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The Journal of Clinical Endocrinology & Metabolism Vol. 83, No. 12 4284-4288
Copyright © 1998 by The Endocrine Society


From the Clinical Research Centers

Relation among Left Ventricular Mass, Insulin Resistance, and Blood Pressure in Nonobese Subjects1

Robert A. Phillips, Lawrence R. Krakoff, Andrea Dunaif, Diane T. Finegood2, Richard Gorlin3 and Seiichi Shimabukuro

Mount Sinai Medical Center (R.A.P., L.R.K., R.G.), New York, New York 10029; Brigham and Women’s Hospital (A.D.), Boston, Massachusetts 00000; Simon Fraser University (D.T.F.), Burnaby, British Columbia, Canada; and Hirano General Hospital (S.S.), Gifu, Japan

Address all correspondence and requests for reprints to: Robert A. Phillips, M.D., Ph.D., Section of Hypertension, Prevention, and Rehabilitation, Zena and Michael A. Wiener Cardiovascular Institute, Box 1085, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029. E-mail: robert_phillips{at}smtplink.mssm.edu

Because left ventricular (LV) mass (LVM) is a powerful predictor of future cardiovascular events, it is important to identify hemodynamic and nonhemodynamic factors that increase LVM. We studied the separate contribution to LVM of daily arterial blood pressure (BP) and insulin resistance in a consecutive series of 29 (mean ± SD age, 43 ± 13 yr) nonobese (body mass index, 24 ± 1.8 kg/m2), nondiabetic, glucose-tolerant subjects with untreated borderline or mild hypertension. The insulin sensitivity index (SI) was quantitatively determined from the frequently sampled iv glucose tolerance test. BP was characterized by ambulatory 24-h BP monitoring, and LVM index (LVMI) was determined by two-dimensional directed M-mode echocardiography. LVMI was directly related to 24-h mean BP (r = 0.47; P = 0.01). LMVI was also significantly related to SI (r = -0.43; P = 0.02). In this nonobese group, neither LVMI nor SI was related to body mass index or age. After adjustment for the influence of BP on LVMI, a significant relation remained between LVMI and SI (P < 0.05).

We conclude that in nonobese subjects with high normal BP, insulin sensitivity is related to LVM independently of BP and may be an important modulator of LV growth. In addition to a reduction of arterial BP, optimal prevention of LV hypertrophy in hypertensives may require improved insulin sensitivity.




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