Does heart failure confer a hypercoagulable state? Virchow's triad revisited.
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 compared with mortality or hospital readmissions. It may well have been that the incidence of thrombotic events are underestimated. The problem of thrombus formation (thrombogenesis) in heart failure may therefore be a much more significant problem than is currently recognized. The pathophysiology of thrombogenesis in heart failure could well be explained in the context of Virchow's original triad. In addition to "abnormal flow" through low cardiac output, dilated cardiac chambers and poor contractility, patients with heart failure also demonstrate abnormalities of hemostasis and platelets (that is "abnormal blood constituents") and endothelial dysfunction ("vessel wall abnormalities"). These abnormalities contribute to a prothrombotic or hypercoagulable state, which increases the risk of thrombosis in heart failure and impaired left ventricular systolic function. Some observational data are available on the role of anticoagulants in heart failure, and there is sound evidence to support the use of antithrombotic therapy in patients with heart failure and atrial fibrillation. However, there are no large-scale prospective randomized controlled trials of antithrombotic therapy in patients with heart failure who remain in sinus rhythm, although important studies are in progress. Although the results of these studies 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 hypercoagulability in patients with heart failure, the association between hemostatic variables and the severity of heart failure, and the effects of different treatments.
Lip
G Y
GY
University Department of Medicine, City Hospital, Birmingham, United Kingdom.G.Y.H.LIP@bham.ac.uk
Gibbs
C R
CR
D000925:Anticoagulants / Q000627:therapeutic use; D001777:Blood Coagulation / Q000502:physiology*; D001779:Blood Coagulation Factors / Q000378:metabolism*; D018450:Disease Progression; D006333:Heart Failure / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D009200:Myocardial Contraction; D011379:Prognosis; D012307:Risk Factors; D013923:Thromboembolism / Q000097:blood / Q000209:etiology* / Q000517:prevention & control
D000925:Anticoagulants; D001779:Blood Coagulation Factors