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普萘洛尔在变异型心绞痛中诱发冠状动脉痉挛:事实还是未经证实的推断?

Facilitation of coronary spasm by propranolol in Prinzmetal's angina: fact or unproven extrapolation?

作者信息

De Cesare N, Cozzi S, Apostolo A, Berti M, Carbucicchio C, Selva A, Guazzi M D

机构信息

Istituto di Cardiologia dell'Università degli Studi, Milan, Italy.

出版信息

Coron Artery Dis. 1994 Apr;5(4):323-30. doi: 10.1097/00019501-199404000-00008.

DOI:10.1097/00019501-199404000-00008
PMID:8044344
Abstract

BACKGROUND

Alpha-adrenergic activation enhances coronary vascular tone; beta-blockade leaves alpha-adrenergic vasoconstriction unopposed. Whether beta-adrenergic blockade facilitates coronary spasm in patients with Prinzmetal's angina is unknown.

METHODS

Using quantitative angiography, we evaluated the response of normal and narrowed coronary arteries to intravenous propranolol, a cold pressor test (an alpha-stimulus), and the combination of the two in 15 patients with Prinzmetal's (group 1) and in 19 with classic (group 2) angina. From measurements of heart rate, systemic and pulmonary arterial pressures, and left and right ventricular ejection times, we derived the tension-time index per minute as a measure of the oxygen need (O2 demand) of the whole heart.

RESULTS

In group 1, cold invariably constricted normal and diseased vessels, and in two patients elicited spasm at sites of significant lesions; these changes did not correlate with those in O2 demand. In group 2, the vasomotor reaction of normal and narrowed vessels in response to cold correlated with the modifications in O2 demand. After propranolol administration, (1) in normal vessels in both groups, the baseline luminal diameter varied in parallel with the changes in myocardial O2 demand; (2) narrowings in group 1 patients invariably dilated and in group 2 the caliber varied according to changes in O2 demand; (3) during cold stimulation, luminal narrowing in group 1 varied in parallel with O2 demand, and, in group 2, vessels were uniformly constricted.

CONCLUSION

These results do not support the facilitation of coronary spasm by propranolol in Prinzmetal's angina and support the hypothesis that the contractility of coronary vessels in patients with this form of angina is different from that in the classic form.

摘要

背景

α-肾上腺素能激活会增强冠状动脉血管张力;β受体阻滞剂会使α-肾上腺素能血管收缩未受拮抗。β受体阻滞剂是否会促使变异型心绞痛患者发生冠状动脉痉挛尚不清楚。

方法

我们采用定量血管造影术,评估了15例变异型心绞痛患者(第1组)和19例典型心绞痛患者(第2组)的正常和狭窄冠状动脉对静脉注射普萘洛尔、冷加压试验(一种α刺激)以及两者联合应用的反应。通过测量心率、体循环和肺动脉压以及左、右心室射血时间,我们得出每分钟张力-时间指数,作为衡量全心氧需求(O2需求)的指标。

结果

在第1组中,寒冷总是会使正常和病变血管收缩,并且在2例患者中,在显著病变部位引发痉挛;这些变化与O2需求的变化无关。在第2组中,正常和狭窄血管对寒冷的血管运动反应与O2需求的改变相关。给予普萘洛尔后,(1)在两组的正常血管中,基线管腔直径与心肌O2需求的变化平行;(2)第1组患者的狭窄部位总是扩张,而第2组的管径根据O2需求的变化而变化;(3)在冷刺激期间,第1组的管腔狭窄与O2需求平行变化,而在第2组中,血管均匀收缩。

结论

这些结果不支持普萘洛尔在变异型心绞痛中促使冠状动脉痉挛的观点,并支持这样一种假说,即这种类型心绞痛患者的冠状动脉收缩性与典型类型不同。

相似文献

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Facilitation of coronary spasm by propranolol in Prinzmetal's angina: fact or unproven extrapolation?普萘洛尔在变异型心绞痛中诱发冠状动脉痉挛:事实还是未经证实的推断?
Coron Artery Dis. 1994 Apr;5(4):323-30. doi: 10.1097/00019501-199404000-00008.
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Eur J Cardiol. 1978 Jun;7(4):327-35.

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