Calcium in atrial fibrillation — pulling the trigger or not?

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Abstract

Atrial fibrillation (AF) is the most common sustained arrhythmia disease. Current drug- and surgical-based therapies are ineffective in about 40% to 50% of AF patients; therefore, there is a great need to better understand the underlying mechanisms of this disease and identify potential therapeutic targets. In this issue of the JCI, Greiser and coworkers discovered that atrial remodeling in response to sustained tachycardia silences Ca²⁺ signaling in isolated rabbit and human atrial myocytes. This Ca²⁺ release silencing was attributable to a failure of subcellular propagated Ca²⁺ release due to an increased cytosolic buffering strength. The results from this study challenge the current paradigm that Ca²⁺ release instability underlies AF. Instead, Ca²⁺ silencing could be protective against the massive cellular Ca²⁺ loading that occurs during chronic AF.

Authors

Nieves Gomez-Hurtado, Björn C. Knollmann