Relation of Various Degrees of Body Mass Index in Patients With Systemic Hypertension to Left Ventricular Mass, Cardiac Output, and Peripheral Resistance (The Hypertension Genetic Epidemiology Network Study) Vittorio Palmieri, MD, Giovanni de Simone, MD, Donna K. Arnett, PhD, Jonathan N. Bella, MD, Dalane W. Kitzman, MD, Albert Oberman, MD, MPH, Paul N. Hopkins, MD, MSPH, Michael A. Province, PhD, and Richard B. Devereux, MD The impact of different methods of indexation of left ventricular (LV) mass and systemic hemodynamic vari- ables on prevalences and correlates of cardiovascular abnormalities in relation to level of obesity in popula- tions remains unclear. We evaluated 1,672 participants in the Hypertension Genetic Epidemiology Network Study to investigate the relations of overweight and level of obesity to LV mass and prevalences of LV hypertro- phy, abnormal cardiac output, and peripheral resistance detected using different indexations for body size. In our study population, 1,577 subjects were clinically healthy nondiabetic hypertensive and 95 were normotensive normal-weight nondiabetic reference subjects. Fat-free mass (FFM) did not differ between the reference group and the normal-weight hypertensive subjects, and in- creased with overweight. In hypertensive subjects, LV mass and cardiac output increased and total peripheral resistance decreased with overweight. Indexation of LV mass for FFM or body surface area (BSA) resulted in no difference or even lower prevalence of LV hypertrophy in severely obese compared with normal-weight hyper- tensive subjects. In contrast, indexation of LV mass for height 2.7 identified an increased prevalence of LV hyper- trophy with overweight and obesity. Absolute cardiac output increased and total peripheral resistance de- creased with overweight. Prevalence of elevated cardiac output indexed for height 1.83 increased and for elevated total peripheral resistance-height 1.83 index decreased with greater overweight, whereas opposite trends were seen when cardiac output and total peripheral resis- tance were indexed for BSA or FFM. Thus, in hyperten- sive subjects, FFM increases with overweight and is di- rectly related to LV mass, stroke volume, and cardiac output, and inversely related to total peripheral resis- tance. Indexations of LV mass and systemic hemody- namics for FFM or BSA obscured associations of LV hypertrophy and abnormal cardiac and total peripheral resistance indexes with overweight, whereas LV mass/ height 2,7 , cardiac output/height 1.83 , and total periph- eral resistance-height 1.83 detected significant preclinical cardiovascular abnormalities with obesity. 2001 by Excerpta Medica, Inc. (Am J Cardiol 2001;88:1163–1168) A verage body weight has been increasing in the past 10 years in the United States. 1 Obesity is associated with a preclinical manifestation of cardio- vascular disease, 2,3 which is prognostically rele- vant. 4–6 Obesity is associated with increases in car- diovascular event rates. 7,8 Previous reports 2,3,9 showed that indexation of left ventricular (LV) mass for the allometric power of its relation to body height (height 2.7 ) facilitates identification of LV hypertrophy among obese subjects because height 2.7 parallels ideal body size for body height as opposed to actual body weight. Because the LV mass-body height relation is not linear, it requires use of a mathematic transforma- tion of height by an exponent called the allometric signal. 9 LV hypertrophy defined by LV mass/height 2.7 criteria, appears to predict an adverse prognosis as well as hypertrophy as defined by other indexation meth- ods. 10,11 However, different methods of indexation of LV mass result in considerably different prevalences of LV hypertrophy. 11,12 The impact of different meth- ods of indexing LV mass and systemic hemodynamic parameters on prevalences of cardiovascular abnor- From Weill Medical College of Cornell University, New York, New York; University of Minnesota, Minneapolis, Minnesota; Wake Forest University School of Medicine, Winston-Salem, North Carolina; University of Alabama at Birmingham, Birmingham, Alabama; University of Utah School of Medicine, Salt Lake City, Utah; and Washington University Medical School, St. Louis, Missouri. This study was supported in part by Grant 5 R01 HL55673 and cooperative agreement Grants 5 U10 HL54471, HL 54472, HL54473, HL54496, HL54509, and HL 54515 from the National Heart, Lung, and Blood Institute, Bethesda; and Grant M10RR0047-34 (GCRC) from the National Institutes of Health, Bethesda, Maryland. Manuscript received May 29, 2001; revised manuscript received and accepted July 18, 2001. Address for reprints: Vittorio Palmieri, MD, Division of Cardiology, Box 222, Weill Medical College of Cornell University, 525 East, 68th Street, New York, New York 10021. E-mail: vpalmier@ med.cornell.edu. 1163 ©2001 by Excerpta Medica, Inc. All rights reserved. 0002-9149/01/$–see front matter The American Journal of Cardiology Vol. 88 November 15, 2001 PII S0002-9149(01)02054-9