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Echocardiographic Assessment of Cardiac Anatomy and Function in Adult Rats
Published on: December 13, 2019
The angiotensin infusion test as a method of evaluating left ventricular function
Insights
The angiotensin infusion method for measuring left ventricular function is unreliable. This study found variable responses in patients with and without heart disease, making it difficult to differentiate between groups.
Area of Science:
- Cardiology
- Physiology
Background:
- Assessing left ventricular function is crucial in cardiology.
- The angiotensin infusion method has been explored as a diagnostic tool.
Purpose of the Study:
- To evaluate the reliability of the angiotensin infusion method for measuring left ventricular function.
- To compare ventricular responses to angiotensin infusion in healthy individuals versus patients with coronary artery disease.
Main Methods:
- Left ventricular function was assessed using angiotensin infusion in 15 patients.
- Patients were divided into two groups: those without heart disease (n=7) and those with coronary artery disease (n=8).
- Cardiac index and heart rate changes were monitored during infusion, and ventricular function curves were analyzed.
Main Results:
- Angiotensin infusion caused decreased cardiac index in both healthy subjects and those with coronary artery disease.
- Ventricular function curves showed variable responses, with many exhibiting flat or descending slopes.
- The method failed to reliably differentiate between patients with and without heart disease due to similar curve patterns.
Conclusions:
- The angiotensin infusion method yields highly variable results in left ventricular function assessment.
- Factors like baroreceptor reflex, increased coronary resistance, and afterload likely contribute to the observed variability.
- The angiotensin infusion method is not a reliable tool for evaluating ventricular function.
Abstract:
Fifteen patients had left ventricular function measured by the angiotensin infusion method. Seven patients had no evidence of heart disease, and eight patients had angina pectoris and coronary arteriographic evidence of coronary disease without congestive heart failure. During angiotensin infusion, those patients without heart disease had a decrease in cardiac index (average, 0.63 L. per minute per square meter) and a decrease in heart rate (average, 12 beats per minute.) The ventricular function curve had a poor SWI response in four of the seven subjects. The patients with coronary artery disease also had a reduction in cardiac index during angiotensin (average, 0.44 L. per minute per square meter) and the heart rate was unchanged in four subjects, increased in two subjects, and decreased in two subjects. Six of the subjects had flat or descending slopes on the function curve, and in one subject there was only a very gradual ascending slope. Many of the curves of both groups looked similar so that the function curves did not differentiate between those patients with or without heart disease. The mechanism for production of bradycardia, reduction of cardiac output, and depressed function curves with angiotensin is multifactorial, but is probably due to the baroreceptor reflex response, the increase in coronary artery resistance, and possible to the direct effect of increased left ventricular afterload itself. The ventricular response to angiotensin is so variable that the angiotensin infusion method of evaluating ventricular function is not reliable.
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