1. ¹Division of Epidemiology, University of Minnesota, Minneapolis, Minnesota, USA
2. ²Division of Biostatistics, Washington University, St. Louis, Missouri, USA
3. ³Case-Western Reserve University, Cleveland, Ohio, USA
4. ⁴Division of Preventive Medicine, University of Alabama, Birmingham, Alabama, USA
5. ⁵Department of Internal Medicine (Cardiology Section), Bowman Gray School of Medicine, Winston-Salem, North Carolina, USA
6. ⁶Department of Cardiovascular Genetics, University of Utah, Salt Lake City, Utah, USA
7. ⁷Division of Cardiology, Cornell University Medical College, New York, New York, USA

Correspondence: Donna K. Arnett PhD, Division of Epidemiology, University of Minnesota, 1300 South Second Street, Suite 300, Minneapolis, MN 55454-1015 USA. E-mail: arnett@epi.umn.edu

^* The HyperGEN network is funded by National Heart, Lung, and Blood Institute R01 HL55673 and cooperative agreements (U10) with National Heart, Lung, and Blood Institute: HL54471 (UT FC), HL54472 (MN Lab), HL54473 (DCC), HL54495 (AL FC), HL54496 (MN FC), HL54509 (NC), HL54515 (UT DNA Lab).

Received 12 October 2000; Accepted 12 June 2001.

Abstract

Background: Evidence suggests that left ventricular (LV) mass is under genetic control, independently of risk factors known to influence LV size and geometry.

Methods: As part of the HyperGEN study, four field centers recruited African American and white hypertensive siblings (n = 1664), aged 23 to 87 years. Two-dimensionally guided M-mode echocardiography was performed, and LV mass and relative wall thickness (RWT) were measured at a central reading center. Familial correlations were calculated separately for each ethnic group using maximum likelihood methods, adjusted for the potential confounding influences of age, gender, systolic blood pressure, and obesity.

Results: In African Americans, brother-sister, brother-brother, and sister-sister correlation coefficients and standard errors for LV mass were 0.29 (0.08), 0.44 (0.10), and 0.33 (0.05). In whites, the corresponding correlations were lower than in African Americans at 0.05 (0.08), 0.12 (0.11), and 0.22 (0.09), respectively. Sibling correlation of LV geometry, assessed by RWT, was less in African Americans than in whites: brother-sister, 0.04 (0.10) v 0.21 (0.10), brother-brother, 0.12 (0.22) v 0.28 (0.09), and sister-sister, 0.11 (0.07) v 0.19 (0.11).

Conclusions: LV mass is strongly correlated in hypertensive African American siblings, and modestly correlated in their white counterparts, whereas RWT has stronger sibling correlation in whites. The patterns of familial correlation of echocardiographic LV mass and RWT suggest that the genetic underpinnings of LV hypertrophy and geometric remodeling may differ among ethnic groups.