Clinical Studies
Angiotensinogen gene M235T polymorphism predicts left ventricular hypertrophy in endurance athletes

https://doi.org/10.1016/S0735-1097(99)00199-0Get rights and content
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Abstract

OBJECTIVES

We studied whether left ventricular mass in athletes associates with polymorphisms in genes encoding components of the renin–angiotensin system.

BACKGROUND

Adaptive left ventricular hypertrophy is a feature of the athlete’s heart. However, similarly training athletes develop left ventricular mass to a different extent, suggesting that genetic factors may modulate heart size.

METHODS

We measured left ventricular mass by echocardiography in 50 male and 30 female elite endurance athletes aged 25 ± 4 (mean ± SD) years. Deoxyribonucleic acid samples were prepared for genotyping of angiotensinogen (AGT) gene M235T polymorphism, angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and angiotensin II type 1 receptor (AT1) gene A1166C polymorphism.

RESULTS

The AGT gene M235T genotypes were significantly associated with left ventricular mass independently of blood pressure in both genders (p = 0.0036 for pooled data). TT homozygotes had greater mass compared with MM homozygotes in both men (147 ± 12 g/m vs. 132 ± 15 g/m, p = 0.032) and women (121 ± 12 g/m vs. 101 ± 13 g/m, p = 0.019). There was a gender difference in the relation between myocardial mass and AGT genotype, MT heterozygotes resembling MM homozygotes among women and TT homozygotes among men. The other studied gene polymorphisms were not associated with left ventricular mass.

CONCLUSIONS

Angiotensinogen gene M235T polymorphism is associated with the variability in left ventricular hypertrophy induced by endurance training, with athletes homozygous for the T allele having the largest hearts. We found no association between ACE gene I/D or AT1 gene A1166C polymorphisms and left ventricular mass.

Abbreviations

ACE
angiotensin-converting enzyme
AGT
angiotensinogen
ANCOVA
analysis of covariance
AT1
angiotensin II type 1 receptor
I/D
insertion/deletion
LV
left ventricular
PCR
polymerase chain reaction
RAS
renin–angiotensin system

Cited by (0)

This study was supported by grants from the Finnish Defense Forces, The Council of Health Sciences of the Finnish Academy, the Finnish Heart Foundation, the Sigrid Juselius Foundation and the Aarno Koskelo Foundation.