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)

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Abstract

The impact of different methods of indexation of left ventricular (LV) mass and systemic hemodynamic variables on prevalences and correlates of cardiovascular abnormalities in relation to level of obesity in populations 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 hypertrophy, 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 increased 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 hypertensive subjects. In contrast, indexation of LV mass for height2.7 identified an increased prevalence of LV hypertrophy with overweight and obesity. Absolute cardiac output increased and total peripheral resistance decreased with overweight. Prevalence of elevated cardiac output indexed for height1.83 increased and for elevated total peripheral resistance-height1.83 index decreased with greater overweight, whereas opposite trends were seen when cardiac output and total peripheral resistance were indexed for BSA or FFM. Thus, in hypertensive subjects, FFM increases with overweight and is directly related to LV mass, stroke volume, and cardiac output, and inversely related to total peripheral resistance. Indexations of LV mass and systemic hemodynamics for FFM or BSA obscured associations of LV hypertrophy and abnormal cardiac and total peripheral resistance indexes with overweight, whereas LV mass/height2,7, cardiac output/height1.83, and total peripheral resistance-height1.83 detected significant preclinical cardiovascular abnormalities with obesity.

Section snippets

Population

The Hypertension Genetic Epidemiology Network study is part of the National Heart, Lung, and Blood Institute Family Blood Pressure Program, which assesses the genetic basis of hypertension in population-based samples,14 primarily relying on a sib-pair design that recruited hypertensive members of sibships. Hypertension was defined as receiving treatment or having systolic blood pressure ≥140 mm Hg and/or diastolic blood pressure ≥90 mm Hg. Criteria for eligibility were onset of high blood

LV mass and hemodynamics in normal-weight and overweight subjects

Hypertensive adults with mild to moderate or severe obesity were younger (53 and 50 years old, respectively) than normal-weight and overweight hypertensive subjects (55 and 56 years, both p <0.01), whereas no difference existed between the reference (53 years old) and any hypertensive (all p >0.7) group. The proportion of women was higher with mild to moderate and severe obesity (61% and 82%) than in normal-weight or overweight hypertensive or reference groups (56%, 54%, and 54%, respectively,

Discussion

In our study, overweight and obese hypertensive subjects had an absolute LV mass 15% to 41% higher than that in a reference normal group of normal-weight normotensive subjects, independent of gender and systolic blood pressure as important confounders. Of note, in overweight participants, FFM was 9% to 39% higher than in the reference groups, whereas an increase in fat mass ranged from 27% to 216%. Therefore, in hypertensive subjects, an increase in LV mass with overweight paralleled an

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    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.

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