Günter Breithardt

TL;DR: The authors observed significantly longer conduction intervals on baseline ECG in patients with established SCN5A mutations (PQ and HV interval and, upon class I drugs, more QRS increase) which concur with the observed loss of function of mutated BS-related sodium channels.

TL;DR: It is shown that macrolide antibiotics lead to similar prolongation of repolarization but show a different proarrhythmic potential (erythromycin > clarithromycin • azithromyzin > azithrocin) than previously reported, which may be related to a rectangular pattern of action potential prolongation.

TL;DR: Genetic testing of SCN5A is especially useful in familial disease to identify individuals at cardiac risk and in sporadic cases, however, a genetic basis and the value of mutation screening has to be further determined.

TL;DR: It is reported that the lysosomal cysteine peptidase cathepsin L (CTSL) is critical for cardiac morphology and function and echocardiographic and electrocardiographic findings to some degree point to left ventricular hypertrophy that most likely represents an adaptive response to cardiac impairment.

TL;DR: All patients with aborted sudden death or unexplained syncope without demonstrable structural heart disease and family members of affected individuals should presently undergo drug testing for unmasking BS using ajmaline using a protocol with fractionated drug administration.