Wilhelm Schmitz

TL;DR: It is shown that mice with a genetic gain-of-function defect in Ryr2 did not exhibit spontaneous AF but that rapid atrial pacing unmasked an increased vulnerability to AF in these mice compared with wild-type mice, suggesting that increased RyR2-dependent Ca2+ leakage due to enhanced CaMKII activity is an important downstream effect of CaMK II in individuals susceptible to AF induction.

TL;DR: It is conceivable that an increase in myocardial Gi-proteins is causally related to heart failure due to idiopathic dilated cardiomyopathy, and in the preparation from the patient with inflammatory heart disease the contractile response to isoprenaline was not reduced and likewise content of Gi- Proteins was not changed.

TL;DR: A novel pathophysiological role is established for CMNLRP3 inflammasome signaling, with a mechanistic link to the pathogenesis of AF, and the inhibition of NLRP3 is established as a potential novel AF therapy approach.

TL;DR: In AF, increasedprotein phosphatase activity contributes to impaired basal ICa,L and it is proposed that protein phosphatases may be potential therapeutic targets for AF treatment.

TL;DR: Enhanced activity of phosphatases may be causally related to heart failure and/or may aggravate the well known decreased cardiac responsiveness to positive inotropic agents in end-stage heart failure.