C K Phoon1, N H Silverman. 1. Division of Pediatric Cardiology, New York University Medical Center, New York 10016, USA.
Abstract
OBJECTIVES: We modeled the utility of preoperative potential left ventricular (LV) volume in predicting postoperative volume in conditions causing LV compression. BACKGROUND: With right ventricular (RV) overload lesions, LV "hypoplasia" may be primarily due to compression by reverse septal bowing. If so, preoperative potential LV volume should correspond 1:1 with postoperative volume. The potential volume for a given endocardial circumference can be calculated from the maximal potential cross-sectional area (where A = circumference(2)/4pi) and LV length. METHODS: We studied echocardiographic variables from 22 patients with RV overload lesions perioperatively. RESULTS: Preoperative LV volume was 15.0 +/- 7.1 ml/m2 (59% of patients had a volume <15 ml/m2); potential volume was 20.0 +/- 9.8 ml/m2. Postoperative volume increased to 28.2 +/- 8.6 ml/m2 (100% of patients had a volume >15 ml/m2). Preoperative potential volume correlated well with, but generally underestimated, postoperative volume (r = 0.75, p < 0.0001). Postoperative increases in both LV circumference and length contributed to this discrepancy. CONCLUSIONS: In RV overload lesions, LV "hypoplasia" is primarily due not to compression; rather it is due to underfilling. Even "hypoplastic" ventricles can achieve an adequate cavity after operation normalizes loading conditions. Both true and potential preoperative volume can predict postoperative volume well. However, potential volume, which is less prone to underestimating ventricular adequacy, may better help to determine suitability for biventricular repair in lesions of RV overload associated with a "hypoplastic" LV.
OBJECTIVES: We modeled the utility of preoperative potential left ventricular (LV) volume in predicting postoperative volume in conditions causing LV compression. BACKGROUND: With right ventricular (RV) overload lesions, LV "hypoplasia" may be primarily due to compression by reverse septal bowing. If so, preoperative potential LV volume should correspond 1:1 with postoperative volume. The potential volume for a given endocardial circumference can be calculated from the maximal potential cross-sectional area (where A = circumference(2)/4pi) and LV length. METHODS: We studied echocardiographic variables from 22 patients with RV overload lesions perioperatively. RESULTS: Preoperative LV volume was 15.0 +/- 7.1 ml/m2 (59% of patients had a volume <15 ml/m2); potential volume was 20.0 +/- 9.8 ml/m2. Postoperative volume increased to 28.2 +/- 8.6 ml/m2 (100% of patients had a volume >15 ml/m2). Preoperative potential volume correlated well with, but generally underestimated, postoperative volume (r = 0.75, p < 0.0001). Postoperative increases in both LV circumference and length contributed to this discrepancy. CONCLUSIONS: In RV overload lesions, LV "hypoplasia" is primarily due not to compression; rather it is due to underfilling. Even "hypoplastic" ventricles can achieve an adequate cavity after operation normalizes loading conditions. Both true and potential preoperative volume can predict postoperative volume well. However, potential volume, which is less prone to underestimating ventricular adequacy, may better help to determine suitability for biventricular repair in lesions of RV overload associated with a "hypoplastic" LV.