Elevated immune monitoring as measured by increased adenosine triphosphate production in activated lymphocytes is associated with accelerated development of cardiac allograft vasculopathy after cardiac transplantation.

Background: Elevated immune monitoring (IM), as measured by adenosine triphosphate (ATP) release from activated lymphocytes, has been suggested to represent an under-immunosuppressed state. Its association with the development of angiographic cardiac allograft vasculopathy (CAV) is unknown.

Methods: Patients transplanted between January 2007 and December 2011 with annual angiograms and at least 1 IM assay were included in the analysis.

Elevated immune monitoring early after cardiac transplantation is associated with increased plaque progression by intravascular ultrasound.

Background: Immune monitoring (IM) has not been shown to be associated with cardiac allograft vasculopathy (CAV).

Methods: Maximal intimal area, average percent stenosis, plaque volume, and maximal intimal thickness (MIT) were measured for matched baseline and one-yr IVUS segments in a blinded fashion. Patients were divided into quartiles by IM scores and outcomes compared.

Inhibition of Coxsackievirus-associated dystrophin cleavage prevents cardiomyopathy.

Heart failure in children and adults is often the consequence of myocarditis associated with Coxsackievirus (CV) infection. Upon CV infection, enteroviral protease 2A cleaves a small number of host proteins including dystrophin, which links actin filaments to the plasma membrane of muscle fiber cells (sarcolemma). It is unknown whether protease 2A-mediated cleavage of dystrophin and subsequent disruption of the sarcolemma play a role in CV-mediated myocarditis.

Cortactin is required for N-cadherin regulation of Kv1.5 channel function.

The intercalated disc serves as an organizing center for various cell surface components at the termini of the cardiomyocyte, thus ensuring proper mechanoelectrical coupling throughout the myocardium. The cell adhesion molecule, N-cadherin, is an essential component of the intercalated disc. Cardiac-specific deletion of N-cadherin leads to abnormal electrical conduction and sudden arrhythmic death in mice.

Coxsackievirus and adenovirus receptor (CAR) mediates atrioventricular-node function and connexin 45 localization in the murine heart.

The coxsackievirus and adenovirus receptor (CAR) is a transmembrane protein that belongs to the family of adhesion molecules. In the postnatal heart, it is localized predominantly at the intercalated disc, where its function is not known. Here, we demonstrate that a first degree or complete block of atrioventricular (AV) conduction developed in the absence of CAR in the adult mouse heart and that prolongation of AV conduction occurred in the embryonic heart of the global CAR-KO mouse.