Left Ventricular Hypertrophy in Severe Obesity

Abstract

Obese subjects have a high prevalence of left ventricular (LV) hypertrophy. It is unclear to what extent LV hypertrophy results directly from obesity or from associated conditions, such as hypertension, impaired glucose homeostasis, or obstructive sleep apnea. We tested the hypothesis that LV hypertrophy in severe obesity is associated with additive effects from each of the major comorbidities. Echocardiography and laboratory testing were performed in 455 severely obese subjects with body mass index 35 to 92 kg/m 2 and 59 nonobese reference subjects. LV hypertrophy, defined by allometrically corrected (LV mass/height 2.7 ), gender-specific criteria, was present in 78% of the obese subjects. Multivariable regression analyses showed that average nocturnal oxygen saturation <85% was the strongest independent predictor of LV hypertrophy ( P <0.001), followed by systolic blood pressure ( P <0.015) and then body mass index ( P <0.05). With regard to LV mass, there were synergistic effects between hypertension and body mass index ( P interaction <0.001) and between hypertension and reduced nocturnal oxygen saturation. Severely obese subjects had normal LV endocardial fractional shortening (35±6% versus 35±6%) but mildly decreased midwall fractional shortening (15±2% versus 17±2%; P <0.001), indicating subtle myocardial dysfunction. In conclusion, more severe nocturnal hypoxemia, increasing systolic blood pressure, and body mass index are all independently associated with increased LV mass. The effects of increased blood pressure seem to amplify those of sleep apnea and more severe obesity.