Cardiac Release and Kinetics of Endothelin After Severe Short-Lasting Myocardial Ischemi

Objectives. The aim of this study was to investigate the release kinetics of endothelin after induced short-lasting myocardial ischemia. Background. Endothelin is an endothelium-derived vasoactive peptide. Unequivocal proof of its cardiac release in ischemic syndromes has not yet been demonstrated. Methods. coronary sinus study with atrial pacing was performed in 23 patients with coronary artery disease. Endothelin (ET), cardiac troponin-T (TnT), myoglobin (Mb) and creatine kinase (CK) samples were withdrawn from the coronary sinus and peripheral vein before and 1, 5, 10, 30 and 45 min and 1, 2, 3 and 6 h after pacing. The appearance of angin pectoris, abnormal cardiac lactate metabolism and ST segment depression were further criteri for myocardial ischemia. Results. In the study group, pacing stress induced severe ischemi (mean duration ± SD 6.1 ± 1.2 min), with maximum of 0.34 ± 0.12-mV ST segment depression in 21 of 23 patients and angin pectoris in 22 of 23. The maximal cardiac lactate production was 42.8 ± 17.3% (p < 0.03). TnT and CK levels in the total group were normal; in 14 of 23 patients transient elevation of Mb with maximum after 3 h was detected (86.4 ± 27.1 μg/liter, p < 0.03). The ET concentrations increased significantly (p < 0.001) in the coronary sinus (from 4.6 ± 0.8 [baseline] to 12.9 ± 2.7 pg/ml at 1 min after cessation of pacing) and the peripheral vein, respectively (from 4.7 ± 0.7 [baseline] to 8.3 ± 2.1 pg/ml at 1 min). ET further remained elevated for 1 h with persisting higher coronary sinus than peripheral venous concentrations, indicating cardiac ET release. In control group of 18 patients without heart disease, all variables were unchanged. Conclusions. Short-lasting severe myocardial ischemi was associated with significant ET release of cardiac origin that lasted up to 1 h.