Premature Ventricular Contraction-Induced Systolic Heart Failure: A Treatable Condition

Several clinical predictors of VPD-induced cardiomyopathy and HF have been identified. Classically, a high VPD burden of more than 24% has been associated with impaired LVEF and HF [13]. A longitudinal study found subclinical deterioration in LVEF over 5 years in those with a high burden of VPDs (≥ 10-20%) [14]. Despite the absence of a definitive and clear cutoff, the risk of developing NICM appears to be greater with a higher VPD burden. A threshold of approximately 10,000 VPDs/day appears required to induce LVEF dysfunction, HF and NICM [13]. Other factors suggested to confer an increased risk of developing NICM include male sex, increased BMI, an epicardial origin, shorter VPD coupling interval (600 ms), interpolated VPDs, the presence of retrograde p waves and asymptomatic nature of VPDs [15-17]. In addition, patients developing VPD NICM were more likely to be paucisymptomatic or to present prolonged palpitations [18]. Other recently published study indicated that patients with VPDs of right ventricular origin presented a higher risk to develop NICM [19]. However, another study has convincingly demonstrated that VPDs from non-outflow tract sites can also induced a NICM Editorial