent, placing special emphasis on the benefits andrisks in various patient populations.
Lingua originaleEnglish
pagine (da-a)2373-2383
Numero di pagine11
RivistaNew England Journal of Medicine
Volume353
DOI
Stato di pubblicazionePubblicato - 2005

Keywords

  • Arteriosclerosis
  • Aspirin
  • Cyclooxygenase 1
  • Cyclooxygenase Inhibitors
  • Drug Interactions
  • Drug Resistance
  • Gastrointestinal Hemorrhage
  • Humans
  • Male
  • Medicine (all)
  • Myocardial Infarction
  • Platelet Aggregation Inhibitors
  • Risk
  • Stroke
  • Thrombosis
  • Thromboxane A2

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