This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Murakami, T. Articles by Takahashi, H. Search for Related Content PubMed PubMed Citation Articles by Murakami, T. Articles by Takahashi, H.

(Arteriosclerosis, Thrombosis, and Vascular Biology. 1995;15:1107-1113.)
© 1995 American Heart Association, Inc.

Articles

Evaluation of Factor XIa–₁-Antitrypsin in Plasma, a Contact Phase–Activated Coagulation Factor–Inhibitor Complex, in Patients With Coronary Artery Disease

Takashi Murakami; Yutaka Komiyama; Midori Masuda; Masahiro Karakawa; Toshiji Iwasaka; Hakuo Takahashi

From the Departments of Clinical Sciences and Laboratory Medicine (T.M., Y.K., M.M., H.T.) and Second Internal Medicine (M.K., T.I.), Kansai Medical University, Osaka, Japan.

Correspondence to Takashi Murakami, MD, Department of Clinical Sciences and Laboratory Medicine, Kansai Medical University, 10-15 Fumizonocho, Moriguchi, Osaka 570, Japan.

Abstract Excess activated factor XI (FXIa) in plasma indicates increased activation during the contact phase of blood coagulation. To investigate the relationship between such elevations and coronary atherosclerosis, we examined FXIa values in patients with coronary artery disease (CAD) by an enzyme-linked immunorsorbent assay method that we developed that detects FXIa in plasma samples as an FXIa–₁-antitrypsin complex (FXIa-₁AT). The presence and extent of CAD were documented by coronary angiography and assessed by a recently developed scoring system for semiquantitative estimation of coronary atherosclerosis. Plasma FXIa-₁AT levels were significantly increased in patients with angiographically proven CAD (13.9±3.0 µg/L, n=42) compared with age-matched, healthy control subjects (11.9±1.7 µg/L, n=20) as well as patients with angiographically normal coronary arteries (12.0±2.3 µg/L, n=25). Moreover, in the total patient population, the FXIa-₁AT level was related to the number of significant coronary artery stenoses as well as to the total coronary score. FXIa-₁AT showed a positive correlation with thrombin–antithrombin III complex, fibrinogen, and Lp(a) and an inverse correlation with apo A-I, as determined by multivariate analysis. Our studies provide evidence that increased activation of the contact pathway occurs in patients with CAD and is related to the severity of the disease. Although it is unknown whether this abnormality is the cause or the result of the vascular lesion, it may be important for progression of the underlying atherosclerosis or for propagation of the atherosclerotic process itself.

Key Words: factor XI • activated coagulation factor–inhibitor complex • hypercoagulability • coronary artery disease

This article has been cited by other articles:

				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, and H. t. Cate Activation of Clotting Factors XI and IX in Patients With Acute Myocardial Infarction Arterioscler. Thromb. Vasc. Biol., November 1, 2000; 20(11): 2489 - 2493. [Abstract] [Full Text] [PDF]

				M. C. Minnema, M. E. Wittekoek, N. Schoonenboom, J. J. P. Kastelein, C. E. Hack, and H. t. Cate Activation of the Contact System of Coagulation Does Not Contribute to the Hemostatic Imbalance in Hypertriglyceridemia Arterioscler. Thromb. Vasc. Biol., October 1, 1999; 19(10): 2548 - 2553. [Abstract] [Full Text] [PDF]