Chest pain and “normal” coronary arteries—Role of small coronary arteries

doi:10.1016/0002-9149(85)90613-7

The American Journal of Cardiology

Volume 55, Issue 3, 25 January 1985, Pages B50-B60

https://doi.org/10.1016/0002-9149(85)90613-7 Get rights and content

Abstract

To study the mechanism of chest pain in patients with insignificant epicardial coronary artery disease, 50 patients underwent great cardiac vein (GCV) flow, oxygen content and lactate determinations at rest and during pacing, and left ventricular end-diastolic pressure (LVEDP) measurements at rest and after pacing. Twenty-four patients having typical chest discomfort during pacing demonstrated significantly lower increase in flow from baseline (36 ± 18% versus 86 ± 24%, p < 0.001) and decrease in coronary resistance (−17 ± 12% versus −43 ±7%, p < 0.001) compared with 26 patients without pacing-induced chest pain, despite no significant difference in myocardial oxygen consumption (MVO₂) between the 2 groups. Lactate consumption at a heart rate (HR) of 150 beats/min was significantly less (28.3 ± 21.5 versus 51.3 ± 35.8 mM· ml/min, p < 0.001) and the increase in LVEDP from rest to after pacing was significantly greater (5 ±2 versus 1 ± 2 mm Hg, p < 0.001) in the chest pain group. After administration of ergonovine, 0.15 mg intravenously, to 46 of these patients, 31 had typical pain either at rest (1 patient) or during pacing. This group had significantly lower increase in flow (38 ± 20% versus 107 ± 38%, p < 0.001), and decrease in coronary resistance (-16 ± 12% versus −45 ± 11%, p < 0.001) compared with the 15 patients not having chest pain, despite no significant difference in MVO₂ between the 2 groups. Patients with chest pain also had lower lactate consumption at a HR of 150 beats/min (39.2 ± 23.6 versus 65.3 ± 46.3 mM·ml/min, p < 0.01), greater arterial-GCV oxygen difference (12.5 ± 1.3 versus 11.6 ± 1.0 ml O₂/100 ml, p < 0.05), and a more marked increase in LVEDP from rest to after pacing (11 ± 3 versus 5 ± 2 mm Hg, p < 0.001). Quantitative coronary arteriography demonstrated no significant luminal narrowing of the epicardial coronary arteries in response to ergonovine. These data are consistent with the hypothesis that some patients with chest pain and angiographically normal epicardial coronary arteries have dynamic abnormalities of the small coronary arteries or coronary microcirculation that cause abnormal vasodilator reserve or vaso-constriction, resulting in myocardial ischemia and angina pectoris.

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Chest pain and “normal” coronary arteries—Role of small coronary arteries

Abstract

Am J Cardiol

JACC

Am J Cardiol

Am J Cardiol

Am J Cardiol

Am J Cardiol

Am J Cardiol

Am J Cardiol

JACC

Am J Cardiol

Am J Med

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JACC

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Circulation

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JAMA

Importance of the design of an exercise protocol in the evaluation of patients with angina pectoris

Circulation

Origin of great cardiac vein and coronary sinus drainage within the left ventricle

Am J Physiol