Arterial Load and Ventricular-Arterial Coupling Physiologic Relations With Body Size and Effect of Obesity

Accurate quantification of arterial function is crucial to distinguishing disease states from normal variants. However, there are little data regarding methods to scale arterial load to body size in humans. We studied 2365 adults aged 35 to 55 years free of overt cardiovascular disease. We assessed arterial hemodynamics and ventricular-vascular coupling with carotid tonometry and Doppler echocardiography. To define normal (physiological) relationships between hemodynamic indices and body size, we used nonlinear regression to analyze a selected reference subsample (n = 612) with normal weight (body mass index 18 to 25 kg/m(2)), waist circumference, and metabolic parameters. Most arterial hemodynamic indices demonstrated important relationships with body size, which were frequently allometric (nonlinear). Allometric indexation using appropriate powers (but not ratiometric indexation) effectively eliminated the relationships between indices of arterial load and body size in normal subjects. In the entire sample (n = 2365), the adverse effects of obesity on arterial load and end-systolic ventricular stiffening were clearly demonstrated only after appropriate indexation to account for the expected normal relationship to body size. After adjustment for age and sex, a progressive increase in indexed systemic vascular resistance, effective arterial and ventricular end-systolic elastance, and a decrease in total arterial compliance were seen from normal weight to obesity (P < 0.0001). Arterial load relates to body size in an allometric fashion, calling for scaling with the use of appropriate powers. Obesity exerts adverse effects on arterial load and ventricular stiffening that go beyond the normal relationship with body size. Allometric normalization should allow more accurate quantification of arterial load in future studies. (Hypertension. 2009;54:558-566.)