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Coronary vasoconstrictor effect of indomethacin in patients with coronary-artery disease
Insights
Indomethacin significantly reduced coronary blood flow and increased vascular resistance in patients with coronary artery disease. This suggests caution is needed when using this drug in such individuals.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Prostaglandins are potential regulators of coronary blood flow.
- Indomethacin is a nonsteroidal anti-inflammatory drug that inhibits prostaglandin synthesis.
Purpose of the Study:
- To investigate the effect of indomethacin-induced prostaglandin synthesis blockade on coronary blood flow in patients with coronary artery disease.
Main Methods:
- Nine patients with coronary artery disease received intravenous indomethacin (0.5 mg/kg).
- Coronary sinus blood flow, mean arterial pressure, and myocardial arteriovenous oxygen difference were measured before and 20 minutes after indomethacin administration using thermodilution and blood sampling.
Main Results:
- Indomethacin significantly increased mean arterial pressure, coronary vascular resistance, and myocardial arteriovenous oxygen difference.
- Coronary blood flow significantly decreased after indomethacin administration.
- The observed coronary vasoconstriction may be due to blockade of vasodilatory prostaglandins or a direct drug effect.
Conclusions:
- Indomethacin causes coronary vasoconstriction and reduces coronary blood flow in patients with coronary artery disease.
- The use of indomethacin in patients with severe coronary artery disease warrants caution due to potential adverse effects on coronary hemodynamics.
Abstract:
Prostaglandins may be important regulators of coronary blood flow. To investigate this possibility, we studied the effect of blockade of prostaglandin synthesis by indomethacin in nine patients with coronary-artery disease. Coronary-sinus blood flow (determined with the thermodilution technique) was recorded, together with mean arterial blood pressure and the myocardial arteriovenous oxygen difference from simultaneously obtained arterial and coronary-sinus blood samples, before and 20 minutes after an intravenous dose of indomethacin (0.5 mg per kilogram of body weight). There were significant increases (P less than 0.05) in mean arterial pressure (from 99 +/- 4 to 118 +/- 5 mm Hg [+/- S.E.M.]), coronary vascular resistance (+73 per cent), and myocardial arteriovenous oxygen difference (from 107 +/- 5 to 138 +/- 4 ml per liter) after indomethacin, but coronary blood flow fell significantly, from 181 +/- 29 to 111 +/- 14 ml per minute (P less than 0.05). Thus, despite an increase in myocardial oxygen demand, coronary blood flow fell and coronary vascular resistance increased. This coronary vasoconstrictor effect may have been due to blockade of vasodilatory prostaglandin synthesis or to a direct drug effect. Whatever the mechanism, indomethacin should be used with caution in patients with severe coronary-artery disease.