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(Hypertension. 2007;49:34.)
© 2007 American Heart Association, Inc.

Original Articles

Left Ventricular Hypertrophy in Severe Obesity

Interactions Among Blood Pressure, Nocturnal Hypoxemia, and Body Mass

Erick Avelar; Tom V. Cloward; James M. Walker; Robert J. Farney; Michael Strong; Robert C. Pendleton; Nathan Segerson; Ted D. Adams; Richard E. Gress; Steven C. Hunt; Sheldon E. Litwin

From the Divisions of Cardiology (E.A., N.S., S.E.L.), Pulmonary and Critical Care (J.M.W.), General Internal Medicine (M.S., R.C.P.), and Cardiovascular Genetics (T.D.A., R.E.G., S.C.H.), University of Utah School of Medicine, Salt Lake City; the Intermountain Sleep Disorders Center (T.V.C., J.M.W., R.J.F.), LDS Hospital, Salt Lake City, Utah; and Salt Lake City Veterans Affairs Hospital (S.E.L.), Utah.

Correspondence to Sheldon E. Litwin, Cardiology 4A100 SOM, University of Utah, 30 N 1900 E, Salt Lake City, UT 84121. E-mail Sheldon.Litwin{at}hsc.utah.edu or Erick Avelar, Division of Cardiology, Massachusetts General Hospital, Blake 02:260, 55 Fruit St, Boston, MA 02114. E-mail Eavelar@partners.org

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/m² 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.

Key Words: obesity • echocardiography • left ventricular hypertrophy • myocardial contraction • hypertension • diabetes • metabolic syndrome • obstructive sleep apnea

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