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Updated: Aug 19, 2026

Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders
Published on: August 18, 2016
Diffuse and severe left ventricular dysfunction induced by epicardial coronary artery spasm
K Sakata1, R Nawada, K Ohbayashi
1Department of Cardiology, Shizuoka General Hospital, Japan.
Insights
Epicardial coronary artery spasm can cause severe left ventricular dysfunction, mimicking dilated cardiomyopathy (DCM). Early identification via acetylcholine testing and treatment with antianginal drugs significantly improve cardiac function in these vasospastic angina patients.
Area of Science:
- Cardiology
- Vascular Biology
- Cardiac Imaging
Background:
- Dilated cardiomyopathy (DCM) may involve coronary artery spasm.
- Investigating epicardial coronary artery spasm as a cause of severe cardiac dysfunction.
Observation:
- 34 patients with unexplained left ventricular hypokinesis underwent acetylcholine testing.
- 9 patients (35%) diagnosed with DCM-like vasospastic angina (VSA) showed spasm.
- DCM and DCM-like VSA groups had similar clinical and biopsy data.
Findings:
- DCM-like VSA patients had acetylcholine-induced diffuse, multivessel coronary spasm.
- Left ventricular end-systolic volume was greater in DCM than DCM-like VSA.
- Both groups improved with treatment, but DCM-like VSA showed greater ejection fraction and fractional shortening increases.
Implications:
- Epicardial coronary artery spasm can induce DCM-like left ventricular dysfunction.
- Acetylcholine testing is crucial for diagnosing DCM-like VSA.
- Antianginal drugs significantly improve cardiac function in DCM-like VSA.
Abstract:
Endothelial dysfunction and effectiveness of treatment of calcium antagonists are suggestive of coronary artery spasm as an underlying disorder in dilated cardiomyopathy (DCM). The aim of this study is to determine whether or not the epicardial coronary artery spasm can induce severe cardiac dysfunction like DCM. Thirty-four consecutive patients with angiographically normal coronary arteries and diffuse left ventricular hypokinesis whose causes had been unknown underwent acetylcholine provocation test and left ventricular biopsy. Eight patients were excluded according to the clinical and laboratory data and biopsy findings suggesting myocarditis or other systemic diseases. According to the results of the acetylcholine provocation test, 17 patients were finally diagnosed as having DCM, and nine patients (35% of the study patients), who had acetylcholine-induced diffuse and multivessel coronary spasm, were diagnosed as having DCM-like vasospastic angina pectoris (VSA). Clinical and cardiac catheterization data including hemodynamics and biopsy findings were similar between the two groups except that left ventricular end-systolic volume was significantly greater in DCM than in DCM-like VSA. After the acetylcholine provocation test, DCM patients received both a beta blocker and an angiotensin-converting enzyme inhibitor, and DCM-like VSA patients received antianginal drugs. In echocardiographic findings at predischarge and those after 6-month drug treatment, both DCM-lke VSA and DCM showed significant reduction in end-diastolic and end-systolic diameters and significant increase in fractional shortening and ejection fraction, whereas changes in ejection fraction and fractional shortening were significantly greater in DCM-like VSA than those in DCM. Epicardial coronary artery spasm can induce diffuse and severe left ventricular dysfunction like DCM in VSA. Although antianginal drugs markedly improve left ventricular function of these patients, only the acetylcholine provocation test can identify DCM-like VSA.
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