Cardiomyopathy-inducing premature ventricular contractions: Not all animals are equal?

Abstract

Isolated premature ventricular contractions (PVCs) are common in clinical practice and occur in patients with any form of structural heart and valvular disease as well as in normal hearts when they are usually considered benign. However, an improvement in the left ventricular (LV) systolic function after pharmacologic PVC suppression or ablation in patients with cardiomyopathy (CMP) 1,2 has led to the realization that frequent PVCs themselves sometimes can cause reversible LV dysfunction and PVC-induced CMP (PVC-CMP). At the first clinical encounter, patients often present with both PVCs and LV dysfunction, raising the question which condition came first. 3 Factors associated with the risk to develop PVC-CMP have been in the focus of intense investigations and include the PVC burden, duration of symptoms, QRS width, site of origin, and others. 4‐8 A significant overlap in these parameters usually exists between groups with and without PVC-CMP, limiting their prognostic utility. The current issue of HeartRhythm presents 2 retrospective studies examining the role of the PVC QRS duration on the development and regression of PVC-CMP. 7,9 Both studies used similar criteria to define PVC-CMP (ejection fraction [EF] 50%) and technical criteria for ablation success (80% PVC suppression) and had comparable PVC frequency in PVC-CMP groups (27%‐32%). Yokokawa et al 7 studied 294 patients with frequent PVCs referred for ablation. Of those, 113 were found to have a decreased LV EF. Other causes of CMP were excluded by thorough evaluation including cardiac magnetic resonance imaging (CMRI), rendering ventricular ectopy the only presumed cause of CMP. Patients with decreased LV function had longer PVC QRS duration than did those with normal LV EF (mean 164 ms vs 149 ms), and successful ablation resulted in the reversal of PVC-CMP in all cases. The study by Deyell et al 9 included 114 patients with frequent PVCs of which 48 had reduced LV EF. Longer PVC QRS duration also was associated with the presence of CMP. However, in a subgroup of patients with very wide PVCs (mean QRS duration 173 ms), successful suppression of PVCs failed to normalize LV function. There are several possible explanations for the difference in the study outcomes. First, some of the patients in the “irreversible” group of Deyell et al could have had a component of LV dysfunction unrelated to PVCs. (CMRI was not routinely performed in all patients but in 2 out of 3 patients in that group was abnormal.) Such patients would have been excluded by routine MRI screening in the study of Yokokawa et al. Of note, PVC frequency in the “irreversible” group was lower than in the “reversible” PVCCMP group, further suggesting that PVCs were an epiphenomenon.