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(Circulation. 2002;106:1748.)
© 2002 American Heart Association, Inc.

Editorial

Acute Pulmonary Embolism

Don’t Ignore the Platelet

Piotr Sobieszczyk, MD; Michael C. Fishbein, MD; Samuel Z. Goldhaber, MD

From the Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (P.S., S.Z.G.); and the Department of Pathology and Laboratory Medicine, UCLA Medical Center, Los Angeles, Calif (M.C.F.).

Correspondence to Samuel Z. Goldhaber, MD, Cardiovascular Division, Department of Medicine, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115. E-mail sgoldhaber@partners.org

Key Words: Editorials • platelets • embolism • thrombosis • pulmonary heart disease

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Acute pulmonary embolism (PE) remains a dreaded and frequent cardiovascular emergency, with an estimated annual incidence of almost 200 000 cases in the United States alone.¹ Despite therapeutic advances, ² the International Cooperative Embolism Registry of 2454 patients³ reported a surprisingly high 90-day all-cause mortality of 17.4%. The cause of death in 45% of patients was PE itself. Recurrent PE, fatal or nonfatal, occurred in 8% of patients within 90 days. It is clear that a novel therapeutic pharmacological strategy with a safe and easy-to-administer agent is needed to reduce adverse outcomes from this common illness. Clinical and experimental evidence suggests that antiplatelet agents, usually overlooked in the treatment of PE, may fulfill this role by preventing the initiation and propagation of the venous thrombus and by minimizing the adverse physiological consequences of PE.

Venous thrombosis has been traditionally associated with red blood cell and fibrin-rich "red clot," whereas arterial thrombi superimposed on atherosclerotic lesions are rich in platelets, giving the appearance of "white clot." This simple but somewhat dogmatic concept has had important therapeutic implications: "red clot" has been traditionally treated with heparin and warfarin, while platelet inhibition has been utilized for acute coronary syndromes caused by "white clot." However, careful morphological analysis of thrombi formed in veins reveals tangled pale strands of aggregated platelets and fibrin within the mass of red blood cells.⁴ Experimentally induced venous thrombus in the presence of radiolabeled platelets shows early platelet accumulation at the "head" of the venous thrombus.^5,6 As the thrombi age, acquisition . . . [Full Text of this Article]

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