Therapeutic interventions to lower plasma fibrinogen concentration

Abstract

A causal link between plasma fibrinogen levels and the risk of cardiovascular disease is now reasonably well established. Therefore the therapeutic lowering of fibrinogen has become a relevant area of research. Several options to achieve this aim have been reported in the literature. Changes in lifestyle can affect the fibrinogen level, of which smoking cessation is by far the most effective; weight or stress reduction or an increase in regular physical activity may have less pronounced effects; dietary changes appear to have even less effect, though a regular, moderate alcohol consumption may result in a small reduction. Many oral drugs have been shown to lower fibrinogen; however, the data should be viewed critically. In particular, the clinical situation in which a drug is administered must be considered and risk:benefit analyses should be performed before a drug is recommended for this indication. Among the oral fibrinogen-lowering drugs, fibrates rank first (e.g. bezafibrate has been reported to reduce increased fibrinogen by as much as 40%, and ticlopidine can induce a reduction of about 15% if fibrinogen was elevated at baseline). Whether concentration within the normal range can be altered by oral medication is less clear. Finally (and obviously), intravenous fibrinolytic agents or heparin-induced extracorporeal low-density lipoprotein precipitation will lower fibrinogen dramatically; yet these procedures are rarely indicated for this purpose alone. All options to lower fibrinogen also have prominent effects on other cardiovascular functions; thus, an intervention trial may not be the most appropriate method of testing the validity of the hypothesis of fibrinogen as a cardiovascular risk factor.

Lifestyle and Hemostatic Risk Factors for Ischemic Heart Disease

“…Increasing body mass index was also associated with increasing levels of fibrinogen and plasma viscosity, consistent with the literature, 4,6,16,39,40,42 although, overall, there is little evidence that weight reduction reduces fibrinogen or viscosity levels. 42 Interestingly, body mass index was associated with total (nephelometrically assayed) fibrinogen rather than clottable fibrinogen (Table 6), which may be relevant to our finding that the former assay was a better predictor of incident IHD than the latter in this cohort. 8 Many cohort studies indicate that physical activity, particularly during leisure time, is a protective lifestyle activity against IHD, even in moderate doses.…”

“…Likewise, the association between fibrinogen and physical activity was no longer statistically significant after adjustment for smoking and social class in the Scottish Heart Health Study. 44 In combination with the conflicting data from intervention studies, 42 a causal association between leisure activity and fibrinogen remains to be proven by further studies. We observed no significant independent association of leisure activity with tPA or PAI-1 levels, which again is consistent with data from intervention studies.…”

Assessment of the 10-year risk of cardiovascular events among a group of Sub-Saharan African post-menopausal women

“…Regular physical activity reduces the risk of CHD, stroke, diabetes, and breast and colon cancers [2]. Specifically, physical activity is associated with beneficial changes in circulating lipids and lipoproteins [24,25], body weight, blood pressure, insulin sensitivity [26], and coagulation parameters [27,28]. There is overwhelming evidence of an association between regular physical training and lowering of plasma TG, TC and LDL-C concentrations, and an increase in the plasma HDL-C titers, hence a significant reduction in CVR [24,29,30].…”

Plasma haemostatic markers, endothelial function and ambulatory blood pressure changes with home versus hospital cardiac rehabilitation: the Birmingham Rehabilitation Uptake Maximisation Study

“…41 Conversely, improvements of these risk factors have been associated with a lower prothrombotic tendency. [42][43][44][45] Despite this, the precise mechanism(s) by which the package of programmed cardiac rehabilitation (with all its individual components) can improve haemostatic profile in patients with CHD are unclear.…”