A genetic variant of the atrial natriuretic peptide gene is associated with left ventricular hypertrophy in a non-diabetic population – the Malmö preventive project study
- Equal contributors
1 Department of Biomedical Laboratory Science, Malmö University, Malmö, Sweden
2 Department of Cardiology, Skåne University Hospital Malmö, and Lund University, Malmö, Sweden
3 Department of Clinical Sciences, Lund University, Skåne University Hospital Malmö, Malmö, Sweden
4 Center of Emergency Medicine, Skåne University Hospital Malmö, Malmö, Sweden
BMC Medical Genetics 2013, 14:64 doi:10.1186/1471-2350-14-64Published: 24 June 2013
Epidemiological studies have shown considerable heritability of blood pressure, thus suggesting a role for genetic factors. Previous studies have shown an association of a single nucleotide polymorphism rs5068 in the NPPA locus gene with higher levels of circulating atrial natriuretic peptide as well as with lower intra individual blood pressure, but up to date, no association between rs5068 and cardiac organ damage, i.e. left ventricular hypertrophy, has been accounted for in humans. We sought to explore if rs5068 is associated with left ventricular hypertrophy as measured by echocardiographic examination in a non-diabetic population.
968 non-diabetic individuals from the Malmö Preventive Project (mean age 67 years; 31% women) were genotyped and examined with echocardiography. Logistic regression was used to adjust for covariates.
The minor allele of rs5068 was associated with decreased prevalence of left ventricular hypertrophy (p = 0.021) after adjustment for sex and age. In the multivariate logistic analysis including; age, sex, systolic blood pressure, antihypertensive and/or cardioprotective treatment, body mass index and fasting plasma glucose, the association of rs5068 with left ventricular hypertrophy was, as expected, attenuated (p = 0.061).
In a non-diabetic population, the minor allele of rs5068 was associated with lower left ventricular mass. These findings suggest that rs5068, or genetic variants in linkage disequilibrium, might affect susceptibility to left ventricular hypertrophy and support the possible protective role of natriuretic peptides.