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(Circulation. 2006;114:196-200.)
© 2006 American Heart Association, Inc.

Congenital Heart Disease

The Coronary Microcirculation in Cyanotic Congenital Heart Disease

Eduard I. Dedkov, MD, PhD; Joseph K. Perloff, MD; Robert J. Tomanek, PhD; Michael C. Fishbein, MD; David D. Gutterman, MD

From the Department of Anatomy and Cell Biology and the Cardiovascular Center (E.I.D., R.J.T.), University of Iowa Carver College of Medicine, Iowa City; the Cardiovascular Center, Medical College of Wisconsin (D.D.G.), Milwaukee; and the Ahmanson/UCLA Adult Congenital Heart Disease Center and the Department of Pathology and Laboratory Medicine (J.K.P., M.C.F.), Geffen School of Medicine at the University of California at Los Angeles, Los Angeles.

Correspondence to Joseph K. Perloff, MD, Ahmanson/UCLA Adult Congenital Heart Disease Center, 650 Charles E. Young Dr S, Room 47-123-CHS, Box 951679, Los Angeles, CA 90095-1679. E-mail josephperloff{at}earthlink.net

Received November 19, 2005; revision received April 15, 2006; accepted May 5, 2006.

Background— Despite an appreciable increase in basal coronary blood flow in cyanotic congenital heart disease, flow reserve remains normal. We hypothesized that preservation of flow reserve resides in remodeling of the coronary microcirculation. Microcirculatory morphometric analyses were performed to test this hypothesis.

Methods and Results— Necropsy specimens from 4 sources were studied: (1) hearts from patients with Eisenmenger’s syndrome (A; n=5), (2) structurally abnormal hearts with ventricular hypertrophy (B; n=8), (3) structurally normal hearts with ventricular hypertrophy (C; n=6), and (4) normal hearts (D; n=5). To compare responses of the microcirculation to hypoxia versus hypertrophy, sections were taken from the left ventricular free wall, which in group A, was hypoxemic but not hypertrophied; in groups B and C, was hypertrophied but not hypoxemic; and in group D, was neither hypertrophied nor hypoxemic. Coronary arterioles were immunolabeled for smooth muscle -actin. Measured morphometric parameters included long and short axes, area, and perimeter. Arteriolar length, volume and surface densities were calculated. There was a significant intergroup difference for arteriolar length density (P=0.03) and diameter (P=0.03). Total length density in group A hearts was markedly lower, but mean arteriolar diameter was significantly greater (34%) compared with group B (P=0.03). Arteriolar volume density was similar to that in the other groups.

Conclusions— Remodeling of the coronary microcirculation is the key mechanism for preservation of flow reserve in cyanotic congenital heart disease. The increase in short axis (diameter) compensated for lower arteriolar length density and was the principal anatomic basis for maintenance of normal flow reserve.

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