Effects of sibutramine on ventricular dimensions and heart valves in obese patients during weight reduction.

BACKGROUND: Obesity enhances hemodynamic alterations that predispose to a subsequent increase in left ventricular (LV) wall stress leading to LV hypertrophy. In obese subjects, weight reduction regresses LV mass (LVM), regardless of blood pressure. Sibutramine can increase blood pressure and heart rate, which may attenuate the reductions in LVM associated with weight loss. METHODS: Outpatients (n = 184, age 18-65 y, body mass index > or =30 to <40 kg/m2) were randomly assigned to 6 months of once daily double-blind treatment with sibutramine 10 mg or 20 mg, or placebo. LV dimensions, status and function of the valves, weight loss, blood pressure, heart rate, and electrocardiogram were assessed. RESULTS: For end point data sets, the mean +/- SD LVM index (LVM/height) changes were -3.0 +/- 11.9 g/m for placebo (n = 56), -4.4 +/- 10.7 g/m for sibutramine 10 mg (n = 61), and -4.3 +/- 10.9 g/m for sibutramine 20 mg (n = 56). The reductions observed in the sibutramine groups were statistically significant compared with baseline (P <.01), but pairwise comparison results with placebo were not statistically significant. There was no difference in overall status of the cardiac valves. A statistically significant greater weight loss was found in patients on both doses of sibutramine compared with placebo (P <.001). No statistically significant differences between the groups were observed in respect to blood pressure and electrocardiographic intervals, but a statistically significant increase in pulse rate (7 beats/min) was noted for patients with sibutramine treatment. CONCLUSION: A 6-month treatment with sibutramine does not affect ventricular dimensions, heart valves, and electrocardiogram variables.

Noninvasive quantitation of blood flow turbulence in patients with aortic valve disease using online digital computer analysis of Doppler velocity data.

Previous experimental studies have demonstrated that aortic valve disease is associated with significant downstream turbulence (T). In this study, we developed a noninvasive method on the basis of Doppler velocity recording for quantitating aortic blood flow T in patients with aortic valve disease. The instantaneous blood velocity at a point in the aorta is equal to the sum of a mean periodic velocity component with a random or turbulent velocity component. According to the ensemble average method, time mean absolute T intensity is the root-mean-square value of turbulent velocity averaged over time and T is better quantitated by the relative T intensity (TIr), which is the ratio of absolute T intensity to the ensemble average velocity averaged over time. We computed TIr in 18 patients with mild to severe aortic stenosis and in 13 healthy volunteers from instantaneous modal velocities of 70 cycle length-matched heart beats recorded in the proximal part of the descending aorta by pulsed Doppler using an ultrasound system with an output port for online digital data transfer into a microcomputer. TIr was greater in patients with aortic valve disease (18.4 +/- 5.1%, range 11.2%-28.9%) than in control patients (7.9 +/- 1.9%, range 4.8%-9.8%; P =.0001). In patients with aortic valve disease, TIr was better linearly related to the ratio of postvalvular aorta to valvular orifice cross-sectional areas (r = 0.89, P =.0001) than to other parameters of valve restriction: transvalvular pressure gradient (r = 0.78, P =.0001); valve area (r = -0.56, P =.01); and valve resistance (r = 0.72, P =.0002). Thus, T that can be computed noninvasively from direct digital transfer of Doppler velocity data appears to be linearly related to indices of aortic valve restriction. Our data support the concept of the postvalvular aorta to valvular orifice cross-sectional areas ratio as a new important hemodynamic parameter in patients with aortic valve disease.