Abstract 4146591: Burden of Premature Ventricular Complexes is Unrelated to Prediction of Cardiomyopathy

Background: Premature ventricular complexes (PVCs) are commonly seen on cardiac monitoring. Several studies have suggested that frequent PVCs can directly cause cardiomyopathy. Understanding why only certain patients with PVCs develop cardiomyopathy remains a challenge. The current guidelines suggest a cutoff of 10% burden to indicate risk; other studies have suggested thresholds as low as 4% and as high as 24%. In this observational study, we aim to evaluate the association between PVC burden and cardiomyopathy in a larger population than assessed previously. Methods: We performed a cross-sectional analysis of >35K ambulatory monitors obtained on patients seen across the health system from April 22, 2017 and February 20, 2023. Subjects were included if they had ≥24 hours of monitoring, a PVC burden of ≥5%, and a transthoracic echocardiogram (TTE) performed within 3 months before or after monitoring. The presence of cardiomyopathy was defined as left ventricular ejection fraction (LVEF) <50%. Clinical factors including comorbidities and relevant medications were included if they were in the patient’s chart at the time of the monitor. Results: The population included a total of 1451 patients, with age 68.2±14.5 years, female sex in 39.6%, and main indications of PVCs (20.3%), palpitations (15.0%), paroxysmal AF (8.1%), and bradycardia (5.9%). The average PVC burden was 12.4 ±7.4% (5% - 43.4%). Of 746 subjects with a TTE, the mean LVEF was 55.6 ± 9.2% (25% - 76.8%), with 171 subjects (22.9%) having an LVEF <50%. We identified no significant association between PVC burden and LVEF (p = 0.78), nor with PVC burden and depressed LVEF (p = 0.13), with or without adjustment for risk factors. We also failed to identify a significant trend in PVC burden and EF (p=0.75), and a cutoff of 20% was not associated with an increase in depressed LVEF (OR 1.3, 95%CI 0.87 – 2.0, p = 0.20). Conclusions: In this analysis, we found no association between PVC burden and LV function, and could not validate the clinical cutoff of 20% as being a higher risk. These findings suggest that additional patient or PVC characteristics contributing to the development of PVC-induced cardiomyopathy have yet to be fully defined.