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Premature ventricular contractions (PVCs) have undergone a major conceptual evolution over the past two decades. Frequent PVCs are now recognised as a potentially reversible cause of ventricular dysfunction and adverse remodelling.1 2 The identification of PVC-induced cardiomyopathy (PVC-CM), particularly the observation that suppression of PVCs can improve left ventricular (LV) function, has fundamentally reshaped the understanding of ventricular ectopy. Yet an important question remains unresolved: what degree of PVC burden meaningfully increases the risk of ventricular remodelling?