Contemporary management of ventricular arrhythmias in heart failure

Abstract

Enhanced ventricular arrhythmogenesis is commonly experienced by patients in the end-stage of heart failure spectrum. A high burden of ventricular arrhythmias can affect the ventricular systolic function, lead to unexpected hospitalizations and further deteriorate the prognosis. Management of ventricular arrhythmias in this population is challenging. Implantable cardioverter-defibrillators are protective for the immediate termination of life-threatening arrhythmias but they have no impact in reducing the arrhythmic burden. Combination treatment with invasive (catheter ablation, mechanical hemodynamic support, sympathetic denervation) and noninvasive (antiarrhythmic drugs, medical therapy for heart failure, programming of implantable devices) therapies is commonly required. The aim of this review is to present the available therapeutic options, with main focus on recently published data for catheter ablation and provide a stepwise treatment approach.

Keywords: ICD programming; Ventricular arrhythmias; severe heart failure; ventricular tachycardia ablation.

Figure 1

Arrhythmogenesis in heart failure is multifactorial. Early repolarization is affected by the downregulation of the I_to1 current leading to prolonged action potential duration. Cellular repolarization is additionally impaired by downregulation of genes encoding the inward rectifier potassium current I_K1. Early and delayed afterdepolarizations are triggered by defective calcium and potassium homeostasis. Repolarization changes do not equally affect all myocardial layers leading to transmural heterogeneity. I_na: sodium current, I_to1: transient outward potassium current, I_ca: calcium current through L-type calcium channels, I_ks: delayed rectifier potassium channel (slow), I_kr: rapid delayed rectifier potassium channel, I_k1: inwardly rectifying potassium channel, CaMKII: calcium/calmodulin-dependent protein kinase II, APD: action potential duration, EADs: early afterdepolarizations, DADs: delayed afterdepolarizations.

Figure 2

Combined epicardial (A) and endocardial (B) substrate modification in a patient with non-ischemic cardiomyopathy and electrical storm.

Figure 3

Optimal strategy for antitachycardia pacing (ATP) programming. T-CL: tachycardia cycle length, CL: cycle length.

Figure 4

Management of electrical storm in severe heart failure. S-HF: severe heart failure, AADs: Antiarrhythmic drugs, VT: ventricular tachycardia, ATP: antitachycardia pacing, LV: left ventricle, CRT-D: cardiac resychronization therapy-defibrillator, MHS: mechanical hemodynamic support, IABP: intra-aortic balloon pump, ECMO: extracorporeal membrane oxygenation, LVAD: left ventricular assist device, biVAD: biventricular assist device.