Diffuse and severe left ventricular dysfunction induced by epicardial coronary artery spasm.
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.
Sakata
K
K
Department of Cardiology, Shizuoka General Hospital, Japan.
Nawada
R
R
Ohbayashi
K
K
Tamekiyo
H
H
Yoshida
H
H
D000109:Acetylcholine; D000328:Adult; D000368:Aged; D001706:Biopsy; D006328:Cardiac Catheterization; D002311:Cardiomyopathy, Dilated / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D002317:Cardiovascular Agents / Q000494:pharmacology / Q000627:therapeutic use; D017023:Coronary Angiography; D003329:Coronary Vasospasm / Q000150:complications*; D004730:Endothelium, Vascular / Q000473:pathology; D005260:Female; D006352:Heart Ventricles / Q000473:pathology; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D012720:Severity of Illness Index; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology
D002317:Cardiovascular Agents; D000109:Acetylcholine