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心动过速性心力衰竭起搏停止后左心房的收缩和舒张功能

Left atrial systolic and diastolic function after cessation of pacing in tachycardia-induced heart failure.

作者信息

Hoit B D, Shao Y, Gabel M, Pawloski-Dahm C, Walsh R A

机构信息

Department of Internal Medicine, University of Cincinnati Medical Center, Ohio 45267, USA.

出版信息

Am J Physiol. 1997 Aug;273(2 Pt 2):H921-7. doi: 10.1152/ajpheart.1997.273.2.H921.

Abstract

Studies in the rapid-pacing model of heart failure have shown that left ventricular (LV) systolic function normalizes on cessation of pacing and LV diastolic dysfunction persists, but there is no information regarding atrial function under these conditions. To determine the effects of cessation of pacing on left atrial (LA) systolic and diastolic function, ten dogs with rapid pacing-induced heart failure (250 beats/min for 3-4 wk), six dogs with regression of heart failure (4 wk after cessation of rapid pacing), and seven control dogs were instrumented with LA sonomicrometers and micromanometers. At matched LA pressure, LA ejection (10.2 +/- 3.0 vs. 17.4 +/- 5.5%), reservoir volume fractions (19 +/- 8 vs. 35 +/- 11%), and heart rate-corrected mean normalized systolic ejection rate (1.25 +/- 0.33 vs. 1.60 +/- 0.44 EF/s) were significantly less, and the volume-normalized diastolic stiffness constant (4.9 +/- 0.8 vs. 3.2 +/- 1.1) was significantly greater, in regression versus control dogs; these changes were associated with incomplete regression of LA hypertrophy and a persistent 77.4% increase in beta-myosin heavy chain (beta-MHC) in the LA body. LV systolic function and weight were not significantly different, whereas the time constant of LV relaxation was longer (52.5 +/- 4.4 vs. 40.8 +/- 7.6 ms; P < 0.05) and LV end-diastolic pressure was greater (12.2 +/- 1.8 vs. 7.1 +/- 2.0 mmHg; P < 0.05) in regression compared with control dogs. Thus, unlike the normalization of LV systolic function observed with cessation of rapid pacing, LA systolic function is persistently abnormal, owing in part to persistent LV diastolic dysfunction, residual LA hypertrophy, and MHC isoform switches.

摘要

在心力衰竭快速起搏模型中的研究表明,起搏停止后左心室(LV)收缩功能恢复正常,而左心室舒张功能障碍持续存在,但在这些情况下关于心房功能尚无相关信息。为了确定起搏停止对左心房(LA)收缩和舒张功能的影响,对10只快速起搏诱导心力衰竭的犬(250次/分钟,持续3 - 4周)、6只心力衰竭恢复的犬(快速起搏停止后4周)和7只对照犬植入了左心房超声微测仪和微压计。与对照犬相比,在匹配的左心房压力下,心力衰竭恢复犬的左心房射血(10.2±3.0%对17.4±5.5%)、储备容积分数(19±8对35±11%)以及心率校正的平均标准化收缩射血率(1.25±0.33对1.60±0.44 EF/s)显著降低,而容积标准化的舒张僵硬度常数(4.9±0.8对3.2±1.1)显著升高;这些变化与左心房肥厚未完全恢复以及左心房体部β - 肌球蛋白重链(β - MHC)持续增加77.4%相关。左心室收缩功能和重量无显著差异,然而与对照犬相比,心力衰竭恢复犬的左心室舒张时间常数更长(52.5±4.4对40.8±7.6毫秒;P < 0.05)且左心室舒张末期压力更高(12.2±1.8对7.1±2.0毫米汞柱;P < 0.05)。因此,与快速起搏停止后观察到的左心室收缩功能恢复正常不同,左心房收缩功能持续异常,部分原因是左心室舒张功能障碍持续存在、左心房残余肥厚以及MHC亚型转换。

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