ASSOCIATION OF PLASMA-FIBRINOGEN LEVELS WITH CORONARY-ARTERY DISEASE,SMOKING AND INFLAMMATORY MARKERS

Citation
Mpm. Demaat et al., ASSOCIATION OF PLASMA-FIBRINOGEN LEVELS WITH CORONARY-ARTERY DISEASE,SMOKING AND INFLAMMATORY MARKERS, Atherosclerosis, 121(2), 1996, pp. 185-191
Citations number
31
Categorie Soggetti
Cardiac & Cardiovascular System","Peripheal Vascular Diseas
Journal title
ISSN journal
00219150
Volume
121
Issue
2
Year of publication
1996
Pages
185 - 191
Database
ISI
SICI code
0021-9150(1996)121:2<185:AOPLWC>2.0.ZU;2-G
Abstract
The plasma level of fibrinogen is associated with the risk of ischaemi c heart disease (IHD) and the severity of atherosclerosis. It has been suggested that an increased plasma level of fibrinogen is a coronary risk indicator because it reflects the inflammatory condition of the v ascular wall. An inflamed vascular wall may increase the production of the cytokines interleukin 6 (IL6), interleukin 1 beta (IL1 beta), and tumour necrosis factor alpha (TNF alpha), which have a major role in the regulation of synthesis in the liver of acute phase proteins, incl uding fibrinogen. Smoking has also been reported to increase the level s of fibrinogen and C-reactive protein (CRP). This may indicate that s moking induces an inflammatory reaction, probably of the pulmonary bro nchi and alveolae. Therefore, we anticipated that with both types of i nflammation the levels of acute phase proteins and cytokines would be related. We have investigated the contribution of inflammation to the plasma levels of fibrinogen in 34 patients with severe coronary artery disease (CAD) and 30 healthy controls comparable for age and smoking habits. We did not find a parallel in the effects of smoking and ischa emic heart disease on the plasma levels of fibrinogen, CRP, IL6, IL1 b eta and TNF alpha. Cardiovascular disease had its most important effec t on the plasma fibrinogen level, while smoking appeared to increase t he CRP. levels, while both CAD and smoking seemed to affect the IL6 le vels. Our results indicate that both smoking and CAD induce an inflamm atory condition but that the increase of plasma levels of different in flammatory markers is complex. Although the acute phase reaction is th e main regulatory mechanism of fibrinogen, the increase of fibrinogen in our group of CAD patients could not be fully explained by increased inflammation.