急性冠状动脉闭塞患者的动脉压力感受器反射功能受损。

Arterial baroreflex impairment in patients during acute coronary occlusion.

作者信息

Airaksinen K E, Tahvanainen K U, Eckberg D L, Niemelä M J, Ylitalo A, Huikuri H V

机构信息

Department of Medicine, University of Oulu, Finland.

出版信息

J Am Coll Cardiol. 1998 Nov 15;32(6):1641-7. doi: 10.1016/s0735-1097(98)00452-5.

DOI:10.1016/s0735-1097(98)00452-5

PMID:9822091

Abstract

OBJECTIVES

We tested whether acute coronary occlusion interferes with arterial baroreceptor control of heart rate in humans.

BACKGROUND

Subnormal baroreflex sensitivity (BRS) is an important risk indicator for sudden death. Animal research indicates that both chronic myocardial infarction and acute coronary occlusion impair baroreflex modulation of heart rate.

METHODS

We measured RR interval prolongation after phenylephrine-induced systolic pressure increases before and during 2-min coronary occlusions in 47 patients (27 men) undergoing clinically indicated single-vessel coronary angioplasty for stenoses in the proximal or midportion of the vessel causing >50% reduction in the arterial diameter, with normal antegrade flow (33 anterior descending, 10 circumflex, 4 right coronary artery). A control group of 11 patients treated for chronic total occlusion of a coronary artery was assessed to evaluate nonspecific changes in baroreflex function during a 2-min balloon inflation in the occluded artery.

RESULTS

The BRS decreased from 5.2+/-3.8 (mean+/-SD) to 4.1+/-3.5 ms x mm Hg(-1) (p=0.01) during the coronary occlusion in the 28 patients with preserved arterial baroreceptor control of heart rate-that is, adequate blood pressure responses and correlation coefficients of the slopes both in baseline and during coronary occlusion. The same phenylephrine dose increased systolic pressure less during than before coronary artery occlusion (21+/-21 versus 36+/-16 mm Hg, p < 0.0001), and in 6 patients it failed to prevent systolic pressure reduction during occlusion. Correlation coefficients of the baroreflex regressions decreased from 0.81+/-0.27 to 0.47+/-0.44 (p < 0.0001) during coronary artery occlusion in the 41 patients with adequate systolic pressure rises in both phenylephrine tests, and the association between RR intervals and rising systolic pressures was lost in 13 patients during coronary occlusion. Balloon inflation in a chronic total occlusion of a coronary artery did not cause significant changes in BRS (from 5.3+/-4.0 to 5.2+/-3.7 ms x mm Hg(-1)), correlation coefficient of the slope or phenylephrine-induced pressure rise.

CONCLUSIONS

Our study shows that abrupt coronary occlusion impairs baroreflex modulation of vagal and sympathetic nervous outflow in humans.

摘要

目的

我们测试了急性冠状动脉闭塞是否会干扰人体动脉压力感受器对心率的控制。

背景

压力反射敏感性（BRS）低于正常水平是猝死的重要风险指标。动物研究表明，慢性心肌梗死和急性冠状动脉闭塞都会损害压力反射对心率的调节。

方法

我们测量了47例（27例男性）因近端或中段血管狭窄导致动脉直径减少>50%且顺行血流正常（33例前降支、10例回旋支、4例右冠状动脉）而接受临床指征的单支冠状动脉血管成形术的患者在冠状动脉闭塞2分钟前和闭塞期间苯肾上腺素诱导收缩压升高后的RR间期延长情况。对11例接受冠状动脉慢性完全闭塞治疗的患者组成的对照组进行评估，以评估在闭塞动脉中进行2分钟球囊扩张期间压力反射功能的非特异性变化。

结果

在28例保留动脉压力感受器对心率控制的患者中，即基线和冠状动脉闭塞期间血压反应充分且斜率相关系数良好，冠状动脉闭塞期间BRS从5.2±3.8（均值±标准差）降至4.1±3.5 ms·mmHg-1（p=0.01）。相同剂量的苯肾上腺素在冠状动脉闭塞期间比闭塞前使收缩压升高幅度更小（21±21与36±16 mmHg，p<0.0001），并且在6例患者中未能防止闭塞期间收缩压降低。在两次苯肾上腺素测试中收缩压升高充分的41例患者中，冠状动脉闭塞期间压力反射回归的相关系数从0.81±0.27降至0.47±0.44（p<0.0001），并且在冠状动脉闭塞期间13例患者中RR间期与收缩压升高之间的关联消失。冠状动脉慢性完全闭塞时的球囊扩张未导致BRS（从5.3±4.0降至5.2±3.7 ms·mmHg-1）、斜率相关系数或苯肾上腺素诱导的压力升高有显著变化。