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Cardiac release and kinetics of endothelin after severe short-lasting myocardial ischemia
D Krüger1, A Sheikhzadeh, E Giannitsis
1Department of Cardiology, University Hospital Lübeck, Germany.
Insights
Short-lasting myocardial ischemia triggers significant endothelin (ET) release from the heart. This cardiac ET release persists for up to one hour following the ischemic event.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Biochemistry
Background:
- Endothelin (ET) is a vasoactive peptide produced by the endothelium.
- Previous studies have not definitively proven cardiac release of ET during ischemic syndromes.
Purpose of the Study:
- To investigate the kinetics of endothelin release following induced short-lasting myocardial ischemia.
- To determine if endothelin is released from the heart during ischemia.
Main Methods:
- Coronary sinus and peripheral vein blood samples were collected from 23 patients with coronary artery disease undergoing atrial pacing.
- Measurements included endothelin (ET), cardiac troponin-T (TnT), myoglobin (Mb), and creatine kinase (CK) at various time points before and after pacing.
- Myocardial ischemia was confirmed by angina, abnormal cardiac lactate metabolism, and ST segment depression.
Main Results:
- Pacing induced severe ischemia in most patients, confirmed by ST depression and angina.
- Endothelin levels significantly increased in both coronary sinus and peripheral veins post-pacing, with higher concentrations in the coronary sinus.
- Transient elevations in myoglobin were observed, while troponin-T and CK remained normal.
Conclusions:
- Short-lasting, severe myocardial ischemia is associated with significant endothelin release originating from the heart.
- Cardiac endothelin release was detectable for up to one hour after the ischemic episode.
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:
A 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 Endothelin (ET), cardiac troponin-T (TnT), myoglobin (Mb) and creatine kinase (CK) samples were withdrawn from the coronary sinus and a peripheral vein before and 1, 5, 10, 30 and 45 min and 1, 2, 3 and 6 h after pacing. The appearance of angina pectoris, abnormal cardiac lactate metabolism and ST segment depression were further criteria for myocardial ischemia.
Results:
In the study group, pacing stress induced severe ischemia (mean duration +/- SD 6.1 +/- 1.2 min), with a maximum of 0.34 +/- 0.12-mV ST segment depression in 21 of 23 patients and angina 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 a transient elevation of Mb with a maximum after 3 h was detected (86.4 +/- 27.1 micrograms/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 a control group of 18 patients without heart disease, all variables were unchanged.
Conclusions:
Short-lasting severe myocardial ischemia was associated with significant ET release of cardiac origin that lasted up to 1 h.