Congestive heart failure and Virchow's triad: a neglected association.
Congestive heart failure (CHF) is associated with significant morbidity and mortality. In particular, patients with CHF have a high risk of venous thromboembolism and stroke, as well as recurrent ischaemia and infarction. However, in large heart failure trials, such thrombotic complications have often been regarded as less important end points than total mortality or readmission to hospital. In addition, a high proportion of mortality in CHF is due to sudden cardiac death (SCD). Although it was long thought that SCD was due to malignant arrhythmias, current evidence suggests that thrombosis also has a significant part to play. Thrombosis in CHF may therefore be a much more significant problem than is generally appreciated. CHF is associated with abnormalities of flow (low cardiac output, dilated cardiac chambers), vessel wall (endothelial dysfunction), and abnormalities of blood constituents (abnormalities of platelets and haemorrheology). Thus it fulfills all of Virchow's triad of characteristics of a prothrombotic state. In view of these findings, antithrombotic therapy ought to provide a substantial morbidity and mortality benefit to patients with CHF. However, current data is conflicting, and comes from non-randomised, retrospective analyses of major heart failure trials, and a few randomised trials of anticoagulants in CHF that are more than 50 years old. Prospective trials of warfarin and antiplatelet agents in CHF are in progress. Measures to identify patients at highest risk of thrombosis may help to guide treatment. Further study into the relationships between such markers and the severity of heart failure, the value of such markers in predicting thrombotic complications in CHF, and the effect of treatments, is therefore needed.
Sosin
Michael D
MD
Haemostasis, Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK.
Bhatia
Gurbir
G
Davis
Russell C
RC
Lip
Gregory Y
GY
D000925:Anticoagulants / Q000627:therapeutic use; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology*; D016757:Death, Sudden, Cardiac / Q000209:etiology / Q000517:prevention & control; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology*; D006801:Humans; D020766:Intracranial Embolism / Q000188:drug therapy / Q000503:physiopathology*; D010974:Platelet Aggregation / Q000187:drug effects / Q000502:physiology*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D016032:Randomized Controlled Trials as Topic; D020246:Venous Thrombosis / Q000188:drug therapy / Q000503:physiopathology*
D000925:Anticoagulants; D005343:Fibrinolytic Agents; D010975:Platelet Aggregation Inhibitors