Obesity raises blood pressure in normal subjects via high cardiac output and impaired vasodilation

Obesity is an emerging concern in the US and Western Countries. The effect of rising body mass index (BMI) on blood pressure and hemodynamics in normotensive populations is not known. We examined blood pressure (BP, oscillometric), heart rate (HR) and hemodynamic parameters (cardiac output CO, systemic vascular resistance SVR, by thoracic bioimpedance) in 737 normal subjects evaluated as renal donors by gender and BMI. Mean age was 42±1 years (range 18-75), with 305 males, 432 females. Treated hypertensives were excluded. BP and heart rate rose progressively with rising BMI. Cardiac output increased with BMI accompanied by reduced postural change in impedance. SVR fell slightly at high BMI. Indexing values for body surface area eliminated or reversed the rise in cardiac output with BMI. Indexed values suggested a rise in SVRI with reduced stroke volume and CO as the explanation for higher BP with higher BMI. Taken together, absolute hemodynamic measures demonstrate volume expansion with obesity leading to elevated BP. SVR fails to fall adequately to balance higher cardiac outputs accounting for higher BP with increased BMI. Indexed values reverse this impression and artifactually suggest systemic vasoconstriction. These findings raise concern that indexing to body size may distort vascular patterns particularly at high BMI. (See Table) Mean ± SEM TFI: thoracic impedance, ΔTFI: impedance change with posture. p < 0.05 vs BMI < 25 p < 0.05 vs BMI 25–29.9 p < 0.05 vs BMI 30–34.9. Mean ± SEM TFI: thoracic impedance, ΔTFI: impedance change with posture. p < 0.05 vs BMI < 25 p < 0.05 vs BMI 25–29.9 p < 0.05 vs BMI 30–34.9.