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Catecholamine release in coronary sinus during vasospastic angina induced by ergonovine
Insights
This study found that during coronary vasospasm in angina patients, peripheral catecholamine levels increased, while myocardial catecholamine release decreased. This suggests sympathetic activation and sequestration in ischemic areas.
Area of Science:
- Cardiology
- Neuroscience
- Pharmacology
Background:
- Spontaneous angina involves coronary artery spasms.
- Catecholamines, like norepinephrine and epinephrine, play roles in cardiac function and stress responses.
- Understanding catecholamine dynamics during angina is crucial for diagnosis and treatment.
Purpose of the Study:
- To investigate myocardial and arterial catecholamine levels and release during ergonovine-induced coronary vasospasm in patients with spontaneous angina.
- To correlate hemodynamic changes with catecholamine responses during ischemic events.
Main Methods:
- Assessed aortic and coronary sinus norepinephrine and epinephrine concentrations in seven angina patients and three controls.
- Measured hemodynamic parameters (heart rate, blood pressure, LVEDP, coronary sinus flow) at rest and during ergonovine testing.
- Analyzed net myocardial release and arterial concentrations of catecholamines.
Main Results:
- Ergonovine induced coronary spasm, reduced coronary sinus flow, and slightly increased arterial epinephrine and norepinephrine in ischemic patients.
- A significant decrease in net myocardial norepinephrine and epinephrine release was observed in angina patients during vasospasm.
- Control subjects showed no significant changes in catecholamine levels or release after ergonovine.
Conclusions:
- Increased peripheral catecholamine concentrations during angina may indicate reflex sympathetic activation due to ischemia-induced ventricular dysfunction.
- Decreased myocardial catecholamine release during angina could be due to sequestration in ischemic areas or reflex inhibition of cardiac sympathetic tone.
Abstract:
In seven patients with spontaneous angina and three control subjects, aortic and coronary sinus norepinephrine and epinephrine were assessed. Samples were taken in basal conditions and during ergonovine test in coronary sinus and aorta. The behaviour of some hemodynamic parameters as heart rate, blood pressure, left ventricular end diastolic pressure and coronary sinus flow was also studied. Resting myocardial norepinephrine and epinephrine flux was similar for both groups. In ischemic patients ergonovine induced a coronary spasm accompanied by an evident reduction of coronary sinus flow and a slight increase in arterial epinephrine and norepinephrine concentrations. However, a significant decrease in the net myocardial norepinephrine and epinephrine release was evidenced. After ergonovine, not significant changes in norepinephrine and epinephrine concentration and release resulted in control subjects. The increase in peripheral catecholamine concentrations found in ischemic patients during ergonovine test could represent a reflex activation of sympathetic activity induced by an ischemia dependent ventricular mechanical disfunction. The decrease in myocardial catecholamine release during angina could be justified by sequestration of epinephrine and norepinephrine in ischemic areas induced by vasospasm or reflex inhibition of cardiac sympathetic tone.