Atrial Myocyte NLRP3/CaMKII Nexus Forms a Substrate for Postoperative Atrial Fibrillation.

Authors

Jordi Heijman
Azinwi Phina Muna
Tina Veleva
Cristina E Molina
Henry Sutanto
Marcel Tekook
Qiongling Wang
Issam H Abu-Taha
Marcel Gorka
Stephan Künzel
Ali El-Armouche
Hermann Reichenspurner
Markus Kamler
Viacheslav Nikolaev
Ursula Ravens
Na Li
Stanley Nattel
Xander H T Wehrens
Dobromir Dobrev

Publication Date

9-25-2020

Journal

Circulation Research

DOI

10.1161/CIRCRESAHA.120.316710

PMID

32762493

PMCID

PMC7604886

PubMedCentral® Posted Date

9-25-2021

PubMedCentral® Full Text Version

Author MSS

Published Open-Access

yes

Keywords

Action Potentials, Aged, Animals, Atrial Fibrillation, Calcium Signaling, Calcium-Calmodulin-Dependent Protein Kinase Type 2, Cardiac Surgical Procedures, Case-Control Studies, Cell Line, Female, Heart Atria, Heart Rate, Humans, Inflammasomes, Inflammation Mediators, Male, Mice, Middle Aged, Myocytes, Cardiac, NLR Family, Pyrin Domain-Containing 3 Protein, Phosphorylation, Ryanodine Receptor Calcium Release Channel, Sarcoplasmic Reticulum

Abstract

RATIONALE: Postoperative atrial fibrillation (POAF) is a common and troublesome complication of cardiac surgery. POAF is generally believed to occur when postoperative triggers act on a preexisting vulnerable substrate, but the underlying cellular and molecular mechanisms are largely unknown.

OBJECTIVE: To identify cellular POAF mechanisms in right atrial samples from patients without a history of atrial fibrillation undergoing open-heart surgery.

METHODS AND RESULTS: Multicellular action potentials, membrane ion-currents (perforated patch-clamp), or simultaneous membrane-current (ruptured patch-clamp) and [Ca

CONCLUSIONS: Preexisting Ca