Stanley Nattel

TL;DR: The results indicate that, in human atrial cells at 36 degrees C, the properties of L-type ICa contribute importantly to the rate-dependent and autonomic control of APD.

TL;DR: This article reviews the contributions of some of this recent work to the understanding of electrophysiological, ionic and molecular mechanisms of AF and of its clinical pathophysiology and management.

TL;DR: There are major unanswered questions relating to the limited ability to determine which individuals with this common electrocardiographic variant are at risk for sudden death, the incomplete understanding of underlying mechanisms, the inadequate information regarding genetic determinants and therapeutic responses, and the unclear relationship between early repolarization and other conditions involving accelerated repolarized and sudden arrhythmic death such as Brugada and short-QT syndromes.

TL;DR: How potentially adaptive repolarization changes with congestive heart failure and atrial fibrillation can have arrhythmogenic consequences is focused on.

TL;DR: Differences in the underlying mechanisms were elucidated by studying contractile function, electrophysiology and sarcoplasmic reticulum (SR) Ca2+ load in atrial muscle bundles and by analyzing expression and phosphorylation levels of key Ca2-handling proteins, myofilaments and the expression and activity of their upstream regulators.