Thrombotic Complications in Heart Failure
An Underappreciated Challenge
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Advances in pharmacologic and device therapy have greatly improved prognosis in patients with systolic heart failure. Despite this, congestive heart failure still bears a very grim prognosis, particularly in patients with more advanced stages of the disease, who are so frequently seen on hospital wards.
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Which pathogenic pathways may need to be addressed to improve prognosis in heart failure? The current treatment of this condition is primarily focused on performance of the heart itself and aims to inhibit unfavorable cardiac remodeling (eg, amelioration of impact of activated catecholamine and renin-angiotensin-aldosterone systems), optimization of cardiac hemodynamics (eg, cardiac resynchronization therapy), and prevention of life-threatening arrhythmia (eg, insertion of implantable defibrillators). However, accumulating evidence suggests that thrombotic complications may play a major role in morbidity and outcomes in patients with heart failure, especially as the cardiac targets (largely neurohumoral) are being better managed.
The 2 major thrombotic sources in heart failure are related to atrial fibrillation (AF) and venous thromboembolism (VTE). Although oral anticoagulation in heart failure with known AF is well established and highly successful, the role of oral anticoagulation in heart failure without documented AF is controversial and is not recommended for routine use at present.
Heart failure is undoubtedly associated with a significant prothrombotic shift, which predisposes to thrombi formation both within cardiac chambers (particularly in AF) and blood vessels. Endothelial damage/dysfunction is a hallmark of heart failure irrespective of any cause.1 It has been related to severity of heart failure, and its presence is consistently linked to poor prognosis. Although most studies have focused on arterial endothelial dysfunction, venous dysfunction is also present in heart failure, and it is likely to contribute to the prothrombotic state seen in this condition. Blood stasis in edematous legs with a background of poor mobility and increased …