Genetic contribution to the variance in left ventricular mass: the Tecumseh Offspring Study.

Objective To estimate the contribution of heredity to the variance in left ventricular mass (LVM), and to ascertain whether genetic factors may interact with non-genetic factors in promoting LVM growth. Subjects and setting The study population consisted of 290 healthy parents and 251 healthy children living in Tecumseh, Michigan, USA. Main outcome measure Correlation of parents’ LVM with offspring's LVM adjusting for a number of clinical variables. Methods LVM in parents and offspring was measured with M-mode echocardiography by the same investigators. Results Parents unadjusted LVM was unrelated to offspring unadjusted LVM , but after removing the confounding effect of age, sex, anthropometric measurements, systolic blood pressure, plasma insulin and urinary sodium excretion, parent–child correlation for LVM was 0.28 (P = 0.006). The relative contribution of parental-adjusted LVM and of several offspring phenotypic and environmental variables on offspring LVM was evaluated by multivariable regression analysis. When age, gender, anthropometric measurements and systolic blood pressure were accounted for, adjusted LVM of parents explained only 1.6% of the total variance in offspring LVM. However, after inclusion of insulin and urinary sodium in the model heredity explained 7.6% of the total variance in offspring LVM, and its predictive power was second only to that of child's height. Furthermore, an interactive effect of parental LVM with offspring systolic blood pressure was found on child's left ventricular mass. Conclusion Heredity can explain a small, but definite proportion of the variance in LVM. Higher blood pressure favors the phenotypic expression of the genes that regulate LVM growth.