A look back: the quest for thrombosis in heart failure continues after COMMANDER HF

Heart failure (HF) has been associated with an increased incidence of thromboembolic events, while many HF deaths have been thought to be of thrombotic aetiology.1 In terms of pathophysiology, HF bears several prothrombotic features. The deceleration of peripheral and intracardiac blood flow due to peripheral congestion and impaired cardiac contractility, respectively, the prolonged bed rest in severely ill cases, the associated endothelial dysfunction, the increased risk for atrial fibrillation (AF) due to structural and electrical atrial remodelling in the presence of elevated atrial pressures due to left ventricular dysfunction, and the presence of coagulation defects as, for example, in the case of ventricular assist devices are only some of the potential thrombophilic mechanisms in HF.2,3 At the molecular level, endothelial dysfunction with impaired vascular but also platelet response to nitric oxide (NO) has been observed in HF patients with either reduced or preserved ejection fraction, leading to impaired vascular tone and increased platelet aggregation, respectively.4 Impaired NO response seems to result in turn from NO scavenging and reduced activity of soluble guanylate cyclase (sGC), the principal NO sensor.5 In this complex association, HF may be the cause of the prothrombotic state but also the result of common pathogenetic pathways leading to both conditions.

Source: Cardiovascular Research - October 22, 2019 Category: Cardiology Source Type: research