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Beta-1 adrenergic receptor polymorphism may increase LVH risk.
3 September 2010
MedWire News: The Arg389 polymorphism of the beta-1 adrenergic receptor (β1AR) is associated with a higher risk for left ventricular hypertrophy (LVH) than is the Gly389 polymorphism in non-diabetic acute myocardial infarction (AMI) survivors, researchers report.
However, “the aforementioned association is not universal, since it does not exist among diabetic AMI survivors,” say Anna Hakalahti from the University of Oulu in Finland, and team.
They hypothesize that the absence of this association among diabetics “is caused by the strong association between diabetes and LVH, which may mask the presumably weaker effect of the β1AR Arg389 variant on the left ventricular structure.”
The researchers used M-mode echocardiography to measure the left ventricular parameters of 452 patients 2 to 7 days after an AMI. In all, 93 (20.6%) patients had diabetes.
The team also determined the presence of the Gly389 or Arg389 polymorphism using a polymerase chain reaction (PCR) polymorphism assay.
As reported in the journal Cardiovascular Diabetology, Hakalahti et al found that patients homozygous for Arg389 had a significantly increased left ventricular mass index (LVMI) compared with patients carrying the Gly389 polymorphism (heterozygous or homozygous), at 62.7 and 58.4, respectively.
This increase was primarily reflected by diastolic interventricular septal (IVSd) measurements, which were significantly greater among the Arg389 homozygotes than the Gly389 carriers, at 13.2 and 12.3 mm, respectively.
When diabetic and non-diabetic patients were analyzed separately, the team found that non-diabetic Arg389 homozygotes had higher LVMI and IVSd measurements than Gly389 carriers, with LVMI values of 60.6 versus 56.3 and IVSd measures of 13.1 versus 12.0 mm, respectively.
However, among the patients with diabetes, no difference was found in the LVMI and IVSd measurements of Arg389 homozygotes and Gly389 carriers.
Hakalahti and colleagues say: “Our results support the notion that there is a direct genetic impact of the β1AR Arg389 homozygosity on the left ventricular structure.”
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