4.7 Article

Functional abnormalities in patients with permanent right ventricular pacing - The effect of sites of electrical stimulation

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
卷 40, 期 8, 页码 1451-1458

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ELSEVIER SCIENCE INC
DOI: 10.1016/S0735-1097(02)02169-1

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OBJECTIVES We sought to evaluate the long-term effects of alternative right ventricular pacing sites on myocardial function and perfusion. BACKGROUND Previous studies have demonstrated that asynchronous ventricular activation due to right ventricular apical (RVA) pacing alters regional myocardial perfusion and functions. METHODS We randomized 24 patients with complete atrioventricular block to undergo permanent ventricular stimulation either at the RVA (n = 12) or right ventricular outflow (RVOT) (n = 12). All patients underwent dipyridamole thallium myocardial scintigraphy and radionuclide ventriculography at 6 and 18 months after pacemaker implantation. RESULTS After pacing, the mean QRS duration was significantly longer during RVA pacing than during RVOT pacing (151 +/- 6 vs. 134 +/- 4 ms, p = 0.03). At six months, the incidence of myocardial perfusion defects (50% vs. 25%) and regional wall motion abnormalities (42% vs. 25%) and the left ventricular ejection fraction (LVEF) (55 +/- 3% vs. 55 +/- 1%) were similar during RVA pacing and RVOT pacing (p > 0.05). However, at 18 months, the incidence of myocardial perfusion defects (83% vs. 33%) and regional wall motion abnormalities (75% vs. 33%) were higher and LVEF (47 3 vs. 56 1%) was lower during RVA pacing than during RVOT pacing (all p < 0.05). Patients with RVA pacing had a significant increase in the incidence of myocardial perfusion defects (p < 0.05) and a decrease in LVEF (p < 0.01) between 6 and 18 months, but patients with RVOT pacing did not (p > 0.05). CONCLUSIONS This study demonstrates that preserved synchronous ventricular activation with RVOT pacing prevents the long-term deleterious effiects of RVA pacing on myocardial perfusion and function in patients implanted with a permanent pacemaker. (J Am Coll Cardiol 2002;40: 1451-8) (C) 2002 by the American College of Cardiology Foundation.

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