Background: This study tested two hypotheses: 1) regional left ventricular radius-to-wall thickness ratios (R/T) are uniform in normal subjects, and 2) patients with left ventricular hypertrophy secondary to compensated volume overload normalize global and regional R/T.
Methods and results: Ultrafast computed tomography was used to measure regional short-axis ventricular R/T in 11 normal subjects and 13 patients with compensated aortic insufficiency (AI) of moderate severity (regurgitant fraction, greater than or equal to 25%). Radius and wall thickness dimensions were calculated by two different methods. In method 1, the average radius and wall thickness were determined for each planimetric transaxial tomographic image. In method 2, the left ventricle was three-dimensionally reconstructed; then, new radii and wall thickness were recalculated as if all the images were acquired orthogonal to the endocardial surface at each tomographic level. In normals, the mean R/T ratio was 1.75 +/- 0.11 (SEM) with method 1 and 1.80 +/- 0.07 with method 2. The R/T ratios varied as a function of the relative apex-to-base position. R/T ratios at the basal four levels were relatively uniform, whereas R/T at the lower three tomographic levels were significantly less than those at the base (p less than 0.01). Patients with AI had a mean regurgitant fraction of 44 +/- 3.8% (range, 25-63%). The mean R/T ratio was 2.18 +/- 0.16 with method 1 and 2.55 +/- 0.18 with method 2. Similar to the pattern observed in normals, the regional R/T ratios at the lower three or four levels were significantly less than the basal R/T ratios (p less than 0.01). Regional comparison of the normal to the volume-overloaded ventricles demonstrated that R/T ratios in the AI patients were significantly greater at the upper five levels with method 1 and at all eight levels with method 2 (p less than 0.01-0.001, AI versus normal).
Conclusions: These findings demonstrate that regional R/T ratios are heterogeneous in both normals and patients with left ventricular hypertrophy secondary to compensated aortic insufficiency. Furthermore, these findings challenge the accepted hypothesis that global and regional R/T ratios normalize in patients with compensated volume-overload hypertrophy.