Key result
Homozygous alpha-adducin polymorphism linked to increased LV mass and ~15-fold higher odds of LVH.
Why the study?
The association between individual gene polymorphisms and left ventricular mass is inconsistent and contradictory, necessitating investigation of specific genetic influences on LV mass and plasma renin activity.
Does the alpha-adducin polymorphism associate with increased left ventricular mass and altered plasma renin activity in men with mild, never-treated hypertension?
Observational (n=162)
Does the alpha-adducin polymorphism associate with increased left ventricular mass and altered plasma renin activity in men with mild, never-treated hypertension?
Answers are grounded in this paper and cite their sources.
The homozygotic state of the alpha-adducin polymorphism is associated with increased left ventricular mass and low plasma renin activity in men with mild, untreated hypertension.
OBJECTIVE: Left ventricular hypertrophy (LVH) is associated with an increased risk for cardiovascular morbidity and mortality. Epidemiological studies suggest that LVH may be influenced by genetic factors. However, the evidence associating individual genes with left ventricular (LV) mass is inconsistent and contradictory. METHODS: We investigated the association between angiotensin-converting enzyme insertion/deletion, angiotensinogen and alpha-adducin polymorphisms with LV mass and plasma renin activity (PRA) in 162 men with mild, never-treated hypertension who were recruited for the Hypertension and Ambulatory Recording Venetia Study. The effect of each polymorphism on LV mass and PRA was tested in one-way analysis of covariance using LV mass index or PRA as the dependent variable after adjusting for covariates. RESULTS: The alpha-adducin polymorphism was the only individual polymorphism independently associated with LV mass index (F = 7.78, P= 0.006). Patients homozygous for the allele of that polymorphism had a LV mass index (123.4 +/- 10.5 g/m(2) ) significantly higher compared with heterozygotes (90.8 +/- 2.5 g/m(2) , P<0.01) or homozygotes (94.7 +/- 1.7 g/m(2) , P<0.05). These subjects also have significantly lower PRA (F = 4.2, P= 0.017). Albeit uncommon, 40% of homozygotes of the alpha-adducin polymorphism had LVH (odds ratio, 15.1; 95% confidence interval, 3.0-82.1). CONCLUSIONS: The homozygotic state of the allele of alpha-adducin polymorphism is independently associated with increased LV mass and low PRA. These data suggest that genetic considerations may contribute importantly to risk stratification, and perhaps therapeutic interventions targeted at LVH and the renin-angiotensin system in hypertensive patients.
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Winnicki et al. (2002) conducted an observational in mild, never-treated hypertension (n=162). alpha-adducin polymorphism vs. heterozygotes or other homozygotes was evaluated on Left ventricular hypertrophy (LVH) (OR 15.1, 95% CI 3.0-82.1). The homozygotic state of the alpha-adducin polymorphism was independently associated with increased left ventricular mass and a higher odds of left ventricular hypertrophy.
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