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血管紧张素转换酶抑制可恢复高血压患者冠状动脉中血流依赖性扩张及冷加压试验诱导的扩张。

Angiotensin-converting enzyme inhibition restores flow-dependent and cold pressor test-induced dilations in coronary arteries of hypertensive patients.

作者信息

Antony I, Lerebours G, Nitenberg A

机构信息

Service d'Explorations Fonctionnelles, Centre Hospitalier, Universitaire Xavier Bichat, Paris, France.

出版信息

Circulation. 1996 Dec 15;94(12):3115-22. doi: 10.1161/01.cir.94.12.3115.

Abstract

BACKGROUND

Cold pressor test (CPT)-induced and flow-dependent epicardial coronary artery dilations are impaired in patients with hypertension. ACE inhibition can attenuate sympathetic coronary constriction and potentiate or restore endothelium-dependent relaxations. This study was designed to determine whether the ACE inhibitor perindoprilat can restore normal coronary dilative responses in hypertensive patients.

METHODS AND RESULTS

Coronary vasomotor responses to CPT and to maximal increase of blood flow induced by papaverine were studied in 10 untreated patients with essential hypertension, no other risk factors, and angiographically normal coronary arteries before and after intravenous ACE inhibition by perindoprilat. Diameters of proximal and distal left anterior descending (LAD) and circumflex coronary arteries were measured by quantitative angiography. Estimates of coronary blood flow and resistance index were calculated with an intracoronary Doppler catheter in the distal LAD. Perindoprilat did not modify the hemodynamic responses to CPT and papaverine. In response to CPT, perindoprilat changed the epicardial coronary constriction (-8.4 +/- 5.8%, P < .001) into a significant dilation (+12.0 +/- 6.4%, P < .001). Perindoprilat significantly increased the coronary blood flow (from 33.7 +/- 10.0 to 57.9 +/- 20.5 mL/min, P < .01) and enhanced the decrease in coronary resistance (from 4.28 +/- 1.27 to 2.96 +/- 0.84 mm Hg.mL-1.min-1, P < .001) caused by CPT. Flow-dependent dilation of the proximal LAD was abolished in the control condition and was restored after perindoprilat (12.6 +/- 4.7%, P < .001).

CONCLUSIONS

ACE inhibition restored CPT-induced and flow-mediated coronary artery dilations in patients with essential hypertension. These results indicate that impaired coronary vasomotor responses may be reversible in recently diagnosed hypertension.

摘要

背景

高血压患者冷加压试验(CPT)诱导的和血流依赖性心外膜冠状动脉扩张受损。血管紧张素转换酶(ACE)抑制可减弱交感神经介导的冠状动脉收缩,并增强或恢复内皮依赖性舒张。本研究旨在确定ACE抑制剂培哚普利是否能恢复高血压患者正常的冠状动脉扩张反应。

方法与结果

在10例未经治疗的原发性高血压患者中,研究了静脉注射培哚普利抑制ACE前后,冠状动脉对CPT以及罂粟碱诱导的最大血流增加的血管舒缩反应。这些患者无其他危险因素,冠状动脉造影正常。通过定量血管造影测量左前降支(LAD)近端和远端以及回旋支冠状动脉的直径。使用冠状动脉内多普勒导管在LAD远端计算冠状动脉血流和阻力指数估计值。培哚普利未改变对CPT和罂粟碱的血流动力学反应。对CPT的反应中,培哚普利使心外膜冠状动脉收缩(-8.4±5.8%,P<.001)转变为显著扩张(+12.0±6.4%,P<.001)。培哚普利显著增加冠状动脉血流(从33.7±10.0增至57.9±20.5 mL/min,P<.01),并增强CPT引起的冠状动脉阻力降低(从4.28±1.27降至2.96±0.84 mmHg·mL-1·min-1,P<.001)。在对照条件下,近端LAD的血流依赖性扩张消失,培哚普利治疗后恢复(12.6±4.7%,P<.001)。

结论

ACE抑制恢复了原发性高血压患者CPT诱导的和血流介导的冠状动脉扩张。这些结果表明,新诊断的高血压患者受损的冠状动脉血管舒缩反应可能是可逆的。

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