Pathophysiological Mechanisms of Premature Ventricular Complexes

Abstract

Premature ventricular complexes (PVCs) are the most common ventricular arrhythmia. Despite the high prevalence, the cause of PVCs remains elusive in most patients. A better understanding of the underlying pathophysiological mechanism may help to steer future research. This review aims to provide an overview of the potential pathophysiological mechanisms of PVCs and their differentiation.

Keywords: arrhythmia; cardiomyopathy; pathophysiology; premature ventricular complex; review.

FIGURE 1

Schematic overview of the mechanisms of premature ventricular complexes covered in this review.

FIGURE 2

Illustration of modulated parasystole. A Purkinje fiber and ventricular myocardium are shown on the left and their transmembrane potentials on the right. The Purkinje fiber is protected from reset by the ventricular activation due to functional conduction block and is activated by its intrinsic automaticity. This automatic rhythm in the Purkinje fiber is influenced by the subthreshold depolarization by the surrounding myocardium. Subthreshold depolarization during the early phase 4 depolarization is followed by hyperpolarization (highlighted by an asterisk) which delays phase 4 depolarization reaching threshold potential. Subthreshold depolarization during later stage of phase 4 depolarization is not followed by hyperpolarization and advances the next automatic activation. The automatic activation of the Purkinje fiber activates the myocardium because the functional conduction block is unidirectional.

FIGURE 3

Illustration of continuous activation (left) and reflection (right) as mechanism of premature ventricular complexes. In continuous activation, a second activation front traveling through a separate pathway reactivates the myocardium. This separate pathway activates in only one direction which requires unidirectional block (asterisk) at the distal site. Furthermore, sufficient activation delay is required over this pathway to reactivate the myocardium after its refractory period. In reflection, activation delay over an inexcitable gap is sufficiently long for the myocardium to recover from refractoriness resulting in reactivation of the proximal myocardium.