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Incidence and predictors of pacemaker-induced cardiomyopathy with comparison between apical and non-apical right ventricular pacing sites

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SPRINGER
DOI: 10.1007/s10840-019-00602-2

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Right ventricular pacing; Left ventricular dysfunction; Pacemaker-induced cardiomyopathy; Apical lead position; Non-apical lead position

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Background Asynchronous activation of left ventricle (LV) due to chronic right ventricular (RV) pacing has been known to predispose to LV dysfunction. The predictors of LV dysfunction remain to be prospectively studied. This study was designed to follow up patients with RV pacing to look for development of pacing-induced cardiomyopathy (PiCMP), identify its predictors and draw comparison between apical vs non-apical RV pacing sites. Methods Three hundred sixty-three patients undergoing dual-chamber and single-chamber ventricular implants were enrolled and followed up. Baseline clinical parameters; paced QRS duration and axis; RV lead position by fluoroscopy; LV ejection fraction (LVEF) by Simpson's method on transthoracic echocardiography (TTE); intraventricular dyssynchrony (septal-posterior wall contraction delay) and interventricular dyssynchrony (aortopulmonary ejection delay) on TTE were recorded. The patients were followed up at 6-12 monthly interval with estimation of LVEF and pacemaker interrogation at each visit. Pacemaker-induced cardiomyopathy (PiCMP) was defined as a fall in ejection fraction of 10% as compared to the baseline LVEF. Patients developing PiCMP were compared to other patients to identify predictors. Results The mean age of study population was 59.8 years, 68.3% being males. Fifty-one percent and 49% patients underwent VVIR and DDDR pacemaker implantation, respectively. After attrition, 254 patients were analysed. PiCMP developed in 35 patients (13.8%) over a mean follow-up of 14.5 months. After multivariate analysis, burden of ventricular pacing > 60% [HR 4.26, p = 0.004] and interventricular dyssynchrony (aortopulmonary ejection delay > 40 msec) [HR 3.15, p = 0.002] were identified as predictors for PiCMP in patients undergoing chronic RV pacing. There was no effect of RV pacing site (apical vs non-apical) on incidence of PiCMP [HR 1.44, p = 0.353). Conclusions Incidence of PiCMP with RV pacing was found to be 13.8% over a mean follow-up of 14.5 months. Burden of right ventricular pacing and interventricular dyssynchrony were identified as the most important predictors for the development of PiCMP. Non-apical RV pacing site did not offer any benefit in terms of incidence of PiCMP over apical lead position.

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