Dobutamine stress testing is a useful diagnostic tool for identifying reduced adrenergic myocardial contractile reserve related to altered myocardial expression of beta(1)-adrenergic receptor, sarcoplasmic reticulum Ca(2+)-adenosine triphosphatase, and phospholamban genes even in asymptomatic or mildly symptomatic patients with DCM.
In summary, this meta-analysis suggests that no statistically increased risk was found between β1-adrenergic receptor gene polymorphisms and susceptibility to IDCM among Europeans.
In vitro, the Gly389 variant of beta1-AR mediates less adenylyl cyclase activities than the Arg389 variant, so Arg389Gly polymorphism was investigated with regard to the genesis, progression, or arrhythmogenesis of dilated cardiomyopathy (DCM).
We have explored the effects of beta(1)AR autoantibodies obtained from DCM patients on extracellular signal-regulated kinase (ERK) activation in murine cardiomyocytes.
Evidence confirms that autoantibodies that bind to M(2) muscarinic (M(2)AChR) and beta(1) adrenergic receptors (beta(1)AR) are present in idiopathic dilated cardiomyopathy and Chagasic patients' sera.
In contrast, a previously used ELISA conducted with a linear 26-meric peptide derived from the second extracellular β1-AR loop yielded a high number of false-positive results precluding any specific identification of DCM patients.
To introduce an animal model, we investigated the β1-AAB associated autoimmunity in Doberman Pinscher (DP) with dilated cardiomyopathy, which has similarities to human DCM.
An autoantibody targeting the β1-adrenergic receptor is related to the persistent myocardial damage resulting in DCM and provides the substrate for fatal ventricular arrhythmias.
Myocarditis/dilated cardiomyopathy (DCM) patients can develop autoantibodies to various cardiac antigens and one major antigen is β1-adrenergic receptor (β<sub>1</sub>AR).