Key result
The aldosterone synthase -344C/T allele was not significantly associated with left ventricular structure, function, blood pressure, or serum aldosterone levels in two population-based samples.
Why the study?
Does the aldosterone synthase -344C/T polymorphism affect left ventricular structure, function, blood pressure, or serum aldosterone levels in a white population?
Observational (n=2,007)
Does the aldosterone synthase -344C/T polymorphism affect left ventricular structure, function, blood pressure, or serum aldosterone levels in a white population?
Answers are grounded in this paper and cite their sources.
The aldosterone synthase -344C/T polymorphism does not appear to significantly influence left ventricular size, function, blood pressure, or serum aldosterone levels in white populations.
BACKGROUND: Cardiac growth and function may be modulated in part by trophic effects of neurohormones. Specifically, aldosterone has been shown to stimulate the growth of cardiac myocytes and the accumulation of cardiac extracellular matrix proteins. Moreover, a variant of the aldosterone synthase gene (a cytosine/thymidine exchange at position -344 in the transcriptional regulatory region) has been associated with enlargement and disturbed filling of the left ventricle (LV) in a small sample of young white adults. The aim of the present study was to reinvestigate the implications of aldosterone synthase -344C/T allele status for serum aldosterone levels, blood pressure, and LV structure and function in large population-based samples. METHODS AND RESULTS: Individuals who participated in the echocardiographic substudy of the third MONICA (MONitoring trends and determinants in CArdiovascular disease) survey (n=1445) or in the second follow-up of the first MONICA survey (n=562) were studied by standardized anthropometric, echocardiographic, and biochemical measurements as well as genotyping for aldosterone synthase -344C/T allele status. In both surveys, the distribution of sex, age, arterial blood pressure, and body mass index was homogeneous in the aldosterone synthase genotype groups. Echocardiographic LV wall thicknesses, dimensions, and mass indexes were not significantly associated with a specific aldosterone synthase genotype. Likewise, no association was detectable with echocardiographic measures of LV systolic or diastolic function. Data were consistent in both samples and not materially different in subgroups defined by age, sex, or intake of antihypertensive medication. Finally, no significant association was observed for aldosterone synthase allele status and serum aldosterone levels in the group of 562 individuals. CONCLUSIONS: The data are not in favor of a significant contribution of the C/T exchange at position -344 in the aldosterone synthase transcriptional regulatory region to the variability of serum aldosterone levels, blood pressure, or cardiac size or function as found in 2 white population-based samples.
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Schunkert et al. (1999) conducted an observational in General population (n=2,007). Aldosterone synthase -344C/T allele vs. Other genotypes was evaluated on Echocardiographic LV wall thicknesses, dimensions, and mass indexes. The aldosterone synthase -344C/T allele was not significantly associated with left ventricular structure, function, blood pressure, or serum aldosterone levels in two population-based samples.
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