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.

译文

肥厚型心肌病 (HC) 的特征是舒张功能受损,在约1/4的患者中,左心室 (LV) 流出道阻塞。房室 (AV) 起搏会减少HC的LV流出道梯度,但会损害实验动物和不同类别患者的舒张功能。为探讨AV起搏对梗阻性HC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时进行的放射性核素血管造影研究。静息左室流出道梯度随AV起搏从60 +/- 34降至38 +/-37毫米Hg (平均值 +/- SD; p <0.001)。区域射血分数在间隔水平上从0.81 +/- 0.21% 显著降低到0.69 +/- 0.27% (p <0.01)。肺动脉楔压从10 +/- 5增加到15 +/-6毫米Hg (p <0.001)。AV起搏引起的异步 (即,收缩末期时间的变异系数从7 +/- 4% 增加到14 +/- 10% (p <0.01)。等容松弛时间常数 (t) 从58 +/- 24增加到74 +/- 33 ms (p <0.02),峰值填充率从491 +/- 221降至416 +/-184毫升/s (p <0.05)。因此,AV起搏通过减少间隔射血分数 (即收缩期左室流出道宽度的增加) 大大减少静息阻塞,但是会损害主动舒张功能并增加充盈压力。这些后一种作用对于存在舒张功能障碍的HC患者可能是有害的。

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