BACKGROUND: Both left ventricular hypertrophy (LVH) and repolarization phase (RP) are known to be attributable to genetic influences, but less is known whether they share same genetic influences. The aim of this study was to investigate to what extent individual differences in electrocardiographic (ECG) LVH and RP are explained by genetic and environmental influences and whether these influences are shared between these two traits. METHODS: Resting ECG recordings were obtained from 186 monozygotic and 203 dizygotic female twin individuals, aged 63 to 76 years. Latent factors, called LVH and RP, were formed to condense the information obtained from LVH indices (Cornell voltage and Cornell product) and T-wave amplitudes (leads V(5) and II), respectively. Multivariate quantitative genetic modeling was used both to decompose the phenotypic variances into additive genetic, common environmental, and unique environmental influences, and for the calculation of genetic and environmental correlations between LVH and RP. RESULTS: Additive genetic influences explained 16% of individual differences in LVH and 74% in RP. The remaining individual differences were explained by both common and unique environmental influences. The genetic correlation and unique environmental correlation between LVH and RP were -0.93 and -0.05, respectively. CONCLUSIONS: In older women without overt cardiac diseases, RP is under stronger genetic control than LVH. The majority of genetic influences are shared between LVH and RP whereas environmental influences are mainly specific to each.
BACKGROUND: Both left ventricular hypertrophy (LVH) and repolarization phase (RP) are known to be attributable to genetic influences, but less is known whether they share same genetic influences. The aim of this study was to investigate to what extent individual differences in electrocardiographic (ECG) LVH and RP are explained by genetic and environmental influences and whether these influences are shared between these two traits. METHODS: Resting ECG recordings were obtained from 186 monozygotic and 203 dizygotic female twin individuals, aged 63 to 76 years. Latent factors, called LVH and RP, were formed to condense the information obtained from LVH indices (Cornell voltage and Cornell product) and T-wave amplitudes (leads V(5) and II), respectively. Multivariate quantitative genetic modeling was used both to decompose the phenotypic variances into additive genetic, common environmental, and unique environmental influences, and for the calculation of genetic and environmental correlations between LVH and RP. RESULTS: Additive genetic influences explained 16% of individual differences in LVH and 74% in RP. The remaining individual differences were explained by both common and unique environmental influences. The genetic correlation and unique environmental correlation between LVH and RP were -0.93 and -0.05, respectively. CONCLUSIONS: In older women without overt cardiac diseases, RP is under stronger genetic control than LVH. The majority of genetic influences are shared between LVH and RP whereas environmental influences are mainly specific to each.
Authors: J Karjalainen; U M Kujala; A Stolt; M Mäntysaari; M Viitasalo; K Kainulainen; K Kontula Journal: J Am Coll Cardiol Date: 1999-08 Impact factor: 24.094
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Authors: H Schunkert; H W Hense; S R Holmer; M Stender; S Perz; U Keil; B H Lorell; G A Riegger Journal: N Engl J Med Date: 1994-06-09 Impact factor: 91.245
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Authors: Claudia Tamar Silva; Jan A Kors; Najaf Amin; Abbas Dehghan; Jacqueline C M Witteman; Rob Willemsen; Ben A Oostra; Cornelia M van Duijn; Aaron Isaacs Journal: Hum Genet Date: 2015-09-18 Impact factor: 5.881