Abstract

Endothelin (ET) is an endothelium-derived vasoactive peptide, its possible contribution to myocardial ischemia and infarction is not yet well understood. was to elucidate whether a brief period of myocardial ischemia (CI) not leading to myocardial infarction may increase plasma ET levels and to determine the kinetics of a possible ET release. A coronary sinus lactate study with incremental atrial pacing was performed in 16 patients (pts) with obstructive coronary artery multivessel disease (CAD). A Zucker-catheter was positioned in the distal coronary sinus for incremental atrial pacing (100–160 bpm) and lactate sampling. ET was measured by a radio-immuno-assay 1100% ET-1, 52% ET-2, 96% ET-3, 7% Big-ET, Nichols Institute). ET, cardiac troponin-T (TnT, Boehringer Mannheim) and creatine phosphokinase (CPK) samples were withdrawn from the coronary sinus (CS) and a peripheral vein (PV) before and at time 1, 5, 10, 30, 45 min, 1, 2, 3, 6 h after pacing. Significant ST depressions in the 12-lead ECG after pacing was a further criterion for CI. A comparison to the results of a control group (CG, n = 13) without heart disease and statistical analysis was done. In CAD pacing stress induced a CI in all pts (duration 6.1 ± 1.2 min). The mean cardiac lactate production was 143.9 ± 19.3% compared with the arterial lactate concentration, all pts suffered from typical angina pectoris, significant ST depressions of 0.32 ± 0.11 mV were found in 14/16 pts. All pts developed pathological elevated ET concentration, whereas the levels in the CG were within the limits of normal (p < 0.003). The mean ET concentrations increased from 5.0 pg/ml in CS and PV before pacing to 10.9 pg/ml in CS and 8.9 pg/ml in PV at 1 min after the end of pacing. The concentrations further remained elevated within 1 h after pacing with higher levels in CS than in PV due to a persisting cardiac release of ET, ET concentrations dropped to the limits of normal (2.3–5.3 pg/ml) after 1 h with identical levels in CS and PV In both groups TnT and CPK were not elevated, no signs of CI were detected in the CG. A short lasting severe myocardial ischemia without myocardial infarction was followed by a significant ET release for 1 h reaching 218% of the base line concentration in CS and 178% in PV respectively. The higher ET levels in CS compared to PV indicate, that the ET release is of cardiac origin.

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