INTRODUCTION: Left ventricular hypertrophy is recognized as one of the most important independent predictors of adverse cardiovascular outcome. The aetiology of LVH includes a number of well-recognized causes but there is considerable interest in the genetics of cardiac muscle hypertrophy. We used a large prospective twin database in order to establish the heritability of left ventricular mass (LVM). METHODS: Normotensive twins were prospectively recruited. Demographic data were collected. The LVM was determined using the Penn formulae derived from data collected from echocardiography. RESULTS: A total of 376 Caucasian twin pairs (182 monozygotic and 194 dizygotic) aged 25-79 years were recruited. All subjects were normotensive with no significant differences in blood pressure (mean blood pressure: monozygotic twins, 132/83 mmHg; dizygotic twins, 131/82 mmHg) or body mass index between the monozygotic and dizygotic twins. The mean LVM for monozygotic twins was 140.9 g, compared with 140.2 g for dizygotic twins. Heritability estimates suggest that the genetic variance of LVM is 0.59 (95% confidence interval, 0.5-0.67). No common shared environmental effects were identified under this model. CONCLUSION: Our data from the largest set of twin pairs studied to date show that LVM has a sizeable genetic basis that is probably polygenic. This result has important implications for the understanding of normal and abnormal cardiac morphology at the molecular level.
INTRODUCTION:Left ventricular hypertrophy is recognized as one of the most important independent predictors of adverse cardiovascular outcome. The aetiology of LVH includes a number of well-recognized causes but there is considerable interest in the genetics of cardiac muscle hypertrophy. We used a large prospective twin database in order to establish the heritability of left ventricular mass (LVM). METHODS: Normotensive twins were prospectively recruited. Demographic data were collected. The LVM was determined using the Penn formulae derived from data collected from echocardiography. RESULTS: A total of 376 Caucasian twin pairs (182 monozygotic and 194 dizygotic) aged 25-79 years were recruited. All subjects were normotensive with no significant differences in blood pressure (mean blood pressure: monozygotic twins, 132/83 mmHg; dizygotic twins, 131/82 mmHg) or body mass index between the monozygotic and dizygotic twins. The mean LVM for monozygotic twins was 140.9 g, compared with 140.2 g for dizygotic twins. Heritability estimates suggest that the genetic variance of LVM is 0.59 (95% confidence interval, 0.5-0.67). No common shared environmental effects were identified under this model. CONCLUSION: Our data from the largest set of twin pairs studied to date show that LVM has a sizeable genetic basis that is probably polygenic. This result has important implications for the understanding of normal and abnormal cardiac morphology at the molecular level.
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