Heart Failure and Wide QRS: Clinical and Pharmacological Perspectives

Abstract

Heart failure (HF) is a highly prevalent cardiovascular clinical syndrome. Health care spending on HF treatment is high. Therefore, its treatment has generated a great deal of interest in pharmacological research in recent years. Recent guidelines have introduced several molecules for the treatment of HF that have demonstrated safety, and above all, efficacy. One of the worst aspects of HF is ventricular dyssynchrony (VD) with a wide QRS interval. Currently, the cornerstone of VD therapy is cardiac resynchronization therapy (CRT). Our comprehensive review aims to analyze the effects of new molecules on QRS width and understand whether these molecules can provide benefits.

Keywords: QRS widening; cardiac remodeling; dapagliflozin; empagliflozin; heart failure; sacubitril/valsartan; ventricular dyssynchrony; vericiguat.

Figure 1

The five pillars of therapy for the pharmacological treatment of chronic heart failure. ACEi: angiotensin-converting enzyme inhibitors; ARBs: angiotensin-receptor blockers; ARNI: angiotensin receptor neprilysin inhibitor; MRA: mineralocorticoid receptor antagonist; SGLT2i: sodium glucose co-transporter 2 inhibitors.

Figure 2

Pathophysiology of intraventricular conduction delay in heart failure. ANS: autonomic nervous system; HF: heart failure; LV: left ventricle; MR: mitral regurgitation; RV: right ventricle; ↑: increase; ↓: decrease.