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硝酸甘油对冠状动脉心肌桥处血管挤压的增强作用:冠状动脉定量血管造影和血管内超声研究

Augmentation of vessel squeezing at coronary-myocardial bridge by nitroglycerin: study by quantitative coronary angiography and intravascular ultrasound.

作者信息

Hongo Y, Tada H, Ito K, Yasumura Y, Miyatake K, Yamagishi M

机构信息

Cardiology Division of Medicine, National Cardiovascular Center, Osaka, Japan.

出版信息

Am Heart J. 1999 Aug;138(2 Pt 1):345-50. doi: 10.1016/s0002-8703(99)70123-7.

DOI:10.1016/s0002-8703(99)70123-7
PMID:10426850
Abstract

BACKGROUND

Nitroglycerin is known to augment vessel wall squeezing at the site with coronary-myocardial bridging (CMB). This study was designed to define the mechanism of nitroglycerin-induced augmentation of CMB in clinical settings.

METHODS

We analyzed nitroglycerin reactivity at the site with CMB in 39 patients. Maximal and minimal diameters of CMB during a cardiac cycle were measured by quantitative angiography before and after intracoronary administration of 250 microgram nitroglycerin. In 15 patients, CMB sites were observed by intravascular ultrasound to determine the intimal thickness and the time-serial change in vessel area.

RESULTS

Before nitroglycerin, CMB was demonstrated with angiography in 25 patients, and the remaining 14 patients showed CMB after nitroglycerin. The maximal diameter during diastole increased from 1. 4 +/- 0.4 mm to 1.9 +/- 0.4 mm after nitroglycerin, whereas the minimal diameter during systole decreased from 1.0 +/- 0.4 mm to 0.7 +/- 0.4 mm (P <.01). Thus nitroglycerin augmented the percent vessel narrowing during systole from 24% +/- 21% to 65% +/- 16% (P <.01). Under these conditions, intravascular ultrasound showed the reduction of the cross-sectional area of the sites with CMB by -38% +/- 16% (P <.01) during systole, and this phenomenon continued to early diastole (-30% +/- 16%). The intimal thickness was 0.32 +/- 0. 10 mm, which suggests the absence of atherosclerotic disease at CMB sites.

CONCLUSIONS

These results indicate that nitroglycerin-induced augmentation of the percent narrowing of CMB can be derived from further systolic compression of the vessel lumen as well as diastolic expansion, probably because of the increase in vessel compliance after nitroglycerin. We suggest that the delayed dilation of coronary lumen during the early diastole may contribute to the occurrence of myocardial ischemia.

摘要

背景

已知硝酸甘油可增强冠状动脉心肌桥(CMB)部位的血管壁挤压。本研究旨在确定临床环境中硝酸甘油诱导CMB增强的机制。

方法

我们分析了39例患者CMB部位的硝酸甘油反应性。在冠状动脉内给予250微克硝酸甘油前后,通过定量血管造影测量心动周期中CMB的最大和最小直径。在15例患者中,通过血管内超声观察CMB部位,以确定内膜厚度和血管面积的时间序列变化。

结果

在给予硝酸甘油前,25例患者通过血管造影显示有CMB,其余14例患者在给予硝酸甘油后显示有CMB。舒张期最大直径在给予硝酸甘油后从1.4±0.4毫米增加到1.9±0.4毫米,而收缩期最小直径从1.0±0.4毫米减少到0.7±0.4毫米(P<0.01)。因此,硝酸甘油使收缩期血管狭窄百分比从24%±21%增加到65%±16%(P<0.01)。在这些情况下,血管内超声显示收缩期CMB部位的横截面积减少了-38%±16%(P<0.01),并且这种现象持续到舒张早期(-30%±16%)。内膜厚度为0.32±0.10毫米,这表明CMB部位不存在动脉粥样硬化疾病。

结论

这些结果表明,硝酸甘油诱导的CMB狭窄百分比增加可能源于血管腔在收缩期的进一步压缩以及舒张期的扩张,这可能是由于硝酸甘油后血管顺应性增加所致。我们认为舒张早期冠状动脉腔的延迟扩张可能导致心肌缺血的发生。

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