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Circulation. 2000;102:2233-2238

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(Circulation. 2000;102:2233.)
© 2000 American Heart Association, Inc.


Clinical Investigation and Reports

Insulin Resistance and Hyperinsulinemia

No Independent Relation to Left Ventricular Mass in Humans

Alfredo Quiñones Galvan, MD; Fabio Galetta, MD; Andrea Natali, MD; Elza Muscelli, MD; Anna Maria Sironi, MD; Giuseppe Cini, MD; Stefania Camastra, MD; Ele Ferrannini, MD

From the Department of Internal Medicine, University of Pisa School of Medicine, and the Metabolism Unit of the CNR Institute of Clinical Physiology, University of Pisa, Italy.

Correspondence to Dr Ele Ferrannini, CNR Institute of Clinical Physiology, Via Savi, 8, 56100 Pisa, Italy. E-mail ferranni{at}ifc.pi.cnr.it

Background—Hyperinsulinemia and insulin resistance may contribute to the development of cardiac hypertrophy. In humans, however, the evidence is inconclusive.

Methods and Results—We studied 50 nondiabetic subjects covering a wide range of age (20 to 65 years), body mass index (BMI, 19 to 40 kg · m-2), and mean blood pressure (72 to 132 mm Hg). Plasma insulin concentrations and secretory rates were measured at baseline and during an oral glucose tolerance test; insulin sensitivity was measured by the insulin clamp technique. Left ventricular mass (LVM) (by 2D M-mode echocardiography) was distributed normally and was higher in obese (BMI >=27 kg · m-2, n=16) or hypertensive patients (blood pressure >140/90 mm Hg, n=21) (50±8 and 55±10 g · m-2.7, respectively) than in 13 nonobese, normotensive subjects (40±8 g · m-2.7, P=0.0004). In a multivariate model adjusting for sex, age, BMI, and blood pressure, neither insulin concentrations (fasting or postglucose) nor insulin sensitivity or secretory rates were significant correlates of LVM. Systolic blood pressure (P=0.003) and BMI (P=0.01) were the only independent correlates of LVM. From the regression, the impact of hypertension (as a systolic pressure of 180 versus 140 mm Hg=+20%) was twice as large as that of obesity (as a BMI of 35 versus 25 kg · m-2=+11%), the two factors being additive.

Conclusions—When adequate account is taken of body mass and blood pressure, insulin, as concentration, secretion, or action, is not an independent determinant of LVM in nondiabetic subjects.


Key Words: hypertrophy • ventricles • insulin • obesity • hypertension




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