Chauhan A, Mullins P A, Taylor G, Petch M C, Schofield P M
Regional Cardiac Unit, Papworth Hospital, Papworth Everard, Cambridge.
Br Heart J. 1993 Jun;69(6):516-24. doi: 10.1136/hrt.69.6.516.
To assess the effect of hyperventilation and mental stress on coronary blood flow and symptom production in patients with syndrome X.
A prospective study. Hyperventilation and mental stress tests were performed on the ward and were repeated in the cardiac catheter laboratory where coronary blood flow velocity was also measured with an intracoronary Doppler catheter in the left anterior descending coronary artery. Oesophageal manometry studies were also performed.
29 patients with syndrome X (typical anginal chest pain, a positive exercise test, and normal coronary angiogram).
A regional cardiothoracic centre.
Hyperventilation produced typical chest pain in 16 patients on the ward. 13 patients experienced their typical chest pain with mental stress test 5. Ten patients experienced chest pain with both hyperventilation and mental stress tests. This pattern was reproduced exactly when the tests were repeated in the cardiac catheter laboratory. Hyperventilation produced a significant increase in the rate-pressure product during ward and laboratory testing. There was, however, no significant change in the rate-pressure product on mental stress tests. The mean (SEM) coronary flow velocity decreased significantly on hyperventilation in the catheter laboratory from 10.0 (0.92) cm/s to 5.9 (0.72) cm/s (p < 0.001). There was also a significant reduction in the mean (SEM) coronary blood flow velocity on mental stress tests from 9.8 (0.86) cm/s to 7.4 (0.6) cm/s (p < 0.001). This reduction in flow velocity occurred in the absence of any changes in diameter of the left anterior descending artery. Further analysis showed that the coronary flow velocity was reduced significantly in only that group of patients in which hyperventilation and mental stress provoked chest pain. There was a significant increase in the arterial concentrations of noradrenaline on both hyperventilation and mental stress testing. Oesophageal manometry showed abnormalities in 17% of patients.
Both hyperventilation and mental stress can produce chest pain in patients with syndrome X and this is associated with a reduction in coronary blood flow velocity. The results of this study suggests that this reduction in coronary flow occurs as a result of increased microvascular resistance.
评估过度通气和精神应激对X综合征患者冠状动脉血流及症状产生的影响。
一项前瞻性研究。在病房进行过度通气和精神应激试验，并在心脏导管实验室重复进行，同时使用冠状动脉内多普勒导管在左前降支冠状动脉测量冠状动脉血流速度。还进行了食管测压研究。
29例X综合征患者（典型心绞痛胸痛、运动试验阳性、冠状动脉造影正常）。
一个地区心胸中心。
在病房，16例患者过度通气时出现典型胸痛。13例患者在精神应激试验时出现典型胸痛。10例患者在过度通气和精神应激试验时均出现胸痛。当在心脏导管实验室重复试验时，这种模式完全再现。在病房和实验室试验中，过度通气使心率 - 血压乘积显著增加。然而，精神应激试验时心率 - 血压乘积无显著变化。在导管实验室，过度通气时平均（标准误）冠状动脉血流速度从10.0（0.92）cm/s显著降至5.9（0.72）cm/s（p < 0.001）。精神应激试验时平均（标准误）冠状动脉血流速度也从9.8（0.86）cm/s显著降至7.4（0.6）cm/s（p < 0.001）。这种血流速度降低发生在左前降支动脉直径无任何变化的情况下。进一步分析表明，仅在过度通气和精神应激诱发胸痛的患者组中冠状动脉血流速度显著降低。过度通气和精神应激试验时去甲肾上腺素的动脉浓度均显著增加。食管测压显示17%的患者有异常。
过度通气和精神应激均可使X综合征患者产生胸痛，且这与冠状动脉血流速度降低有关。本研究结果提示，这种冠状动脉血流减少是微血管阻力增加的结果。
