Ethanol-induced coronary vasodilation in patients with and without coronary artery disease

Ricardo G. Cigarroa, Richard A. Lange, Jeffrey J. Popma, Gary Yurow, Michael N. Sills, Brian G. Firth, L. David Hillis

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

To assess the influence of ethanol on coronary arterial blood flow and dimensions, we measured coronary sinus blood flow in 35 subjects (23 men and 12 women, aged 38 to 69 years; (29 with and 6 without coronary artery disease) before and during a 15- to 30-minute intracoronary infusion of (1) 5% dextrose in water (n=15, controls) or (2) 5% ethanol in 5% dextrose in water (n=20). In the controls heart rate, arterial pressure, and coronary sinus blood flow were unchanged. In those receiving ethanol at a rate that produced a concentration in coronary sinus blood of 285±102 (mean±SD) mg/dl, heart rate-systolic arterial pressure product was unchanged; coronary sinus blood flow rose 27±36%, and coronary vascular resistance fell 17±22% (p<0.05 in comparison to baseline); arterial-coronary sinus oxygen content difference fell (p<0.05), and epicardial coronary arterial dimensions were unchanged. Thus intracoronary ethanol increases coronary blood flow and decreases resistance without inducing a change in epicardial coronary dimensions, suggesting that its effect results from dilatation of the intramyocardial resistance vessels.

Original languageEnglish (US)
Pages (from-to)254-259
Number of pages6
JournalAmerican Heart Journal
Volume119
Issue number2 PART 1
DOIs
StatePublished - 1990
Externally publishedYes

Fingerprint

Coronary Sinus
Vasodilation
Coronary Artery Disease
Ethanol
Arterial Pressure
Heart Rate
Glucose
Water
Vascular Resistance
Dilatation
Oxygen
Blood Pressure

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Cigarroa, R. G., Lange, R. A., Popma, J. J., Yurow, G., Sills, M. N., Firth, B. G., & Hillis, L. D. (1990). Ethanol-induced coronary vasodilation in patients with and without coronary artery disease. American Heart Journal, 119(2 PART 1), 254-259. https://doi.org/10.1016/S0002-8703(05)80013-4

Ethanol-induced coronary vasodilation in patients with and without coronary artery disease. / Cigarroa, Ricardo G.; Lange, Richard A.; Popma, Jeffrey J.; Yurow, Gary; Sills, Michael N.; Firth, Brian G.; Hillis, L. David.

In: American Heart Journal, Vol. 119, No. 2 PART 1, 1990, p. 254-259.

Research output: Contribution to journalArticle

Cigarroa, RG, Lange, RA, Popma, JJ, Yurow, G, Sills, MN, Firth, BG & Hillis, LD 1990, 'Ethanol-induced coronary vasodilation in patients with and without coronary artery disease', American Heart Journal, vol. 119, no. 2 PART 1, pp. 254-259. https://doi.org/10.1016/S0002-8703(05)80013-4
Cigarroa, Ricardo G. ; Lange, Richard A. ; Popma, Jeffrey J. ; Yurow, Gary ; Sills, Michael N. ; Firth, Brian G. ; Hillis, L. David. / Ethanol-induced coronary vasodilation in patients with and without coronary artery disease. In: American Heart Journal. 1990 ; Vol. 119, No. 2 PART 1. pp. 254-259.
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abstract = "To assess the influence of ethanol on coronary arterial blood flow and dimensions, we measured coronary sinus blood flow in 35 subjects (23 men and 12 women, aged 38 to 69 years; (29 with and 6 without coronary artery disease) before and during a 15- to 30-minute intracoronary infusion of (1) 5{\%} dextrose in water (n=15, controls) or (2) 5{\%} ethanol in 5{\%} dextrose in water (n=20). In the controls heart rate, arterial pressure, and coronary sinus blood flow were unchanged. In those receiving ethanol at a rate that produced a concentration in coronary sinus blood of 285±102 (mean±SD) mg/dl, heart rate-systolic arterial pressure product was unchanged; coronary sinus blood flow rose 27±36{\%}, and coronary vascular resistance fell 17±22{\%} (p<0.05 in comparison to baseline); arterial-coronary sinus oxygen content difference fell (p<0.05), and epicardial coronary arterial dimensions were unchanged. Thus intracoronary ethanol increases coronary blood flow and decreases resistance without inducing a change in epicardial coronary dimensions, suggesting that its effect results from dilatation of the intramyocardial resistance vessels.",
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