In patients with documented focal induction of non-permanent AF and absence of structural heart disease, PVI is as effective in endurance athletes as in other patients.

Symptomatic focal atrial tachycardia near His may originate from the NCC and can be treated safely and effectively with radiofrequency ablation.

Mutations in the SCN5A gene are responsible for multiple phenotypical presentations including Brugada syndrome, long QT syndrome, progressive familial heart block, sick sinus syndrome, dilated cardiomyopathy, lone atrial fibrillation and multiple overlap syndromes. These different phenotypic expressions of a mutation in a single gene can be explained by variable expression and reduced penetrance. One of the possible explanations of these phenomena is the co-inheritance of genetic variants. We describe a family where the individuals exhibit a compound heterozygosity in the SCN5A gene including a mutation (R1632H) and a new variant (M858L). Individuals with both the mutation and new variant present with a more severe phenotype including spontaneous atrial tachyarrhythmia at young age. We give an overview of the different phenotypes of "SCN5A disease" and discuss the importance of co-inherited genetic variants in the expression of SCN5A disease.

LV flow pattern analysis by echocardiographic particle image velocimetry reveals that conduction delay due to LBBB or pacemaker stimulation in the right ventricle (DDD) disturbs the transfer of kinetic energy during the cardiac cycle and causes less efficient LV function. These data contribute to a better understanding of hemodynamic consequences of conduction delays and may help in the optimization of therapeutic approaches.

No abstract