Cigarette smoking-induced coronary vasoconstriction in atherosclerotic coronary artery disease and prevention by calcium antagonists and nitroglycerin

Michael D. Winniford, Donald E. Jansen, Gary A. Reynolds, Phillip Apprill, William H. Black, L. David Hillis

Research output: Contribution to journalArticle

52 Citations (Scopus)

Abstract

In patients with coronary artery disease, cigarette smoking increases myocardial oxygen demand but may cause an inappropriate α-adrenergically mediated fall in myocardial oxygen supply. This study was performed to determine if smoking-induced coronary vasoconstriction is prevented by nitroglycerin, verapamil or nifedipine treatment. In 25 smokers with coronary artery disease (20 men, 5 women, aged 32 to 65 years), heart rate-systolic arterial pressure double product and coronary sinus blood flow (thermodilution) were measured before and during smoking both before and 30 to 60 minutes after administration of saline solution (n = 5, control subjects); nifedipine, 10 mg sublingually (n = 6); verapamil, 10 mg intravenously (n = 7); or nitroglycerin, 0.4 mg sublingually (n = 7). During the first smoking period, double product increased, but coronary sinus flow did not change or decreased. During the second smoking period, in the control subjects double product and coronary sinus flow responded in a manner similar to that observed previously. In those given nifedipine, double product did not change, but coronary sinus flow increased (-4 ± 5% during the first smoking period [before nifedipine] and 17 ± 12% during the second period [after nifedipine], p < 0.01). In those given verapamil, double product and coronary sinus flow increased during smoking (-12 ± 8% during the first smoking period [before verapamil], 10 ± 9% during the second period [after verapamil], p < 0.01). In those given nitroglycerin, double product and coronary sinus flow increased with smoking (-1 ± 17% during the first smoking period [before nitroglycerin], 31 ± 18% during the second [after nitroglycerin], p < 0.01). Thus, smoking-induced coronary vasoconstriction is prevented by calcium antagonist drugs and nitroglycerin; these agents may improve the myocardial oxygen supply:demand relation during smoking.

Original languageEnglish (US)
Pages (from-to)203-207
Number of pages5
JournalAmerican Journal of Cardiology
Volume59
Issue number4
DOIs
StatePublished - 1987
Externally publishedYes

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Nitroglycerin
Vasoconstriction
Coronary Artery Disease
Smoking
Calcium
Coronary Sinus
Nifedipine
Verapamil
Oxygen
Thermodilution
Sodium Chloride
Arterial Pressure
Heart Rate
Blood Pressure

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Cigarette smoking-induced coronary vasoconstriction in atherosclerotic coronary artery disease and prevention by calcium antagonists and nitroglycerin. / Winniford, Michael D.; Jansen, Donald E.; Reynolds, Gary A.; Apprill, Phillip; Black, William H.; Hillis, L. David.

In: American Journal of Cardiology, Vol. 59, No. 4, 1987, p. 203-207.

Research output: Contribution to journalArticle

Winniford, Michael D. ; Jansen, Donald E. ; Reynolds, Gary A. ; Apprill, Phillip ; Black, William H. ; Hillis, L. David. / Cigarette smoking-induced coronary vasoconstriction in atherosclerotic coronary artery disease and prevention by calcium antagonists and nitroglycerin. In: American Journal of Cardiology. 1987 ; Vol. 59, No. 4. pp. 203-207.
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abstract = "In patients with coronary artery disease, cigarette smoking increases myocardial oxygen demand but may cause an inappropriate α-adrenergically mediated fall in myocardial oxygen supply. This study was performed to determine if smoking-induced coronary vasoconstriction is prevented by nitroglycerin, verapamil or nifedipine treatment. In 25 smokers with coronary artery disease (20 men, 5 women, aged 32 to 65 years), heart rate-systolic arterial pressure double product and coronary sinus blood flow (thermodilution) were measured before and during smoking both before and 30 to 60 minutes after administration of saline solution (n = 5, control subjects); nifedipine, 10 mg sublingually (n = 6); verapamil, 10 mg intravenously (n = 7); or nitroglycerin, 0.4 mg sublingually (n = 7). During the first smoking period, double product increased, but coronary sinus flow did not change or decreased. During the second smoking period, in the control subjects double product and coronary sinus flow responded in a manner similar to that observed previously. In those given nifedipine, double product did not change, but coronary sinus flow increased (-4 ± 5{\%} during the first smoking period [before nifedipine] and 17 ± 12{\%} during the second period [after nifedipine], p < 0.01). In those given verapamil, double product and coronary sinus flow increased during smoking (-12 ± 8{\%} during the first smoking period [before verapamil], 10 ± 9{\%} during the second period [after verapamil], p < 0.01). In those given nitroglycerin, double product and coronary sinus flow increased with smoking (-1 ± 17{\%} during the first smoking period [before nitroglycerin], 31 ± 18{\%} during the second [after nitroglycerin], p < 0.01). Thus, smoking-induced coronary vasoconstriction is prevented by calcium antagonist drugs and nitroglycerin; these agents may improve the myocardial oxygen supply:demand relation during smoking.",
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