ENDOTHELIN CONCENTRATIONS IN CORONARY SINUS DURING ATRIAL PACING-INDUCED MYOCARDIAL-ISCHEMIA

Citation
J. Vojacek et al., ENDOTHELIN CONCENTRATIONS IN CORONARY SINUS DURING ATRIAL PACING-INDUCED MYOCARDIAL-ISCHEMIA, Cardiology, 85(3-4), 1994, pp. 154-160
Citations number
27
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00086312
Volume
85
Issue
3-4
Year of publication
1994
Pages
154 - 160
Database
ISI
SICI code
0008-6312(1994)85:3-4<154:ECICSD>2.0.ZU;2-1
Abstract
To investigate the possible role of endothelin in coronary vasoconstri ction contributing to the development of myocardial ischemia, plasma e ndothelin concentrations at rest and during atrial pacing-induced myoc ardial ischemia have been measured in blood samples drawn from the aor ta and coronary sinus in 12 patients with significant narrowing of the left anterior descending coronary artery. The plasma endothelin conce ntrations at rest were similar in the aorta (AO/R) and coronary sinus (CS/R) (4.8 +/- 2.4 and 4.5 +/- 1.7 pg/ml, respectively), the differen ce between coronary sinus and aorta plasma endothelin concentration (C S/R-AO/R) being -0.3 +/- 1.7 pg/ml. During atrial pacing-induced myoca rdial ischemia aortic plasma endothelin concentration (AO/P) did not c hange(4.6 +/- 2.6 pg/ml) and only an insignificant increase in the pla sma endothelin concentration in the coronary sinus (CS/P) was observed (5.3 +/- 2.8 pg/ml). The difference between coronary sinus and aortic endothelin plasma concentration (CS/P-AO/P) was 0.6 +/- 2.5 pg/ml. Fin ally, the difference in endothelin concentrations between coronary sin us and aorta rose only insignificantly during pacing as compared to th e resting values ([CS/P-AO/P] - [CS/R-AP/R] being 0.9 +/- 3.2 pg/ml). Thus, atrial pacing-induced myocardial ischemia in patients with signi ficant left anterior descending coronary artery stenosis was not accom panied by significant changes in coronary sinus plasma endothelin conc entrations. This suggests that increased release of endothelin into pl asma is probably not responsible for coronary artery vasoconstriction in patients with significant coronary artery narrowings. However, neit her of two other possibilities can be ruled out: that basal level of e ndothelin secretion is a prerequisite for the effect of another vasoco nstrictor or that local intraluminal or abluminal secretion and uptake of endothelin occurs.