Hypercoagulability and reduced fibrinolysis in hyperlipidemia: relationship to the metabolic cardiovascular syndrome

Abstract

Hypercholesterolemia is seen as an important risk factor for coronary artery disease (CAD), as the incidence of CAD is strongly correlated with the level of serum cholesterol in epidemiological studies. However, hypercoagulability and reduced fibrinolytic capacity, often seen in survivors of myocardial infarction, are associated with hypertriglyceridemia (possibly concomitant with low levels of high-density lipoprotein cholesterol) and not with increased levels of total or low-density lipoprotein cholesterol. The important role of thrombogenesis in CAD is supported by the fact that initial high levels of plasma fibrinogen, coagulation factor VII (VIIc), and plasminogen activator inhibitor (PAI-1) are all independent risk factors for CAD or recurrent myocardial infarction as found in multivariate analyses of epidemiological studies. Furthermore, high plasma levels of VIIc and PAI-1 are associated with hypertriglyceridemia, reduced glucose tolerance, overweight, and hyperinsulinemia. The contribution of thrombogenic risk factors to the metabolic cardiovascular syndrome (MCVS) is thus established. Diet intervention is preferable for the normalization of hypercoagulability and hypofibrinolysis associated with MCVS. In familial combined hyperlipidemia, however, and especially with concomitant thromboembolic disease, diet alone is often not sufficient, and drug treatment with anticoagulants and/or lipid-lowering drugs may be necessary.