How does anticoagulant therapy help in heart failure?

Any cause of relative stasis in a dilated cardiac chamber predisposes to thromboembolic events such as myocardial infarction and stroke. In chronic heart failure, such causes include low cardiac output, poor contractility, abnormal regional wall motion, and atrial fibrillation.

Incidence figures vary widely. In a retrospective study from the Mayo Clinic, Fuster et al reported systemic emboli in 18% of 104 patients with nonischemic dilated cardiomyopathy and an incidence of 3.5 clinically apparent events/100 patient-years. In a prospective study from the Albert Einstein College of Medicine in 264 patients with congestive heart failure, Katz et al reported 1.7 cerebral thromboembolic events per 100 patient-years of follow-up. In a retrospective study from the University of California in Los Angeles, Nat-terson et al found that only 6 of 224 heart transplantation candidates (3%; 3.2/100 patient-years) had an episode of arterial embolization over a mean follow-up of 301 days. In the Vasodilator-Heart Failure Trials (V-HeFT I III), the overall rate of thromboembolism ranged from 2.2 to 2.5/100 patient-years, with no significant difference between ischemic And nonischemic dilated cardiomyopathy. In the Survival And Ventricular Enlargement (SAVE) study, the incidence of stroke was 1.5/100 patient-years. SAVE and V-HeFT patients with an ejection fraction <28% had nearly twice the relative risk of stroke compared with patients with an ejection fraction >28%. A retrospective review from the Studies Of Left Ventricular Dysfunction (SOLVD) has provided the most recent analysis (1998), reporting a similar incidence of thromboembolic events, and the unexpected finding that women are at greater risk than men. In these controlled heart failure studies, the annual risk of stroke was between 1% and 2%, and that of myocardial infarction between

2% and 5.4%. The annual risk of stroke in the Stroke Prevention in Atrial Fibrillation (SPAF) studies (1991-1996) ranged from 3.6% to 4.8%.

Despite the increased risk of thromboembolism in heart failure, there has never been a controlled efficacy and safety study of long-term anticoagulation in this setting. Fuster et al reported systemic emboli in 18% of the patients who did not receive anticoagulants and in none of those who did. Katz et al reported stroke in 9 of their patients, 5 of whom were receiving long-term anticoagulation; however, 3 had a left ventricular thrombus documented by two-dimensional echocardiography, and 1 had atrial fibrillation. Nat-terson et al recorded arterial emboli in 5 of the 142 patients who did not receive warfarin vs in one of the 82 patients who did.

In contrast, V-HeFT I III failed to show protection by anticoagulation: anticoagulated patients had the same or higher rates of thromboembolic events. The SAVE trial found an 81% reduced risk of stroke in anticoagulated patients, but anticoagulant therapy was not randomized, nor was dosage controlled. The SOLVD analysis showed an association between warfarin anticoagulation in left ventricular systolic dysfunction and improved survival and morbidity; the association was independent of age, gender, etiology, functional class, presence or absence of atrial fibrillation, ejection fraction, or use of enalapril. As for safety, major hemorrhage rates in anticoagulated patients in the above studies range from 2.3 to 6.8/100 patient-years, with intracranial bleeding being the most feared event.

Although chronic anticoagulation is clearly indicated in certain subgroups, eg, heart failure patients with a previous thromboembolic event, atrial fibrillation, or newly formed left ventricular thrombus, the literature

provides no convincing evidence that in other subgroups its benefits outweigh the risks: fluctuating metabolic status in heart failure predisposes to bleeding complications; chronically low cardiac output impairs hepatic and renal function; and polymedication tends to interact with warfarin.

Adjusted dose warfarin versus low-intensity, fixed-dose warfarin plus aspirin for high-risk patients with atrial fibrillation:

Stroke Prevention in Atrial Fibrillation III randomised clinical trial. Lancet. 1996;348:633-638.

Al-Khadra AS, Salem DN, Rand WM, Udelson JE, Smith JJ, Konstam MA. Antiplatelet agents and survival: a cohort analysis from the Studies of Left Ventricular Dysfunction (SOLVD) trial. J Am Coll Cardiol. 1998;31:419-425.

Consensus recommendations for the management of chronic heart failure. On behalf of the membership of the advisory council to improve outcomes nationwide in heart failure. Am J Cardiol. 1999:83(2A): 1A-38A. Fuster V, Gersh BJ, Giuliani ER, Tajik AJ, Brandenburg RO, Frye

RL. The natural history of idiopathic dilated cardiomyopathy. Am J Cardiol. 1981;47:525-531.

Katz SD, Marantz PR, Biasucci L, et al. Low incidence of stroke in ambulatory patients with heart failure: a prospective study. Am Heart J. 1993;126:141-146.

Koniaris LS, Goldhaber SZ. Anticoagulation in dilated cardiomyopathy. J Am Coll Cardiol. 1998;31:745-748.

Natterson PD, Stevenson WG, Saxon LA, Middlekauff HR, Stevenson LW. Risk of arterial embolization in 224 patients awaiting cardiac transplantation. Am Heart J. 1995;129:564-570.

Remme WJ, Swed berg 1C Guidelines for diagnosis and treatment of chronic heart failure. Task Force for the Diagnosis and Treatment of Chronic Heart Failure, European Society of Cardiology. Eur Heart J. 2001; 22:1527-1560. Stroke Prevention in Atrial Fibrillation Study. Final results. Circulation. 1991;84:527-539.

Warfarin versus aspirin for prevention of thromboembolism in atrial fibrillation: Stroke Prevention in Atrial Fibrillation II Study. Lancet. 1994;343:687-691.

Keywords

drug; anticoagulant therapy; atrial fibrillation; thromboembolic event; ventricular thrombus; prevention; risk-benefit ratio

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