It is well-recognized that patients with congestive heart failure are at an
increased risk of stroke and venous thromboembolism. Nevertheless, stroke,
thromboembolism and myocardial infarction have generally been regarded to
be end points of secondary importance in large heart failure trials, when c
ompared with mortality or hospital readmissions. It may well have been that
the incidence of thrombotic events are underestimated. The problem of thro
mbus formation (thrombogenesis) in heart failure may therefore: be a much m
ore significant problem than is currently recognized.
The pathophysiology of thrombogenesis in heart failure could well be explai
ned in the context of Virchow's original triad. In addition to "abnormal fl
ow" through low cardiac output, dilated cardiac chambers and poor contracti
lity, patients with heart failure also demonstrate abnormalities of hemosta
sis and platelets (that is "abnormal blood constituents") and endothelial d
ysfunction ("vessel wail abnormalities"). These abnormalities contribute to
a prothrombotic or hypercoagulable state, which increases the risk of thro
mbosis in heart failure and impaired left ventricular systolic function.
Some observational data are available on the role of anticoagulants in hear
t failure, and there is sound evidence to support the use of antithrombotic
therapy in patients with heart failure and atrial fibrillation. However, t
here are no large-scale prospective randomized controlled trials of antithr
ombotic therapy in patients with heart failure who remain in sinus rhythm a
lthough important studies are in progress. Although the results of these st
udies are awaited, measurement of suitable markers of thrombogenesis might
prove to be valuable in identifying "high risk" patients and in determining
the nature, duration and intensity of such treatment. Further information
is also needed on the predictive value of various markers of hypercoagulabi
lity in patients with heart failure, the association between hemostatic var
iables and the severity of heart failure, and the effects of different trea
tments. (C) 1999 by the American College of Cardiology.