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Assessment of left ventricular myocardial perfusion and diastolic function during acetylcholine-induced diffuse
1Division of Cardiology, Shimada Municipal Hospital, Shizuoka, Japan.
Insights
Acetylcholine-induced diffuse coronary vasoconstriction can impair myocardial blood flow and cause diastolic dysfunction. This study highlights a potential mechanism for ischemia in patients without significant coronary stenosis.
Area of Science:
- Cardiology
- Physiology
Background:
- Investigated the link between diffuse coronary vasoconstriction and myocardial ischemia.
- Focused on patients with chest pain and no significant coronary artery disease.
Purpose of the Study:
- To determine if acetylcholine-induced diffuse coronary vasoconstriction leads to myocardial ischemia.
- To assess the impact on left ventricular diastolic function.
Main Methods:
- Acetylcholine provocation test in 30 patients (40 arteries).
- Doppler echocardiography to measure mitral inflow (E:A ratio).
- Thallium-201 scintigraphy for myocardial perfusion assessment.
Main Results:
- Diffuse vasoconstriction occurred in 45% of arteries, decreasing the E:A ratio (0.83 to 0.77, P=0.031).
- Focal spasm occurred in 5 arteries, significantly reducing the E:A ratio (0.83 to 0.66, P=0.043).
- Thallium-201 defects were observed in 80% of diffuse vasoconstriction territories.
Conclusions:
- Intracoronary acetylcholine-induced diffuse coronary vasoconstriction reduces myocardial blood flow.
- This vasoconstriction can cause global left ventricular diastolic dysfunction.
Background:
We investigated whether diffuse coronary vasoconstriction induced by acetylcholine caused myocardial ischemia.
Methods:
We studied 30 patients (40 coronary arteries) with spontaneous chest pain or equivocal studies on treadmill exercise testing and no significant coronary stenosis or previous myocardial infarction. During the acetylcholine provocation test, Doppler echocardiography was performed, and thallium-201 was injected intravenously for scintigraphy. We used Doppler echocardiography to measure the ratio of early-to-late peak mitral flow (E:A ratio).
Results:
When acetylcholine was injected, the coronary arteries showed three different responses. Diffuse coronary vasoconstriction without chest pain or ischemic changes on the ECG was induced in 18 (45%) arteries and the E:A ratio decreased from 0.83 +/- 0.13 to 0.77 +/- 0.13 (P = 0.031). In 17 vessels (control arteries), the E:A ratio did not change significantly (from 0.88 +/- 0.15 to 0.88 +/- 0.18; P = 0.95). In five arteries, focal spasm was induced and the E:A ratio decreased from 0.83 +/- 0.18 to 0.66 +/- 0.13 (P = 0.043). Transient defects on thallium-201 scintigraphy were observed in the territory of eight (80%) arteries with diffuse vasoconstriction and in one (20%) control artery (P = 0.047).
Conclusions:
Diffuse coronary vasoconstriction induced by intracoronary acetylcholine can decrease the regional myocardial blood flow (as shown by thallium-201 scintigraphy) and can cause global left ventricular diastolic dysfunction (as shown by the results of Doppler echocardiography).