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European Heart Journal 2003 24(6):577-582; doi:10.1016/S0195-668X(02)00524-9
Copyright © 2003 by the European Society of Cardiology.
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The genetic determination of left ventricular mass in healthy adults

L. Swan*, D.H. Birnie, S. Padmanabhan, G. Inglis, J.M.C. Connell and W.S. Hillis

Department of Medicine and Therapeutics, University of Glasgow, UK

* Corresponding author. Dr L. Swan, Adult Congenital Heart Disease Unit, Royal Brompton Hospital, London SW3 6NP, U.K. Tel.: +44-20-7351-8602; fax: +44-20-7351-8629
E-mail address: lornaswan{at}yahoo.com

revised 23 July 2002; accepted 24 July 2002

Aims The extent to which left ventricular (LV) mass, an independent cardiovascular risk factor, is determined by genetic factors is unclear. The aim of this study was to assess the heritability of LV mass and its association with three potential candidate genes.

Methods A population-based adult twin study model was utilized. Echocardiographic assessment of LV mass was performed in 110 twin pairs (mean age 55.9±10.9 years). An estimate of genetic determination, heritability, was calculated for the main echocardiographic parameters. The cohort were genotyped for the G-protein beta-3, aldosterone synthase, and beta-1 adrenoceptor genes.

Results The intra-class correlation coefficients for LV mass were 0.69 for monozygotic (r-MZ) twins and 0.32 for dizygotic (r-DZ) twins, P=0.008 (heritability estimate of 0.69). This pattern persisted following correction for known confounding factors. Within-pair differences in the monozygotic, discordant and concordant dizygotic twins showed no differences for the three genes with respect to left ventricular wall thickness or mass. There was a non-significant trend towards a relationship between LV mass and the beta-1 adrenoceptor genotype.

Conclusion Within a normal population left ventricular mass has a significant genetic determination. Further investigation of potential candidate genes is required.

Key Words: Hypertrophy • Genetics • Ventricle


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