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Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:2489-2493

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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:2489.)
© 2000 American Heart Association, Inc.

Thrombosis

Activation of Clotting Factors XI and IX in Patients With Acute Myocardial Infarction

Presented in part at the XVII Congress of the International Society on Thrombosis and Haemostasis, Washington, DC, August 14–18, 1999.

M. C. Minnema; R. J. G. Peters; R. de Winter; Y. P. T. Lubbers; S. Barzegar; K. A. Bauer; R. D. Rosenberg; C. E. Hack; H. ten Cate

From the Department of Vascular Medicine (M.C.M., H.t.C.) and the Department of Cardiology (R.J.G.P., R.d.W.), Academic Medical Center, Amsterdam, the Netherlands; the Central Laboratory of the Red Cross Blood Transfusion Service (M.C.M., Y.P.T.L., C.E.H.), Laboratory for Clinical and Experimental Immunology, Amsterdam, the Netherlands; the Department of Veterans Affairs Medical Center (S.B., K.A.B.), West Roxbury, Mass; Beth Israel Deaconess Medical Center (R.D.R.), Molecular Medicine Unit, Boston, and the Department of Biology (R.D.R.), MIT, Cambridge, Mass; and the Department of Internal Medicine (H.t.C.), Slotervaart Hospital, Amsterdam, the Netherlands.

Correspondence to Monique C. Minnema, MD, Department of Vascular Medicine, F4-159.2, AMC, Meibergdreef 9, PO Box 22700, 1100 DE Amsterdam, Netherlands. E-mail Jasem{at}wxs.nl

Abstract—In acute coronary events, plaque rupture and the subsequent formation of the catalytic tissue factor–factor VIIa complex is considered to initiate coagulation. It is unknown whether clotting factors XI and IX are activated in acute coronary events. Therefore, we prospectively investigated the activation of clotting factors XI and IX as well as activation of the contact system and the common pathway in 50 patients with acute myocardial infarction (AMI), in 50 patients with unstable angina pectoris (UAP), and in 50 patients with stable angina pectoris (SAP). Factor XIa–C1 inhibitor complexes, which reflect acute activation of factor XI, were detected in 24% of the patients with AMI, 8% of the patients with UAP, and 4% of the patients with SAP (P<0.05), whereas factor XIa–{alpha}1-antitrypsin complexes, which reflect chronic activation, were observed equally in all 3 study groups. Factor IX peptide levels were significantly higher in the patients with AMI and UAP compared with the patients with SAP (P<0.01). No differences regarding markers of the common pathway were demonstrated. Fibrinopeptide A levels were elevated in patients with AMI compared with patients with UAP and those with SAP (P<0.01). Factor XIIa– or kallikrein–C1 inhibitor complexes were not increased. In conclusion, this is the first demonstration of the activation of clotting factors XI and IX in patients with acute coronary syndromes. Because these clotting factors are considered to be important for continuous thrombin generation and clot stability, their activation might have clinical and therapeutic consequences.


Key Words: coagulation • thrombosis • myocardial infarction • cardiovascular disease




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