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(Hypertension. 1996;28:276-283.)
© 1996 American Heart Association, Inc.

Articles

Influence of Obesity on Left Ventricular Midwall Mechanics in Arterial Hypertension

Giovanni de Simone; Richard B. Devereux; Gian Francesco Mureddu; Mary J. Roman; Antonello Ganau; Michael H. Alderman; Franco Contaldo; John H. Laragh

the Division of Cardiology, The New York Hospital–Cornell Medical Center, New York (G. de S., R.B.D., M.J.R., M.H.A., J.H.L.); Department of Clinical and Experimental Medicine, Federico II University Hospital, Naples, Italy (G. de S., G.F.M.); and Institute of Clinical Medicine, University of Sassari (Italy) (A.G.).

Correspondence to Dr Giovanni de Simone, Division of Cardiology, Box 222, The New York Hospital–Cornell Medical Center, 525 E 68th St, New York, NY 10021. E-mail mjograd@mail.med.cornell.edu (US); simogi@ds.unina.it (Italy).

The evaluation of the effect of obesity on left ventricular systolic performance may differ in relation to the method used to measure left ventricular function and to the type of study population. Whether obesity worsens left ventricular midwall mechanics in arterial hypertension has never been investigated. Accordingly, we assessed echocardiographic left ventricular midwall shortening–circumferential end-systolic stress relations in 156 normotensive and normal-weight (reference) adults, 94 normotensive and overweight (1985 National Institutes of Health partition values) to obese (body mass index >30 kg/m²) adults, 263 hypertensive and normal-weight adults, and 224 hypertensive and overweight-to-obese adults. There was an inverse relation of midwall shortening to circumferential end-systolic stress in all groups (all P<.005). Left ventricular performance as a ratio of observed to predicted midwall shortening fell below the fifth percentile in 4 of 94 (4%) of overweight-to-obese normotensive individuals. Eighty-eight of 487 hypertensive subjects (18.1%) exhibited depressed midwall shortening as a percentage of the value predicted from wall stress, with no difference between normal-weight (50 of 263 [19%]) and overweight (38 of 224 [17%]) subjects. Sixty-one normotensive and 131 hypertensive subjects were frankly obese. After adjustment for sex and age, midwall shortening, as either absolute values or a percentage of predicted, was not statistically different among obese, overweight, and normal-weight subjects in both normotensive and hypertensive groups. For each quartile of observed-to-predicted midwall shortening ratio, obese subjects had greater left ventricular end-diastolic volume than normal-weight subjects among both normotensive and, more evidently, hypertensive subjects. A predicted midwall shortening was generated from both wall stress and left ventricular volume with the use of multiple regression analysis. High body mass index, mean blood pressure, aging, and male sex independently predicted low afterload and left ventricular volume–independent midwall left ventricular performance (multiple R=.31, P<.0001). Thus, (1) midwall left ventricular systolic performance in asymptomatic overweight or frankly obese individuals is comparable to that in normal-weight individuals in both the presence and absence of arterial hypertension; (2) however, maintenance of normal left ventricular performance in obese individuals is associated with the use of Starling reserve; and (3) this compensatory mechanism is especially evident when arterial hypertension and obesity coexist.

Key Words: obesity • ventricular function • hypertension, arterial • blood pressure • body mass index • echocardiography

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