Year: 2013
Type: other
Abstract: Normal Activation delay Marked activation delay Excitation failure Changes in AP shapeEarly completion of repolarization TQ-segment depressionThe pathophysiological mechanism of arrhythmogenic right ventricular cardiomyopathy Mechanical overload of the myocyte-myocyte junction is considered to be the pivotal mechanism in ARVC.61 This concept arose after the demonstration of mutations in ARVC patients which are located in the genes encoding the so-called desmosomal proteins, which are important components of the adhering junctions between cardiomyocytes.62,63 These mutations can be identified in ~40% of ARVC patients 54 and are located in the genes encoding plakoglobin 64 , desmoplakin 65 , plakophilin-2 66 , desmoglein-2 67 and desmocollin-2 68 .Mouse models based on the altered expression
Author: Mark G. Hoogendijk
Language: English
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W1943442850