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CLINICAL STUDIES

Coronary endothelial dysfunction in patients with acute-onset idiopathic dilated cardiomyopathy

^a Cardiac Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA

Manuscript received March 24, 1997; revised manuscript received March 26, 1998, accepted April 9, 1998.

Address for correspondence: Dr. Marc J. Semigran, Heart Failure/Transplant Office, Gray 645, Massachusetts General Hospital, Fruit Street, Boston, Massachusetts 02114
semigran.marc{at}mgh.harvard.edu

Objectives. This study sought to determine whether coronary endothelial dysfunction exists in patients with acute-onset idiopathic dilated cardiomyopathy (DCM) and to explore its relation to recovery of left ventricular systolic function in this patient population.

Background. Coronary endothelial dysfunction exists in chronic DCM, but its importance in the development and progression of ventricular dysfunction is not known. To address this issue we studied coronary endothelial function in patients with idiopathic DCM <6 months in duration and explored the relation between coronary endothelial function and subsequent changes in left ventricular ejection fraction (LVEF).

Methods. Ten patients with acute-onset idiopathic DCM (duration of heart failure symptoms 2.0 ± 0.4 months [mean ± SEM]) and 11 control patients with normal left ventricular function underwent assessment of coronary endothelial function during intracoronary administration of the endothelium-dependent vasodilator acetylcholine and the endothelium-independent vasodilator adenosine. Coronary cross-sectional area (CSA) was determined by quantitative coronary angiography and coronary blood flow (CBF) by the product of coronary CSA and CBF velocity measured by an intracoronary Doppler catheter. Patients with DCM underwent assessment of left ventricular function before and several months after the study.

Results. Acetylcholine infusion produced no change in coronary CSA in control patients but significant epicardial constriction in patients with DCM (–36 ± 11%, p < 0.01). These changes were associated with increases in CBF in control patients (+118 ± 49%, p < 0.01) but no change in patients with DCM. Infusion of adenosine produced increases in coronary caliber and blood flow in both groups. Follow-up assessment of left ventricular function was obtained in nine patients with DCM 7.0 ± 1.7 months after initial study, at which time LVEF had improved by 0.10 in four patients. Multiple linear regression revealed a positive correlation between both the coronary CSA (r² = 0.57, p < 0.05) and CBF (r² = 0.68, p < 0.01) response to acetylcholine and the subsequent improvement in LVEF.

Conclusions. Coronary endothelial dysfunction exists at both the microvascular and the epicardial level in patients with acute-onset idiopathic DCM. The preservation of coronary endothelial function in this population is associated with subsequent improvement in left ventricular function.

Abbreviations and Acronyms   CBF = coronary blood flow   CHF = congestive heart failure   CSA = cross-sectional area   DCM = dilated cardiomyopathy   LVEF = left ventricular ejection fraction   LVSWI = left ventricular stroke work index   MAP = mean arterial pressure   PCWP = pulmonary capillary wedge pressure   C1 = control solution of 5% dextrose in water (acetylcholine vehicle)   C2 = control solution of 0.9% NaCl (adenosine vehicle)

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