Premature ventricular contractions (PVCs) are “early depolarizations of the myocardium, originating in the ventricle.”1 Once regarded as benign, PVCs—even in the absence of structural heart disease—are now regarded as more insidious, potentially causing or contributing to cardiomyopathy and heart failure.2

Asymptomatic PVCs are often detected incidentally3 and have been described in 1% of the general population on standard ECG and in 40% to 75% on 24 to 48 hour ambulatory ECG recording.4 The prevalence of PVCs tends to be age-dependent, ranging from <1% in children under 11 years to 69% in individuals >75 years.1

“Nearly everyone has PVCs from time to time,” observed Daniel Cantillon, MD, medical director of the Central Monitoring Unit at Cleveland Clinic in Ohio. “But they become pathological in patients with an excessive number.”

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Symptomatic patients may describe PVCs as “palpitations,” “hard heartbeats,” “chest-thumping,” a “catch” or “skipped” heartbeats, according to  Dr Cantillon, who is associate professor of medicine at the Cleveland Clinical Lerner Medical School. Symptoms typically include dyspnea, chest pain, fatigue, lightheadedness, dizziness, or syncope.3

A guide to PVC nomenclature can be found in Table 1.

Pathophysiology of PVCs

In PVCs, ventricular myocytes spontaneously depolarize to create an extra systole that creates mechanical dyssynchrony with the cardiac cycle.2,3 Affected cells are triggered by cyclic adenosine monophosphate-mediated and calcium-dependent delays in after-depolarizations.3

The most common sites of origin for ventricular ectopy, in the absence of structural heart disease, are the left or right outflow tracts (RVOTs) or the epicardial tissues immediately adjacent to the aortic sinuses of Valsalva.3 Most foci are located in the RVOT. Fascicular PVCs originate from within the left ventricular His-Purkinje system.3 Other sites of origin for PVCs include ventricular tissues adjacent to the aortomitral continuity, the tricuspid annulus, the mitral valve annulus, papillary muscles, and other Purkinje-adjacent structures.3

PVCs can be associated with a variety of underlying cardiac conditions, including coronary artery disease, nonischemic dilated cardiomyopathy, arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C), cardiac amyloidosis and sarcoidosis, and hypertrophic cardiomyopathy.3 Frequent PVCs can cause cardiomyopathy through complex transient alterations in intracellular calcium and membrane ionic currents, heart rate dynamics, hemodynamic parameters, and myocardial and peripheral vascular autonomic stimulation and inhibition.1

To Intervene or Not to Intervene?

“The main question is whether and when to intervene,” said Rakesh Latchamsetty, MD, electrophysiologist at the University of Michigan Hospital and clinical lecturer at the University of Michigan Health System. “The 2 primary indications for intervention are whether the patient has disruptive symptoms, and the development of cardiomyopathy.”