4.7 Article

Differences in left ventricular structure between black and white hypertensive adults - The hypertension genetic epidemiology network study

Journal

HYPERTENSION
Volume 43, Issue 6, Pages 1182-1188

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.HYP.0000128738.94190.9f

Keywords

ethnicity; hypertrophy; vascular resistance

Funding

  1. NCRR NIH HHS [M10RR0047-34] Funding Source: Medline
  2. NHLBI NIH HHS [HL54471, HL54496, K23 HL70854, HL55673, HL54509, HL54515, HL54472, HL54473] Funding Source: Medline

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The degree to which ethnic differences in left ventricular structure among hypertensive adults are independent of clinical and hemodynamic factors remains uncertain. We assessed whether left ventricular mass and geometry differ between black and white hypertensives after accounting for differences in such factors. Our study group comprised 1060 black and 580 white hypertensive participants free of valvular or coronary disease in a population-based cohort. Blood pressure was measured during a clinic visit and echocardiography was performed using standardized protocols. After controlling for clinical and hemodynamic parameters ( cardiac index, peripheral resistance index, and pulse pressure/stroke index), both left ventricular mass and relative wall thickness were higher in blacks than whites (173.9 +/- 30.9 versus 168.3 +/- 24.3 grams, P = 0.006, and 0.355 +/- 0.055 versus 0.340 +/- 0.055 grams, P < 0.001). Similarly, the adjusted risk of having left ventricular hypertrophy, whether indexed by height(2.7) or by body surface area, was greater for blacks than for whites (odds ratio: 1.80; 95% CI: 1.29 to 2.51; and odds ratio: 2.50; 95% CI: 1.58 to 3.96, respectively), and this was also true for concentric geometry (odds ratio: 2.28; 95% CI: 1.22 to 4.25). Further adjustment for relatedness in this genetic epidemiological study did not attenuate these differences. Our findings confirm the strong association between black ethnicity and increased left ventricular mass and relative wall thickness in hypertensive adults and demonstrate that these differences are independent of standard clinical and hemodynamic parameters. Whether such differences relate to distinct ambulatory pressure profiles or an ethnic propensity to cardiac hypertrophy requires further investigation.

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