Aims The mechanism responsible for premature ventricular complex (PVC)-mediated left ventricular (LV) dysfunction remains unclear. We sought to determine the electrocardiographic and electrophysiological characteristics of PVC-mediated LV dysfunction. Methods and results One hundred and twenty-seven patients who underwent radiofrequency catheter ablation (RFCA) for frequent PVCs (PVCs burden ≥10%/24 h) and had no significant structural heart disease were investigated. Left ventricular dysfunction (ejection fraction < 50%) was present in 28 of 127 patients (22.0%). The mean PVC burden (31 ± 11 vs. 22 ± 10%, P < 0.001), the presence of non-sustained ventricular tachycardia (53.6 vs. 33.3%, P = 0.05), and the presence of a retrograde P-wave following a PVC (64.3 vs. 30.3%, P = 0.001) were significantly greater in those with LV dysfunction than in those with normal LV function. The cut-off PVC burden related to LV dysfunction was 26%/day, with a sensitivity of 70% and a specificity of 78%. The PVC morphology, QRS axis, QRS width, coupling interval, the presence of interpolation, and PVC emergence pattern during exercise electrocardiogram were not significantly different between the two groups. The origin sites of PVCs, the acute success rate, and the recurrence rate during follow-up after RFCA were similar. In a multivariate analysis, the PVC burden (odds ratio 2.94, 95% confidence interval 0.90-3.19, P = 0.006) and the presence of retrograde P-waves (odds ratio 2.79, 95% confidence interval 1.08-7.19, P = 0.034) were independently associated with PVC-mediated LV dysfunction. Conclusion A higher PVC burden (>26%/day) and the presence of retrograde P-waves were independently associated with PVC-mediated LV dysfunction.
- Left ventricular dysfunction
- Premature ventricular complexes
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)