Elsevier

Progress in Cardiovascular Diseases

Volume 66, May–June 2021, Pages 17-27
Progress in Cardiovascular Diseases

Clinical and translational insights on premature ventricular contractions and PVC-induced cardiomyopathy

https://doi.org/10.1016/j.pcad.2021.04.001Get rights and content

Abstract

The medical community's understanding of the consequences of premature ventricular contractions (PVCs) and PVC-induced cardiomyopathy has been derived mostly from observational and large population-based studies. Due to the difficulty of predicting the development of PVC-cardiomyopathy, the acute and chronic cardiac effects of PVCs and the mechanism of PVC-cardiomyopathy have been derived from pre-clinical studies with large animal models. Recently, these studies have described myocardial substrates that could potentially increase morbidity and mortality in patients with frequent PVCs and PVC-cardiomyopathy. In this paper, we provide an up-to-date comprehensive review of these pre-clinical and clinical studies.

Introduction

Premature ventricular contractions (PVCs) are frequently encountered in clinical practice. Clinical and translational studies have shown that frequent PVCs are associated with an increased risk of cardiomyopathy and heart failure (HF), ventricular arrhythmias (VAs), mortality, and sudden cardiac death (SCD).1, 2, 3, 4, 5, 6, 7, 8, 9 It was not until 2016 that PVC-cardiomyopathy was widely recognized as a unique cause of dilated cardiomyopathy.10 PVC-cardiomyopathy is defined as reversible left ventricular (LV) systolic dysfunction caused by frequent PVCs. The diagnosis of PVC-cardiomyopathy should be suspected if the PVC burden is equal to or greater than 10% and confirmed if LV function improves or recovers after elimination of PVCs. This manuscript aims to provide a comprehensive overview of the pre-clinical and clinical studies of frequent PVCs and PVC-cardiomyopathy.

Section snippets

Prevalence of PVCs and PVC-Cardiomyopathy

PVCs are common, with an estimated prevalence of 1–4% by routine ECG in the general population, and as high as 75% when assessed by 24 to 48-h ambulatory ECG monitoring.4,11 While PVC prevalence in children is low, PVCs increase with age (e.g. 70% in patients over 75 years old) or additional co-morbidities (up to 95%), such as coronary artery disease (CAD), post-myocardial infarction (MI), dilated cardiomyopathy and HF.11

In patients referred for PVC ablation, the prevalence of

Acute cardiac effects of PVCs and trigger(s) of PVC-cardiomyopathy

PVCs have acute intra-ventricular effects including LV dyssynchrony, increased heart rate, heart rate irregularity and post-extrasystolic potentiation, as well as extra-ventricular effects comprising AV dissociation, and changes in hemodynamics and autonomic nerve activity (Fig. 1). These acute effects of PVCs are thought to trigger structural, cellular, and molecular abnormalities responsible for the mechanism of LV systolic dysfunction in PVC-cardiomyopathy.

Clinical syndrome

Patients with frequent PVCs and PVC-cardiomyopathy are often asymptomatic but can also present with intermittent fatigue, dyspnea, dizziness, and palpitations.41 Occasionally, patients with frequent PVCs are referred for pacemaker evaluation due to pseudo-bradycardia, if heart rate is assessed by BP cuff, pulse, or pulse oximetry. Pseudo-bradycardia is a frequent occurrence since PVCs are associated with inadequate ventricular filling with a resultant low pulse pressure that may not be detected

Summary

PVC-cardiomyopathy has unique pathophysiological features distinct from other types of non-ischemic cardiomyopathy. While PVC-cardiomyopathy can be insidious, it has been documented to increase morbidity in the form of HF admissions, implantation of defibrillators and resynchronization devices, malignant VAs, and increased mortality. In addition, PVC-cardiomyopathy can coexist with, and can exacerbate other cardiac substrates including both ischemic and other non-ischemic cardiomyopathies, then

Funding

NIH/NHLBI 1R01HL139874–01 (PI: Huizar), 1R34HL133182–01 (PI: Huizar); BX004861–01 (PI: Huizar); AHA SDG 16SDG3128001 (PI: Tan).

Declaration of Competing Interest

KAE KAE: Research support (RS) from Boston Scientific (BS), Biosense Webster (BSW), Medtronic (MDT), Abbott, NIH, Consultant for BS, Abbott, Atricure, MDT, Honoraria from MDT, BS, Biotronik (BTK), BSW and Atricure; JFH: RS from Abbott. KK: RS from BS and Abbott; AYT: RS from BS, MDT and BTK.

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