Why the study?
Frequent VPDs can cause reversible cardiomyopathy, but many patients maintain normal LV function despite a high burden, and electrocardiographic characteristics of VPD-induced cardiomyopathy have not been elucidated.
Are specific electrocardiographic features associated with the presence of VPD-induced cardiomyopathy in patients with frequent idiopathic VPDs?
Are specific electrocardiographic features associated with the presence of VPD-induced cardiomyopathy in patients with frequent idiopathic VPDs?
Wider VPD QRS duration and terminal QRS delay are associated with VPD-induced cardiomyopathy, suggesting subclinical conduction abnormalities may predispose patients to this condition.
Wider VPD QRS duration and terminal signals may flag higher cardiomyopathy risk; leaves open their value for risk stratification or ablation timing.
Background Frequent ventricular premature depolarizations (VPDs) can cause reversible cardiomyopathy (CMP). However, many patients maintain a normal left ventricular (LV) function with a high VPD burden. The electrocardiographic characteristics of VPD‐induced CMP have not been elucidated. Methods One hundred and eighty (91 men, age; 51 ± 15 years) patients with frequent idiopathic VPDs (>10% VPDs/day or >10 000 VPDs/day) were studied. All patients underwent successful ablation and were then divided into two groups according to the echocardiographic findings before and after the ablation procedure. Results Group A (n = 139) had a normal LV function with VPD frequencies, and Group B (n = 41) had reversible LV dysfunction after ablation. The VPD QRS duration (QRSd) was wider in patients with CMP (Group A vs Group B; 137.2 ± 12.0 milliseconds vs 159.7 ± 5.3 milliseconds, P < .001). VPDs with a terminal QRS delay marked by a notch followed by a discrete lower amplitude signal after the peak R wave in any precordial lead were identified. The incidence of terminal signals was higher in the CMP group (Group A vs Group B; 2.1% vs 53.6%, P < .001). Conclusions The wider VPD QRSd and terminal QRS delay in patients with VPD‐induced CMP suggest subclinical cell‐to‐cell conduction abnormalities as a potential factor predisposing VPD‐induced CMP.
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Im et al. (2020) studied this question.
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