Movsowitz C, Kussmaul W G, Laskey W K
Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, USA.
Am J Cardiol. 1996 Feb 1;77(4):275-80. doi: 10.1016/s0002-9149(97)89393-9.
Exercise produces profound alterations in symptoms and hemodynamics in patients with valvular aortic stenosis (AS). Prior studies have demonstrated marked increases in late left ventricular (LV) diastolic filling pressure with exercise. Little information is available on the exercise response of indexes of early LV diastolic performance. Catheter-tip manometer recordings in 11 patients with AS and 5 age-matched controls were obtained at rest and with supine bicycle exercise at the time of cardiac catheterization. Pressure-derived indexes of LV diastolic performance, isovolumic relaxation rate, and diastolic interval data were examined. At rest, early (patients 22 +/- 6 mm Hg, controls 12 +/- 3 mm Hg; p < 0.01), minimal (patients 9 +/- 4 mm Hg, controls 4 +/- 1 mm Hg; p < 0.01), and late (patients 28 +/- 10 mm Hg, controls 13 +/- 3 mm Hg; p < 0.002) LV diastolic pressures were elevated in patients with AS. The time to onset of isovolumic relaxation (patients 422 +/- 31 ms, controls 363 +/- 40 ms; p < 0.01) and minimal LV diastolic pressure (patients 608 +/- 57 ms, controls 448 +/- 52 ms; p < 0.002) at rest were prolonged in patients with AS. With exercise, early (patients 45 +/- 14 mm Hg, controls 15 +/- 3 mm Hg; p < 0.002), minimal (patients 15 +/- 6 mm Hg, controls 2 +/- 1 mm Hg; p < 0.01), and late (patients 38 +/- 10 mm Hg, controls 18 +/- 5 mm Hg; p < 0.002) LV diastolic pressures were elevated, and the time to minimal LV diastolic pressure (patients 528 +/- 26 ms; controls 393 +/- 56 ms) and peak first derivative of LV pressure decline (-LV dP/dt) patients 395 +/- 41 ms, controls 326 +/- 59 ms) were prolonged in AS. Furthermore, patients with AS failed to comparably increase the rate of LV pressure decay and isovolumic relaxation with exercise. The LV diastolic response to exercise in patients with AS is distinguished from the control response by suboptimal and prolonged relaxation and a diminished rate of LV pressure decay. These abnormal responses in early diastolic function coupled with the known abnormal chamber distensibility in AS contribute to significant elevations in early, mid-, and late diastolic pressures with exercise.
运动可使主动脉瓣狭窄（AS）患者的症状和血流动力学发生显著改变。既往研究表明，运动时左心室（LV）舒张末期充盈压会显著升高。关于LV舒张早期功能指标的运动反应，目前所知甚少。在心脏导管插入术时，对11例AS患者和5例年龄匹配的对照组进行了静息状态及仰卧位自行车运动时的导管尖端压力计记录。检测了LV舒张功能的压力衍生指标、等容舒张速率和舒张间期数据。静息时，AS患者的LV舒张早期压力（患者22±6mmHg，对照组12±3mmHg；p<0.01）、最低压力（患者9±4mmHg，对照组4±1mmHg；p<0.01）和晚期压力（患者28±10mmHg，对照组13±3mmHg；p<0.002）均升高。AS患者静息时等容舒张起始时间（患者422±31ms，对照组363±40ms；p<0.01）和最低LV舒张压力时间（患者608±57ms，对照组448±52ms；p<0.002）延长。运动时，AS患者的LV舒张早期压力（患者45±14mmHg，对照组15±3mmHg；p<0.002）、最低压力（患者15±6mmHg，对照组2±1mmHg；p<0.01）和晚期压力（患者38±10mmHg，对照组18±5mmHg；p<0.002）升高，最低LV舒张压力时间（患者528±26ms；对照组393±56ms）和LV压力下降的峰值一阶导数（-LV dP/dt）（患者395±41ms，对照组326±59ms）在AS患者中延长。此外，AS患者运动时LV压力衰减速率和等容舒张未能相应增加。AS患者运动时的LV舒张反应与对照组不同，表现为舒张欠佳且延长，LV压力衰减速率降低。舒张早期功能的这些异常反应，再加上AS患者已知的心室扩张性异常，导致运动时舒张早期、中期和晚期压力显著升高。
