Decrease of nitric oxide end-products during coronary circulation reflectselevated basal coronary artery tone in patients with vasospastic angina

Citation
T. Hori et al., Decrease of nitric oxide end-products during coronary circulation reflectselevated basal coronary artery tone in patients with vasospastic angina, JPN HEART J, 41(5), 2000, pp. 583-595
Citations number
35
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
JAPANESE HEART JOURNAL
ISSN journal
00214868 → ACNP
Volume
41
Issue
5
Year of publication
2000
Pages
583 - 595
Database
ISI
SICI code
0021-4868(200009)41:5<583:DONOED>2.0.ZU;2-Z
Abstract
The aim of this study was to investigate the role of nitric oxide (NO) in t he coronary circulation and its relation to basal coronary artery tone in p atients with vasospastic angina (VSA). We evaluated the level of nitric oxi de end-products (NOx; nitrite + nitrate) in coronary circulation blood usin g an HPLC-Griess system for nine patients with VSA and nine control patient s. All of the patients with VSA experienced focal spasm in the proximal to middle segments of the left anterior descending coronary artery (LAD) in re sponse to intracoronary injection of ergonovine maleate. The luminal diamet er of the coronary artery was measured in each patient by quantitative coro nary arteriography. Blood samples for NOx measurement were obtained from th e coronary sinus (NOx(V)) and the ostium of the left coronary artery (NOx(A )). The NOx difference, calculated from the coronary venous-arterial differ ence in NOx, was close to zero for the control patients whereas it was clea rly negative for the patients with VSA. In addition, the NOx difference in the patients with VSA showed a negative correlation with basal coronary art ery tone (r = - 0.91, p < 0.01) and a positive correlation with the dose of ergonovine required for spasm provocation (r = 0.77, p < 0.05). These resu lts indicate that increased basal coronary artery tone and higher susceptib ility to ergonovine in patients with VSA would be a consequence of coronary endothelial dysfunction as in indicated by NOx.