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Hemostatic and rheological variables and risk of cardiovascular disease
Gordon D O Lowe1, Ann Rumley, Peter H Whincup
1University Department of Medicine, Royal Infirmary, Glasgow, United Kingdom. gdl1j@clinmed.ac.uk
Increasing blood levels of hemostatic variables may increase the risk of thrombosis, while increasing levels of rheological variables which reduce blood flow may increase the risk of ischemic events. Systematic reviews of prospective cohort studies of hemostatic and rheological variables suggest that increasing blood levels of fibrinogen, von Willebrand factor, tissue plasminogen activator antigen, fibrin D-dimer, hematocrit, viscosity, and erythrocyte sedimentation rate may be predictors of risk of coronary heart disease (CHD), but their causal relevance is unknown. At present, data for the associations of other hemostatic variables with CHD, and for the associations of hemostatic variables with stroke, venous thromboembolism, and mortality, is relatively sparse and inconclusive. More detailed syntheses of existing prospective data (such as the Fibrinogen Studies Collaboration), observational studies of CHD and the genetic determinants of these plasma components, as well as large-scale randomized trials should help to determine whether or not these associations are (1) useful in prediction of cardiovascular risk and/or (2) of causal significance.
Increasing blood levels of hemostatic variables may increase the risk of thrombosis, while increasing levels of rheological variables which reduce blood flow may increase the risk of ischemic events. Systematic reviews of prospective cohort studies of hemostatic and rheological variables suggest that increasing blood levels of fibrinogen, von Willebrand factor, tissue plasminogen activator antigen, fibrin D-dimer, hematocrit, viscosity, and erythrocyte sedimentation rate may be predictors of risk of coronary heart disease (CHD), but their causal relevance is unknown. At present, data for the associations of other hemostatic variables with CHD, and for the associations of hemostatic variables with stroke, venous thromboembolism, and mortality, is relatively sparse and inconclusive. More detailed syntheses of existing prospective data (such as the Fibrinogen Studies Collaboration), observational studies of CHD and the genetic determinants of these plasma components, as well as large-scale randomized trials should help to determine whether or not these associations are (1) useful in prediction of cardiovascular risk and/or (2) of causal significance.
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