Heritability of left ventricular dimensions and mass in American Indians: The Strong Heart Study.
Academic Article
Overview
abstract
OBJECTIVE: We sought to determine the heritability of left ventricular dimensions and mass in adult American Indians. METHODS: Echocardiograms were analysed in 1373 American Indian participants, from 445 families, in the Strong Heart Study (SHS) to determine the heritability of left ventricular dimensions and mass. Heritability calculations were performed using variance component analysis in SOLAR, a computer analysis program. RESULTS: The SHS participants analysed in this study included 1305 relative pairs, predominantly (n = 1077) sib-pairs. After simultaneously adjusting for sex, age and centre, the proportion of the residual phenotypic variance due to additive genetic effects or heritability (h2) of left ventricular mass was 0.27 (SE = 0.08, P < 0.001). Addition of body weight, height, systolic blood pressure, heart rate, medications and diabetes into the polygenic model attenuated the residual h2 of left ventricular mass to 0.17 (SE = 0.09, P < 0.05). The residual h2 for left ventricular end-diastolic chamber diameter (LVID), after simultaneously adjusting for sex, age and centre was 0.36 (SE = 0.08, P < 0.001) for the analysed families. The residual h2 for interventricular septal wall thickness was 0.26 (SE = 0.07), while that of left ventricular posterior wall thickness was 0.19 (SE = 0.08, both P < 0.001). While adjustment for body weight, height, systolic blood pressure, heart rate, medications and diabetes reduced the h2 of LVID to 0.33 (SE = 0.09, P < 0.001), the h2 of septal (0.12, SE = 0.10) and posterior wall thickness (0.09, SE = 0.09) were no longer significant after similar adjustment. The residual h2 for relative wall thickness, a measure of left ventricular geometry, was 0.22 (SE = 0.07, P < 0.001) after adjusting for sex, age and centre, and 0.17 (SE = 0.08, P < 0.05) after additional adjustment for body weight, height, systolic blood pressure, heart rate, medications and diabetes. CONCLUSIONS: A substantial proportion of the variance of left ventricular dimensions and mass can be explained by heredity, independent of the effects of sex, age, body size, blood pressure, heart rate, medications and diabetes. Identification of genes influencing left ventricular size and geometry may provide mechanistic and therapeutic targets to prevent left ventricular hypertrophy.
