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(Circulation. 1971;43:538.)
© 1971 American Heart Association, Inc.

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Changes in the Hemostatic Mechanism After Myocardial Infarction

PAUL B. GOLDENFARB M.D.¹; MARY H. CATHEY B.S., M.T., (A.S.C.P.)¹; STANLEY ZUCKER M.D.¹; PATRICIA WILBER M.D.¹; JAMES J. CORRIGAN JR. M.D.¹

¹ From the Hematology Unit, Laboratory Division, Center for Disease Control, Health Services and Mental Health Administration, Public Health Service, U. S. Department of Health, Education, and Welfare, Atlanta, Georgia, and the Departments of Medicine and Pediatrics, Emory University School of Medicine, Atlanta, Georgia.

Plasma coagulation factors, adenosine diphosphate-induced platelet aggregation, and fibrinolytic activity were studied in male survivors of myocardial infarction and in healthy normal men. Infarction survivors had significant elevations of factors VIII and X and of adenosine diphosphate-induced platelet aggregation. The fibrinolytic system was altered toward reduced plasminogen activation, increased antiurokinase activity, and elevated antiplasmin activity. These findings suggest that some men with prior myocardial infarction have a heightened tendency to thrombogenesis. This tendency may represent a response to previous cardiac insult or may contribute to its pathogenesis.

Key Words: Myocardial infarction • Fibrinolysis • Platelet aggregation • Hypercoagulability • Thrombogenesis • Hemostasis, alterations in • Blood coagulation

Submitted on September 16, 1970
Accepted on December 17, 1970

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