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Right ventricle apex pacing identifies the presence of ventricular premature depolarizations‐induced cardiomyopathy
Author(s) -
Im Sung Il,
Gwag Hye Bin,
Park Youngjun,
Park SeungJung,
Kim June Soo,
On Young Keun,
Park KyoungMin
Publication year - 2019
Publication title -
pacing and clinical electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 101
eISSN - 1540-8159
pISSN - 0147-8389
DOI - 10.1111/pace.13553
Subject(s) - medicine , ventricle , ejection fraction , cardiology , qrs complex , cardiomyopathy , sinus bradycardia , fractional shortening , body surface area , ventricular dyssynchrony , apex (geometry) , heart failure , bradycardia , heart rate , cardiac resynchronization therapy , blood pressure , anatomy
Background A high burden of ventricular premature depolarizations (VPDs) has been associated with potentially reversible left ventricular (LV) dysfunction, termed as VPD‐induced cardiomyopathy (CMP). However, many patients maintain normal LV function despite a high VPD burden. The purpose of this study was to identify CMP by right ventricle apex (RVa) pacing method in patients with high VPD burden. Methods A total of 62 patients (28 male; mean age = 50 ± 15 years) with idiopathic VPDs undergoing ablation were enrolled. RVa pacing was recorded in all patients during the procedure. The paced QRS duration (QRSd) during RV pacing was measured from the pacing spike to the latest QRS deflection on any surface electrocardiogram lead. Patients were divided into two groups: reversible VPD‐induced CMP (Group R; n = 15, 14 males, mean age = 54 ± 14 years) and normal LV function (Group N; n = 47, 23 males, mean age = 54 ± 15 years). Results The LV ejection fraction (%) was significantly lower in Group R as compared with Group N (Group R, Group N = 36 ± 6, 58 ± 4; P < 0.001); however, LV end‐diastolic dimension mm was not significantly different between the two study groups (Group R, Group N = 54 ± 5, 50 ± 6; P = 0.06). Similarly, sinus QRS width ( P = 0.10), VPD‐burden ( P = 0.36), and body surface area ( P = 0.75) were not significantly different between Group R and Group N. The QRSd was significantly longer in Group R compared with Group N (177 ± 8 vs 150 ± 14; P < 0.001). Using a QRSd cut‐off value of 170.1 ms, VPD‐induced CMP was identified with a sensitivity of 73% and a specificity of 97%. Conclusion RVa pacing with transmyocardial conduction time assessment was a useful method for identifying idiopathic VPD‐induced CMP. Using a QRSd cut‐off value of 170.1 ms, VPD‐induced CMP was identified with a sensitivity of 73% and a specificity of 97%.