SEVERITY OF PERIPHERAL ATHEROSCLEROSIS IS ASSOCIATED WITH FIBRINOGEN AND DEGRADATION OF CROSS-LINKED FIBRIN

被引:128
作者
LASSILA, R [1 ]
PELTONEN, S [1 ]
LEPANTALO, M [1 ]
SAARINEN, O [1 ]
KAUHANEN, P [1 ]
MANNINEN, V [1 ]
机构
[1] HELSINKI UNIV, CENT HOSP, DEPT SURG 4, SF-00140 HELSINKI, FINLAND
来源
ARTERIOSCLEROSIS AND THROMBOSIS | 1993年 / 13卷 / 12期
关键词
FIBRINOGEN; FIBRINOPEPTIDE A; THROMBIN-ANTITHROMBIN III COMPLEX; D-DIMER; PERIPHERAL ARTERIAL OCCLUSIVE DISEASE; ATHEROSCLEROSIS;
D O I
10.1161/01.ATV.13.12.1738
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Immunohistochemical studies of human atherosclerotic lesions have demonstrated the occurrence of fibrin deposition and its degradation in the arterial wall. We studied fibrinogen, the generation of thrombin, and the degradation of fibrin in 40 patients with stable peripheral arterial occlusive disease of varying severity, as assessed by the ankle/brachial pressure index and duplex ultrasonography and/or angiography. Circulating fibrinogen (functional and immunological), fibrinopeptide A, thrombin-antithrombin III complex, and D-dimer were measured. The severity of atherosclerosis was associated with both fibrinogen (both functional and immunological) and D-dimer (r=.57, P<.0002, and r=.57, P<.0001, respectively). Fibrinogen and D-dimer showed a significant positive correlation (r=.50, P<.001). Generation of thrombin was detected in 24 patients (60%) by fibrinopeptide A and levels of thrombin-antithrombin III complex. As a sign of coagulation activation and fibrinolysis, we found that thrombin-antithrombin III complex and the degradation of cross-linked fibrin were progressively associated with the extent of vascular disease. The plasmin-mediated fibrin breakdown contributed to increased levels of circulating fibrinogen, an established risk factor for thrombotic complications. The significant correlations between fibrinogen/D-dimer and the severity of atherosclerosis support previous pathological studies and imply that local degradation of cross-linked fibrin is involved in the progression of atherosclerosis.
引用
收藏
页码:1738 / 1742
页数:5
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