Postprandial Vascular Dysfunction Is Associated With Raised Blood Pressure and Adverse Left Ventricular Remodeling in Adolescent Adiposity

Abstract

Background: Left ventricular hypertrophy (LVH) is a major risk factor for cardiovascular disease, including heart failure. Although linked to obesity and hypertension, its pathogenesis is multifactorial. Blunted postprandial sympathetic regulation of gut blood flow has been observed in overweight animals and suggested as a promotor of hypertension and LVH. We hypothesized that blunted postprandial superior mesenteric blood flow responses would be more common in overweight humans and associated with increased blood pressure and LVH. Methods: Left ventricular dimensions and hemodynamic responses to a standardized high-calorie liquid meal were measured in healthy adolescents (n=82; 39 overweight/obese) by magnetic resonance imaging. Covariates such as body mass index, blood pressure, Tanner score, and an index of insulin resistance were included in multiple regression models to examine the independent associations of mesenteric flow response with blood pressure status and LVH. Results: Food ingestion increased cardiac output (Δmean, 0.45 [SD, 0.62] L·min −1 ; P =3.8×10 −8 ) and superior mesenteric artery flow (Δmean, 0.76 [SD, 0.35] L·min −1 ; P =4.2×10 −31 ). A blunted mesenteric flow response was associated with increased left ventricular mass (B=−12.7 g·m −2.7 per L·min −1 ·m − 0.92 ; P =6×10 −5 ) and concentric LVH (log likelihood, −9.9; P =0.001), independently of known determinants of LVH, including body mass index. It was also associated with elevated systolic blood pressure (B=−18.0 mm Hg per L·min −1 ·m − 0.92 ; P =0.001), but this link did not explain the association with left ventricular mass. Conclusions: Postprandial mesenteric vascular dysfunction is associated with LVH and hypertension, independently of common risk factors for those conditions. These findings highlight a new, independent marker of cardiovascular risk in the young.