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Hemodynamic and coronary effects of intravenous eletriptan, a 5HT1B/1D-receptor agonist
1Department of Medicine and Therapeutics, University of Glasgow, Scotland.
Insights
Eletriptan, a migraine medication, did not cause significant coronary artery constriction in patients without heart disease. This suggests potential selectivity for the 5HT1D-receptor subtype, indicating a favorable safety profile for cardiac arteries.
Area of Science:
- Cardiovascular Pharmacology
- Neuropharmacology
Background:
- Eletriptan is a 5HT1B/1D-agonist used for migraine treatment.
- Investigating its cardiovascular effects is crucial for understanding its safety profile.
Purpose of the Study:
- To evaluate the systemic, pulmonary, and coronary artery effects of intravenous eletriptan.
- To assess the impact of eletriptan on hemodynamics in patients undergoing cardiac catheterization.
Main Methods:
- Ten patients received placebo followed by intravenous eletriptan (3.33 microg/kg/min).
- Hemodynamic parameters (pressures, cardiac output) were serially measured.
- Coronary angiography assessed coronary artery dimensions.
Main Results:
- Eletriptan caused minor, statistically significant increases in pulmonary artery pressures and vascular resistance.
- Systemic vascular resistance also increased post-infusion.
- No significant overall effect on coronary arteries was observed, with one case of possible catheter-induced spasm.
Conclusions:
- Eletriptan does not induce significant coronary artery constriction in patients without obstructive coronary artery disease.
- This finding supports a potential relative selectivity for the 5HT1D-receptor subtype.
- Eletriptan appears to have a favorable safety profile regarding coronary artery effects in this population.
Objective:
To investigate the systemic, pulmonary, and coronary artery effects of eletriptan, a new 5HT1B/1D-agonist in patients undergoing cardiac catheterization.
Methods:
Ten patients (two men and eight women) without significant obstructive coronary artery disease were administered 3.33 microg/kg/min intravenous eletriptan after they were given a placebo infusion of 0.9% saline solution. Serial measurements of right heart and systemic pressures were taken at 5-minute intervals during placebo infusion, eletriptan infusion, and a 30-minute postinfusion period. Cardiac output by the thermodilution technique and coronary angiography were performed every 15 minutes. Quantitative coronary angiography was carried out to measure coronary artery dimensions.
Results:
A small but statistically significant increase in occluded wedge pressure (7.4 versus 8.8 mm Hg; 95% confidence interval [CI], 0.74, 2.51; P < .01), right atrial pressure (5.3 versus 6.1 mm Hg; 95% CI, 0.0, 1.4; P < .05), and mean pulmonary artery pressure (13.2 versus 14.6 mm Hg; 95% CI, 0.0, 2.7; P = .05) was observed during the eletriptan infusion compared with placebo. A statistically significant increase in systemic vascular resistance (1256 versus 1519 dyne/sec/cm(-5); 95% CI, 126, 398; P < .01) and pulmonary vascular resistance (76.4 versus 100.8 dyne/sec/cm(-5); 95% CI, 1.9, 46.9; P < .05) was observed in the period after drug infusion. No overall effect was observed on the coronary arteries, although a segmental right coronary artery constriction developed in one patient, possibly as a result of catheter-induced spasm.
Conclusions:
Eletriptan, a 5HT1B/1D-agonist effective in migraine, causes no significant coronary artery constriction in patients without significant obstructive coronary artery disease. This finding may reflect a relative selectivity for the 5HT1D-receptor subtype.