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双腔起搏对肥厚型心肌病患者左心室流出道梗阻及舒张功能的影响。

Effects of dual-chamber pacing in hypertrophic cardiomyopathy on left ventricular outflow tract obstruction and on diastolic function.

作者信息

Betocchi S, Losi M A, Piscione F, Boccalatte M, Pace L, Golino P, Perrone-Filardi P, Briguori C, Franculli F, Pappone C, Salvatore M, Chiariello M

机构信息

Department of Cardiology and Cardiac Surgery, Federico II University School of Medicine, Naples, Italy.

出版信息

Am J Cardiol. 1996 Mar 1;77(7):498-502. doi: 10.1016/s0002-9149(97)89344-7.

Abstract

Hypertrophic cardiomyopathy (HC) is characterized by impaired diastolic function and, in about 1/4 of patients, left ventricular (LV) outflow tract obstruction. Atrioventricular (AV) pacing diminishes LV outflow tract gradient in HC, but impairs diastolic function in the experimental animal and in different categories of patients. To investigate the effects of AV pacing on hemodynamics and LV function in obstructive HC, 16 patients with HC were studied by cardiac catheterization and simultaneous radionuclide angiography during atrial and AV pacing. The resting LV outflow tract gradient decreased with AV pacing from 60 +/- 34 to 38 +/- 37 mm Hg (mean +/- SD; p <0.001). Regional ejection fraction decreased significantly at the septal level from 0.81 +/- 0.21% to 0.69 +/- 0.27% (p <0.01). Pulmonary artery wedge pressure increased from 10 +/- 5 to 15 +/- 6 mm Hg (p <0.001). AV pacing induced asynchrony (i.e., the coefficient of variation of the time to end-systole increased from 7 +/- 4% to 14 +/- 10% (p <0.01). The time constant of isovolumetric relaxation (t) increased from 58 +/- 24 to 74 +/- 33 ms (p <0.02), and peak filling rate decreased from 491 +/- 221 to 416 +/- 184 ml/s (p <0.05). Thus, AV pacing greatly diminishes resting obstruction through a reduction in septal ejection fraction (i.e., an increase in LV outflow tract width in systole), but impairs active diastolic function and increases filling pressures. These latter effects are potentially detrimental in patients with HC in whom diastolic dysfunction is present.

摘要

肥厚型心肌病(HC)的特征是舒张功能受损,约四分之一的患者存在左心室(LV)流出道梗阻。房室(AV)起搏可降低HC患者的LV流出道梯度,但在实验动物和不同类型的患者中会损害舒张功能。为了研究AV起搏对梗阻性HC患者血流动力学和LV功能的影响,对16例HC患者在心房和AV起搏期间进行了心导管检查和同步放射性核素血管造影。静息时LV流出道梯度在AV起搏时从60±34降至38±37 mmHg(平均值±标准差;p<0.001)。室间隔水平的局部射血分数从0.81±0.21%显著降至0.69±0.27%(p<0.01)。肺动脉楔压从10±5升至15±6 mmHg(p<0.001)。AV起搏诱发了不同步(即收缩末期时间的变异系数从7±4%增至14±10%(p<0.01))。等容舒张时间常数(t)从58±24增至74±33 ms(p<0.02),峰值充盈率从491±221降至416±184 ml/s(p<0.05)。因此,AV起搏通过降低室间隔射血分数(即收缩期LV流出道宽度增加)极大地减轻了静息梗阻,但损害了主动舒张功能并增加了充盈压。后一种效应在存在舒张功能障碍的HC患者中可能是有害的。

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