Why the study?
Does pulmonary artery size influence postoperative hemodynamics in patients undergoing the Fontan operation?
Does pulmonary artery size influence postoperative hemodynamics in patients undergoing the Fontan operation?
Smaller pulmonary artery size (PAI < 100 mm2/m2) is hemodynamically disadvantageous after the Fontan operation, leading to increased afterload and peak central venous pressure.
May flag hemodynamic risk in Fontan candidates with small PAI; leaves open whether size optimization improves outcomes.
BACKGROUND: The outcome of the Fontan operation largely depends on patient selection because this procedure is a physiological correction. Among the several selection criteria for the Fontan operation, the importance of adequate size of the pulmonary artery remains controversial. To clarify whether or not pulmonary artery size is indispensable as one of the selection criteria for the Fontan operation, we considered the physiological importance of pulmonary artery size and investigated how pulmonary artery size influenced postoperative hemodynamics of the Fontan operation. METHODS AND RESULTS: In congenital heart disease of decreasing pulmonary blood flow, 40 patients were examined for this analysis. Pulmonary artery indexes (cross-sectional area of the right and left pulmonary arteries divided by body surface area) were measured as the expression of pulmonary artery size, and the relations of pulmonary artery index (PAI) to pulmonary vascular resistance (Rp) and compliance (Cp) were studied. There was no significant correlation between PAI and Rp, whereas a significant correlation was found between PAI and Cp (r = .71, P = .001). Furthermore, Cp influenced postoperative hemodynamics of the Fontan operation by affecting peak central venous pressure and total impedance, which was the afterload to the ventricle. Impedance increased abruptly when PAI was less than approximately 100 mm2/m2. CONCLUSIONS: The smaller pulmonary artery size is hemodynamically disadvantageous after the Fontan operation, with resultant rise in peak control venous pressure and increased afterload to the single ventricle.
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Senzaki et al. (1994) studied this question.
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