In patients with excessive venous thrombosis, genetic defects predisposing
to thrombosis can be found in 60-80%. Increased plasma levels of coagulatio
n proteins such as fibrinogen and plasminogen activator inhibitor-1 (PAI-1)
are associated with an increased risk of myocardial infarction. However, d
espite the presence of polymorphisms that regulate plasma levels of factor
VIII, PAI-1, and fibrinogen the association between common polymorphisms of
these coagulation protein and ischemic cardiac disease remains ambiguous.
Up to 10% of the population have defects that predispose them to excessive
venous thrombosis. In spite of the essential role of thrombosis in coronary
ischemic syndrome, no convincing evidence has implicated the two most comm
on venous hypercoagulable states in ischemic heart disease. Pathogenic poly
morphisms in the platelet fibrinogen and collagen receptors remain an area
of intense research interest. Finally, it has been shown that lipoproteins
can act as mediators Of coagulation processes. Curr Opin Lipidol 10:443-448
. (C) 1999 Lippincott Williams & Wilkins.