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J Thorac Cardiovasc Surg 2003;126:1026-1032
© 2003 The American Association for Thoracic Surgery

Surgery for congenital heart disease

Left ventricular remodeling in hearts with tricuspid atresia: morphologic observations and possible basis for ventricular dysfunction after surgery

^a Department of Pediatric Cardiology and Adult Congenital Heart Disease, Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil
^b Laboratory of Pathology, Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil

Received for publication September 23, 2002; revisions received November 13, 2002; accepted for publication December 2, 2002.

^* Address for reprints: Maria Angelica Binotto, MD, Heart Institute (InCor), University of São Paulo Medical School, Pediatric Cardiology, Av. Higienopolis, 1048/86, São Paulo 01238-000, Brazil
conangelica{at}incor.usp.br

OBJECTIVES: This study was undertaken to assess the pattern of left ventricular hypertrophy, the myocardial capillary network, and the extracellular matrix in hearts with tricuspid atresia.

METHODS: We examined 32 hearts with tricuspid atresia and 27 normal hearts from control subjects with similar age and sex distribution. Wall thickness, inlet length, and outlet length were obtained from the left ventricle. Immunohistochemical staining for von Willebrand factor was used to label myocardial capillaries. By means of computer-assisted morphometry, the following data were obtained from the inlet, apex, and outlet of the left ventricle: transverse myocyte diameter, myocyte nuclear volume fraction, capillary volume fraction, interstitial fibrous volume fraction, and endocardial thickness.

RESULTS: The wall thickness in affected hearts was not different from that in control hearts. The left ventricular outlet length was significantly greater in the malformed hearts (P = .005). The myocyte diameter did not differ from that in control hearts. The capillary volume fraction was decreased in the malformed hearts (P < .001). The interstitial fibrous deposition was greater in the malformed hearts at all sites analyzed (P < .001). Fibrosis was greater in the inlet and apex (P = .004) and also in the subendocardial half of the ventricular wall than in the subepicardial half. According to a logistic regression model, age was the only variable associated with the probability of occurrence of fibrosis.

CONCLUSIONS: Our findings in hearts with tricuspid atresia possibly represent chronically induced volume overload in the presence of ischemia, rather than a typical model of volume overload. A decreased capillary volume fraction may indicate a greater susceptibility to ischemia. Fibrous deposition probably occurs early in life.

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