SummaryWe investigated the vessel status of coronary and peripheral arteries and those arteries supplying the brain in 929 consecutive male patients admitted to a coronary rehabilitation unit. The severity of coronary atherosclerosis was scored using coronary angiography. Changes in extracranial brain vessels and manifest cerebrovascular disease (CVD) were determined by B-mode ultrasound and Doppler examination. Peripheral arterial disease (PAD) was diagnosed using base-line and stress oscillography. We assessed variables of coagulation, fibrinolysis, and the acute phase response.There was a significant increase in plasma fibrinogen, plasminogen, d-dimer and C-reactive protein (CRP) with increasing severity of coronary heart disease. Compared to men with unaffected arteries, men with 3 diseased coronary arteries had 58% greater d-dimer concentrations. Patients with CVD and PAD, respectively, also had significantly higher fibrinogen, d-dimer and CRP concentrations. We did not find an association between plasminogen activator inhibitor activity and the severity of coronary atherosclerosis.In conclusion, plasma fibrinogen, d-dimer and CRP concentrations were significantly related to atherosclerosis in the coronary, peripheral and extracranial brain arteries.

Previous studies have identified moderately elevated plasma concentrations of homocyst(e)ine as an independent risk factor for coronary heart disease (CHD). The atherogenicity of homocyst(e)ine has mostly been attributed to its effects on endothelial cells, platelets, and the hemostatic system. In this case-control study of 199 male CHD patients and 156 age-matched control subjects, we analyzed the role of homocyst(e)ine as a cardiovascular risk marker in the context of traditional risk factors as well as of plasma fibrinogen, plasminogen, and viscosity. Both univariate and multivariate regression analyses revealed that homocyst(e)ine levels were significantly correlated with age, fibrinogen, and plasma viscosity in both study groups. Geometric mean homocyst(e)ine levels by univariate analysis were significantly higher in patients than in control subjects (8.9 versus 7.8 ^mol/L, f<.001). This difference re-H omocysteine is a sulfhydryl-containing amino acid formed by demethylation of methionine. It is catabolized to cysteine by the pyridoxal phosphate-dependent enzymes cystathionine /3-synthase and •y-cystathionase. It is also remethylated to methionine through folate-and vitamin B 12 -dependent enzymes and from demethylation of betaine.1 -2 Oxidation of homocysteine forms homocysteine disulfide (homocysteine), or homocysteine-cysteine mixed disulfide. The free and protein-bound forms are here referred to as homocyst(e)ine, since our method measures both homocysteine and its oxidation products. -4Genetic defects in cystathionine /3-synthase or tetrahydrofolate reductase interfere with the transsulfuration or remethylation of homocysteine and are involved in the pathogenesis of homocystinuria. This rare disease is associated with dramatically increased homocyst(e)ine plasma concentrations and premature arteriosclerosis.1 Furthermore, several case-control studies as well as one nested study have established that moderately elevated homocys- mained significant on multiple logistic function analysis after being adjusted for body mass index, systolic blood pressure, serum cholesterol, and high-density lipoprotein cholesterol but not after additional adjustment for fibrinogen. By contrast, geometric mean fibrinogen levels after adjustment for homocyst(e)ine levels were significantly different between patients and control subjects (296.4 versus 230.8 mg/dL, P<.001). Within the group of CHD patients, both fibrinogen and homocyst(e)ine significantly increased in parallel with the number of stenosed coronary vessels. We conclude that hyperhomocyst(e)inemia is an independent coronary risk factor and that its interrelation with fibrinogen levels merits further study. (Arteriosder Thromb. 1994;14:4

No abstract

Abstract-Several studies have indicated that plasma viscosity contributes to cardiovascular risk in men. So far, a significant relationship between plasma viscosity and the severity of coronary heart disease has not been found. Thus, the present study is the first to report on the relationship of plasma viscosity and the severity of coronary heart disease. In a collective of 1142 male myocardial infarction patients, plasma viscosity and additional laboratory parameters were determined. Atherosclerotic changes were quantified by coronary angiography. Patients were divided into groups without any, and with one to three stenosed vessels. We found a positive relationship between plasma viscosity and the severity of coronary heart disease, even after adjusting groups for age, fibrinogen, and use of diuretics. Mean plasma viscosity ranged from 1.141Ϯ0.035 mPa s in patients without stenosed vessels to 1.162Ϯ0.044 mPa s in patients who had three coronary vessels with stenoses Ͼ50%. Differences between the groups were significant (PϽ0.001 to 0.05), with two exceptions: differences between patients without any and with one stenosed vessel, as well as between patients with one and two stenosed vessels, did not reach the significance level. On the whole, we can give further support to the hypothesis that cardiovascular risk factors and coronary heart disease may be linked by plasma viscosity.(Arterioscler Thromb Vasc Biol. 1998;18:870-875.)Key Words: coronary heart disease Ⅲ myocardial infarction Ⅲ coronary risk factor Ⅲ blood rheology Ⅲ fibrinogen I n the prospective Caerphilly and Speedwell studies, as well as in the MONICA project, plasma viscosity was indicated as a predictive risk factor for CHD. 1,2 In other studies, high plasma viscosity was shown to lead to an increased risk of acute MI in patients with unstable angina pectoris. 3,4 Furthermore, a relationship of an early increase in plasma viscosity during acute MI and reinfarction or death was shown. 5 An elevation of plasma viscosity was found in patients with severe unstable angina pectoris compared with patients with stable angina pectoris and to healthy individuals. 6-8 Additionally, an elevated plasma viscosity in patients with stable angina pectoris, 9 even without coronary artery stenosis at angiography, 10 could be demonstrated. In the MONICA project, geographical differences in plasma viscosity between populations differing in the CHD event rates were found. 11 Evidently, plasma viscosity contributes to the cardiovascular risk and may be of special importance in areas of reduced blood flow, as commonly occurs in patients with advanced atherosclerosis. 12 Lowe et al 13 suggested that blood viscosity is related to the extension of CHD. The study that proposed this suggestion, however, consisted only of a small group of patients, and therefore the results require further investigation. Moreover, in this study, plasma viscosity was not significantly elevated in patients with extensive CHD compared with a control group and to patients with less severe CHD. Thu...