Open AccessIncreased serotonin release across the coronary bed during a nonischemic interval in patients with vasospastic angina
Author(s) -
Murakami Yo,
Ishinaga Yuji,
Sano Kazuya,
Murakami Rinji,
Kinoshita Yoshihisa,
Kitamura Jun,
Kobayashi Kanako,
Okada Seiji,
Shimada Toshio,
Morioka Shigefumi,
Matsubara Kazuo
Publication year - 1996
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960190606
Subject(s) - medicine , cardiology , vasospastic angina , angina , serotonin , interval (graph theory) , anesthesia , myocardial infarction , receptor , mathematics , combinatorics
Background : Platelet activation and coagulation abnormality have been observed during coronary spasm. It is crucial whether platelet activation occurs even during a nonischemic period. Hypothesis : This study was designed to determine whether platelets might be activated across the coronary bed during a nonischemic interval in patients with vasospastic angina. Methods : Plasma levels of serotonin, 6‐keto‐prostaglandin F1 α, and catecholamines in the aorta and the coronary sinus were simultaneously measured in 16 patients with vasospastic angina and 13 control patients with nonischemic heart disease. Results : None of these patients showed myocardial ischemia during sampling. The difference in transcardiac plasma levels of serotonin in patients with vasospastic angina was significantly higher than that in controls (1.48 ± 1.08 ng/ml vs. 0.07 ± 0.12 ng/ml, respectively, p<0.001). Coronary sinus plasma norepinephrine levels in these two groups were almost the same (204.8 ± 110.8 pg/ml vs. 190.4 ± 131.6 pg/ml, respectively). The ratio of 6‐keto‐prostaglandin F1 α in the coronary sinus and the aorta was not different between the two groups (1.17 ± 0.96 in patients with vasospastic angina vs. 1.15 ± 0.68 in controls). Conclusions : These data suggest that platelet activation across the coronary bed should be ascribed to endothelial dysfunction. Lack of compensatory enhancement of prostacyclin production might be concerned with dysfunction of coronary endothelial cells in these patients.