• premature ventricular beats
• ventricular arrhythmia ablation procedures
• heart failure with reduced ejection fraction

The first publications about the relevance of premature ventricular complexes (PVCs) appeared in the late 1970s.1 In patients with frequent PVCs without structural heart disease, the prognosis was no worse than in the general population. Therefore, it has been generally accepted that prognosis is linked to the presence or absence of structural heart disease rather than with the presence of PVC itself. On the other hand, ablation may improve ventricular ejection fraction in patients with frequent PVCs and systolic dysfunction.2 Those initial descriptions of the so-called PVC-induced cardiomyopathy increased the interest in the prognosis of patients with frequent PVCs.

Cohort studies have shown a relation between PVC burden, deterioration of left ventricular ejection fraction (LVEF)3 4 and cardiovascular events.4 5 Patients with the highest PVC burden (first quartile) showed three times greater odds of 5-year decrease in LVEF and an increased risk of heart failure and death.4 Therefore, it seems that frequent PVCs may result in left ventricular deterioration even in the absence of structural heart disease. Ablation of PVCs may improve LVEF in patients with left ventricular dilation or systolic dysfunction,6 and in patients with left ventricle systolic dysfunction, according to a recent multicentre study,7 may decrease the risk of a combined event including cardiac mortality, cardiac transplantation and heart failure hospital admission. However, limited information is available on the probability of PVC-induced ventricular dysfunction in patients with normal heart function.

The study by Lee and colleagues8 sheds some light on the decision-making tree. They have assessed the natural history of consecutive untreated patients with frequent PVCs (>5%/24 hours) and preserved LVEF (100 patients, median PVC burden of 18.1%). Two major findings are of great interest in this study. First, spontaneous suppression of PVC (<1%/24 hours) or >80% reduction of PVC burden occurred in 44% and 52% of the overall study population, respectively. To our knowledge, this is the first study to report the natural course of frequent PVCs in terms of evolution of PVC burden; furthermore, a higher PVC burden was related with the chance of spontaneous resolution. Second, LVEF deteriorated in only 4% of the patients and dropped below 40% in only one patient (1%). The results of this study are aligned with the benign prognosis suggested in the initial classical studies.1 As the authors mention in the manuscript, a conservative strategy of periodically evaluating cardiac function without further intervention seems reasonable. Two strengths of this study must be highlighted. It is the first study to analyse the presence of structural heart disease by cardiac echocardiogram and with late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR), excluding all patients showing fibrosis in CMR despite normal LVEF. The presence of LGE is a very powerful prognostic factor in all types of cardiomyopathy,9 10 even in patients with PVC, so exclusion of these patients permits a true representation of patients with frequent PVC without any structural heart disease and could partially explain the benign prognosis. Finally, not only patients had a long follow-up (53–71 months), but changes in PVC burden and in LVEF were confirmed by serial Holter and echocardiography. The low prevalence of PVC-induced cardiomyopathy in this study is consistent with previous reports of 5.4%3 and 6%–8.1%4 prevalence. Despite the risks associated with frequent PVCs described by Dukes et al,4 it must be clarified that the populations of the two studies are not comparable and may influence the observed discrepancy in prognosis. Participants in the Dukes et al study4 were older (70 years vs 52 years in the study by Lee et al 8), with a higher prevalence of coronary artery disease (16% vs 9%) and cardiovascular risk burden, such as diabetes mellitus (14%–15% vs 10%) and hypertension (54% vs 34%).

Finally, previous studies have established a correlation between the frequency of PVC and LVEF deterioration3 5 and a lower probability for LVEF recovery after PVC ablation.6 7 Classically, a cut-off of 20% of PVC burden was considered as a marker of worst outcomes. However, this cut-off was mainly validated in patients with depressed LVEF at the time of initial diagnosis.6 7 None of the factors previously linked to poor prognosis, such as a PVC origin other than right ventricular outflow tract, short coupling interval with longer PVC duration and associated sustained ventricular tachycardia, have been observed in the present study. However, the authors point out that cohort size and the low incidence of events may limit the statistical power to identify differences.

In conclusion, the results of the study presented by Lee and colleagues8 suggest that a conservative ‘wait and see’ strategy of periodic LVEF evaluation in patients with frequent PVC, in the absence of structural heart disease (including LGE CMR in selected patients), can be reasonable due to the high likelihood of spontaneous resolution and the low rate of cardiac events and PVC-induced cardiomyopathy.

According to the present data, in patients with normal ejection fraction and frequent PVCs, it seems that the decision to ablate should be based on symptom relief rather than prognostic considerations. However, larger studies are needed to better identify which patients are at higher risk of developing PVC-induced cardiomyopathy. In those patients, an earlier invasive treatment may be reasonable.