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European Heart Journal 2008 29(4):525-530; doi:10.1093/eurheartj/ehn028
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2008 The Author(s). Published by Oxford University Press on behalf of the European Society of Cardiology
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Genome-wide linkage analysis of electrocardiographic and echocardiographic left ventricular hypertrophy in families with hypertension

Bongani M. Mayosi1, Peter J. Avery2, Martin Farrall3, Bernard Keavney4,* and Hugh Watkins2

1 Department of Medicine, University of Cape Town, J Floor Old Main Building, Groote Schuur Hospital, Anzio Road Observatory, Cape Town 7925, W Cape, South Africa
2 School of Mathematics and Statistics, University of Newcastle upon Tyne, UK
3 Department of Cardiovascular Medicine, Wellcome Trust Centre for Human Genetics, University of Oxford, UK
4 Institute of Human Genetics, University of Newcastle upon Tyne, Central Parkway, Newcastle NE1 3BZ, UK

Received 8 October 2007; revised 23 December 2007; accepted 10 January 2008.

* Corresponding author. Tel: +44 191 241 8615, Fax: +44 191 241 8666, Email: b.d.keavney{at}ncl.ac.uk

Aims: To localize chromosomal regions (or quantitative trait loci) that harbour genetic variants influencing the variability of electrocardiographic (ECG) and echocardiographic left ventricular hypertrophy (LVH).

Methods and results: We evaluated genetic linkage to ECG Sokolow-Lyon voltage, ECG Cornell voltage product, ECG left ventricular (LV) mass, and to echocardiographic septal wall thickness, LV cavity size, and LV mass in 868 members of 224 white British families. A genome-wide scan was performed with microsatellite markers that covered the genome at 10-cM intervals and linkage was assessed by variance components analysis. We identified chromosomal regions suggestive of linkage for Sokolow-Lyon voltage on chromosome 10q23.1 [log10 of the odds (LOD = 2.21, P = 0.0007)], for ECG Cornell voltage product on chromosome 17p13.3 (LOD = 2.67; P = 0.0002), and for ECG LV mass on chromosome 12q14.1 (LOD = 2.19; P = 0.0007). There was a single region of possible linkage for echocardiographic LV mass on chromosome 5p14.1 (LOD = 1.6; P = 0.003).

Conclusion: Stronger genetic signals for LVH were found using electrocardiographic than echocardiographic measurements, and the genetic determinants of each of these appear to be distinct. Chromosomes 10, 12, and 17 are likely to harbour genetic loci that exert a major influence on electrocardiographic LVH.

Key Words: Electrocardiogram • Echocardiogram • Left ventricular hypertrophy • Genetics • Linkage analysis • Quantitative trait loci


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