Journal of arrhythmia · 2020
Electrocardiographic features of the presence of occult myocardial disease in patients with VPD-induced cardiomyopathy.
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Im Sung Il, Gwag Hye Bin, Park Youngjun, Park Seung-Jung, Kim June Soo, On Young Keun, Park Kyoung-Min
Аннотация
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.
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.