Arrhythmias & electrophysiology
Impaired Intracellular Calcium Buffering Contributes to the Arrhythmogenic Substrate in Atrial Myocytes From Patients With Atrial Fibrillation
Authors' conclusion
Our findings suggest that loss of myofilament proteins, particularly reduced cTnC protein levels, causes diminished cytosolic Ca2+ buffering in persAF, thereby potentiating the occurrence of spontaneous Ca2+ release events and atrial fibrillation susceptibility.
Study context
- Population
- Myocytes from right atrial biopsies of patients in sinus rhythm or with persistent AF; atrial iPSC-derived cardiac myocytes; ex vivo mouse hearts
- Comparison
- Persistent AF vs sinus rhythm atrial myocytes
- Outcome
- Intracellular Ca2+ buffering and its arrhythmogenic role in persAF
Main finding
As reported in the abstract
- Cytosolic Ca2+ buffering decreased in persAF atrial myocytes (depleted Ca2+ buffers)
- Protein levels of selected Ca2+-binding myofilament proteins, incl. cTnC, significantly lower in persAF
- Small interfering RNA (siRNA) knockdown of cTnC in atrial iPSC-CMs phenocopied reduced cytosolic Ca2+ buffering
- si-cTnC iPSC-CMs: more spontaneous Ca2+ release events and action potential alternans at low stimulation frequencies
- Blebbistatin (indirect buffering reduction) in ex vivo mouse heart increased vulnerability to tachypacing-induced atrial arrhythmia
Original publication
Impaired Intracellular Calcium Buffering Contributes to the Arrhythmogenic Substrate in Atrial Myocytes From Patients With Atrial Fibrillation. Circulation. Published 24 June 2024. doi:10.
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