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Plasma endothelin in coronary venous blood from patients with either stable or unstable angina
J T Stewart1, J A Nisbet, M J Davies
1Department of Cardiological Sciences, St George's Hospital Medical School, London.
Insights
This study found no evidence that elevated endothelin levels in coronary blood cause unstable angina. Endothelin concentrations were similar in patients with stable and unstable angina, and healthy controls.
Area of Science:
- Cardiovascular Medicine
- Endocrinology
Background:
- Endothelin is a potent vasoconstrictor implicated in cardiovascular regulation.
- Unstable angina involves acute coronary syndromes where endothelial dysfunction is suspected.
Purpose of the Study:
- To investigate if active coronary endothelial lesions in unstable angina increase endothelin concentration in coronary venous blood.
Main Methods:
- Blood samples were collected from patients with stable or unstable angina during cardiac catheterization.
- Control samples were obtained from healthy individuals and hemodialysis patients.
Main Results:
- Coronary venous endothelin levels in unstable angina (2.32 ng/l) were not significantly different from stable angina (2.77 ng/l).
- Endothelin concentrations did not differ between angina groups, systemic venous blood, or healthy controls.
- Significantly higher endothelin levels were observed in hemodialysis patients.
Conclusions:
- The study does not support the hypothesis that increased coronary endothelin contributes to unstable angina.
- Elevated systemic endothelin post-myocardial infarction may represent a systemic response.
Study Objective:
To test the hypothesis that the active coronary endothelial lesions in unstable angina raise the endothelin concentration in coronary venous blood.
Design:
Systemic and coronary venous blood samples were obtained from unselected patients with the clinical syndromes of either stable or unstable angina at the time of cardiac catheterisation and coronary arteriography. Control venous blood samples were obtained from healthy laboratory workers and from patients with chronic renal failure treated by intermittent haemodialysis.
Patients:
Twelve patients with angina: seven with stable symptoms and five with unstable angina.
Results:
The mean coronary venous endothelin concentration in unstable angina was 2.32 ng/l (range 1.7-3.2 ng/l). In stable angina it was 2.77 ng/l (range 2.1-4.4 ng/l). These values were not significantly different from one another nor from the values obtained in systemic venous blood from either group or from the healthy controls. Circulating endothelin concentrations were much higher in venous blood from the patients treated by haemodialysis.
Conclusions:
These data do not support the hypothesis that raised endothelin concentrations in coronary blood in patients with unstable angina may modulate variations in coronary arterial tone thereby contributing to the clinical syndrome of chest pain and electrocardiographic changes at rest. The raised endothelin concentrations seen in systemic venous blood after myocardial infarction may be part of the systemic response to myocardial infarction.