Abstract

Premature ventricular complexes (PVCs) are one of the most commonly encountered arrhythmias and are ubiquitous in clinical practice, both in the outpatient and inpatient settings. They are often discovered incidentally in asymptomatic patients, however, can cause myriad symptoms acutely and chronically. Long thought to be completely benign, PVCs have been historically disregarded without pursuing any further evaluation. Newer data have revealed that a high burden of PVCs with specific characteristics can significantly increase a patient's risk of developing PVC-induced cardiomyopathy. The aim of this literature review is to provide further clarification on the identification of high-risk PVCs, subsequent workup, and the currently available treatment options. PVCs arise from an ectopic focus within the ventricles. Patients with PVCs can be either asymptomatic or have severe disabling symptoms. The diagnostic workup for PVCs includes electrocardiogram (ECG) and 24-h Holter monitor to assess the QRS morphology and its frequency. A transthoracic echocardiogram (TTE) is done to look for structural heart disease and cardiomyopathy. Management of PVCs should be focused on identifying and treating the underlying causes, such as electrolyte abnormalities, substance use, and underlying structural heart disease. Beta-blockers are first-line therapy for symptomatic PVCs. Nondihydropyridine calcium channel blockers, classic antiarrhythmic agents, and amiodarone can be considered as second-line agents. Patients who are unable to tolerate medical therapy should undergo catheter ablation of the PVC focus to prevent PVC-induced cardiomyopathy. PVCs are common in clinical practice, and it is vital to identify patients at higher risk for PVC-induced cardiomyopathy to facilitate early intervention. Patients with no evidence of structural heart disease and infrequent PVCs should be monitored closely, while those who are symptomatic should be treated medically. For those who have failed medical therapy, catheter ablation of the PVCs focus is recommended. Catheter ablation has been shown to reduce PVCs burden and improve left ventricular ejection fraction (LVEF) in those with PVC-induced cardiomyopathy.

Highlights

  • BackgroundVentricular premature beats (VPBs), premature ventricular complexes/contractions (PVCs), or ventricular extrasystole are ectopic beats that arise from within the ventricles

  • The PVCs usually do not cause any symptoms in asymptomatic individuals

  • Symptomatic patients either present due to the acute effects of PVCs or due to the symptoms that arise from chronic PVCs and their cumulative effects on myocardial contractility

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Summary

Introduction

Ventricular premature beats (VPBs), premature ventricular complexes/contractions (PVCs), or ventricular extrasystole are ectopic beats that arise from within the ventricles. Re-entry is thought to be the most common mechanism for both PVCs and ventricular tachycardia This is an abnormal impulse that fails to propagate through the normal conduction system and instead travels in a retrograde fashion causing re-excitation and circular conduction. Delayed after-depolarizations are thought to occur due to elevated intracellular calcium causing an increased inward current by the sodium-calcium exchange This leads to an influx of sodium resulting in a triggered action potential [14]. Enhanced automaticity occurs when lower diastolic thresholds of transmembrane voltage, most commonly in the Purkinje fibers, results in premature depolarization and impulse propagation. This can be seen with electrolyte abnormalities, acute ischemia and in states of catecholamine excess

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