Objectives. The purpose of this study was to evaluate whether a serotonin blocker, sarpogrelate, improves exercise capacity as a result of vasodilation of coronary collateral channels in patients with effort angina. Background Serotonin has been reported to decrease coronary collateral blood flow by collateral vasoconstriction in a canine model, suggesting that platelet activation in feeding coronary arteries of the collateral network has the potential to cause collateral vasoconstriction. Methods. The subjects consisted of 22 patients with effort angina and reproducible ischemic threshold (group A, 11 patients with thrombolysis in myocardial infarction (TIMI) grade 2 or 3 Bow of the ischemia-related coronary artery and Rentrop's collateral index 0 or 1; group B, 11 patients with TIMI grade 0 or 1 Bow and Rentrop's collateral index 2 or 3). We repeated the symptom limited treadmill exercise test using the Balke-Ware protocol and exercise tetrofosmin myocardial perfusion scintigraphy with and without pretreatment with 200 mg orally administered sarpogrelate. Each exercise test was performed at 9:00 a.m. on different days. The order of tests with and without sarpogrelate was randomized. Results. In group A, sarpogrelate increased neither exercise time at 0.1 mV ST depression nor double product at 0.1 mV ST depression. In contrast, in group B sarpogrelate increased the exercise duration at 0.1 mV ST depression from 181 +/- 112 (SD) to 248 +/- 131 s (p < 0.05) and also increased the double product at 0.1 mV ST depression by 21% (p < 0.01). The severity score using myocardial perfusion scintigraphy at the same workload was significantly (p < 0.01) decreased by 37% in group B, but not in group A (11%), due to the sarpogrelate treatment. Conclusions. Sarpogrelate augments flow reserve of the collateral circulation and improves exercise capacity in anginal patients with well-developed collaterals. These findings indicate that a serotonin blocker, sarpogrelate, is useful not only as an antiplatelet drugs, but as an antianginal drug. (J Am Coll Cardiol 1998;32:1982-6) (C) 1998 by the American College of Cardiology.
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Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LY, England
Royal Brompton Hosp, Inst Cardiovasc Med & Sci, London SW3 6LY, EnglandUniv London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LY, England
Asbury, Elizabeth A.
Webb, Carolyn M.
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Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LY, England
Royal Brompton Hosp, Inst Cardiovasc Med & Sci, London SW3 6LY, EnglandUniv London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LY, England
Webb, Carolyn M.
Probert, Heather
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Royal Brompton & Harefield NHS Fdn Trust, Harefield Hosp, Cardiac Hlth Promot, London, EnglandUniv London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LY, England
Probert, Heather
Wright, Christine
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Royal Brompton Hosp, Inst Cardiovasc Med & Sci, London SW3 6LY, EnglandUniv London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LY, England
Wright, Christine
Barbir, Mahmoud
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Royal Brompton & Harefield NHS Fdn Trust, Harefield Hosp, Cardiac Hlth Promot, London, EnglandUniv London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LY, England
Barbir, Mahmoud
Fox, Kim
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Royal Brompton Hosp, Inst Cardiovasc Med & Sci, London SW3 6LY, EnglandUniv London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LY, England
Fox, Kim
Collins, Peter
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Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LY, England
Royal Brompton Hosp, Inst Cardiovasc Med & Sci, London SW3 6LY, EnglandUniv London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LY, England