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ET-1 levels in cardioischemic patients undergoing atrial pacing
C Parlapiano1, M C Borgia, G Tonnarini
1Dipartimento di Scienze Cliniche, Istituto di Cardiochirurgia, Policlinico Umberto I, Università di Roma La Sapienza, Italia.
Insights
In cardioischemic patients, rapid heart rates during atrial pacing trigger myocardial ischemia and increase endothelin-1 (ET-1) release from the coronary endothelium. This suggests ET-1 plays a role in tachycardia-induced ischemia.
Area of Science:
- Cardiology
- Vascular Physiology
Background:
- Tachycardia can induce myocardial ischemia in patients with coronary artery disease.
- Endothelin-1 (ET-1) is a potent vasoconstrictor implicated in cardiovascular function.
Purpose of the Study:
- To investigate the release of endothelin-1 (ET-1) during tachycardia-induced myocardial ischemia in patients with coronary artery disease.
- To assess the relationship between atrial pacing, myocardial ischemia, and ET-1 levels.
Main Methods:
- Eleven patients with cardioischemia underwent atrial pacing (AP) to induce ischemia.
- Six control subjects underwent maximal pacing.
- Plasma ET-1 and lactate levels were measured in the coronary sinus and aortic root during the procedures.
Main Results:
- Atrial pacing induced electrocardiographic and metabolic signs of myocardial ischemia and reduced left ventricular ejection fraction in patients.
- Coronary sinus ET-1 levels were significantly higher than arterial levels during AP-induced ischemia in patients (p<0.001).
- No significant difference in ET-1 levels was observed between coronary sinus and arterial blood in control subjects at maximum pacing (p=0.186).
Conclusions:
- Tachycardia provokes myocardial ischemia in cardioischemic patients.
- The coronary endothelium releases significant amounts of ET-1 in response to tachycardia-induced ischemia in these patients.
- ET-1 may contribute to the pathophysiology of ischemia during rapid heart rates in coronary artery disease.
Abstract:
Atrial pacing (AP) procedure was carried out in 11 cardioischemic patients to reproduce tachycardia-induced myocardial ischemia. Six control subjects underwent the same procedure until the maximum pacing rate was reached. During the procedure, endothelin-1 (ET-1) and plasma lactate levels were measured in the coronary sinus and in the aortic root. In all the patients, atrial pacing provoked electrocardiographic signs and metabolic evidence of myocardial ischemia and a significant decrease (p<0.001) in left ventricular ejection fraction. At AP-induced ischemia, coronary sinus (17.31 +/- 4.20 pg/mL) and arterial (9.60 +/- 3.31 pg/mL) ET-1 plasma levels were significantly different (p<0.001) in the patients. On the contrary, at maximum pacing rate, no significant difference (p=0.186) emerged between coronary sinus (9.72 +/- 1.09 pg/mL) and arterial (8.95 +/- 0.75 pg/mL) plasma ET-1 levels in the control group. These results suggest that, in cardioischemic patients, tachycardia can induce the coronary endothelium to release significant amounts of ET-1.