Metabolic syndrome (MetS) is associated with increased risk of both atherothrombotic cardiovascular events
and venous thromboembolism. The pro-thrombotic potential of MetS, may explain this association. In this review we discuss
the relationship of MetS with hemostasis focusing on endothelial function, platelet activity, coagulation, fibrinolysis
and hemorheologic markers. Endothelial-dependent vasodilatation is impaired in MetS. This is mostly mediated by a reduced
expression of vasodilators (nitric oxide and prostacyclin) with a concomitant increase of vasoconstrictors (endothelin-
1, angiotensin II and thromboxane A2). Platelet activity is enhanced in MetS. A cross-talk between activated endothelium
and platelets results in a pro-thrombotic vicious cycle. Enhanced coagulation together with impaired fibrinolysis
is also present in MetS. This is mirrored by high fibrinogen and plasminogen activator inhibitor-1 levels. Endothelial dysfunction,
expressed by high von Willebrand factor and tissue plasminogen factor levels, also contributes to this abnormality.
Whole blood and plasma viscosity is increased in MetS.
Lifestyle intervention can improve the MetS-related pro-thrombotic state. These measures include weight reduction and
improved composition of the diet. A Mediterranean-style diet rich in olive oil, as a source of monounsaturated fat, and low
saturated fat consumption may also be beneficial.
Keywords: Metabolic syndrome, hemostasis, endothelium, platelet, coagulation, fibrinolysis, viscosity.
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