Ryanodine receptor-mediated Ca2+ events in atrial myocytes of patients with atrial fibrillation

Xin Liang1, Hong Xie, Pei-Hong Zhu

  • 1Bio-X Life Science Research Center, College of Life Science and Biotechnology, Shanghai Jiao Tong University, Shanghai, China.

Cardiology
|April 1, 2008
PubMed
Abstract

Insights

Atrial fibrillation (AF) alters calcium handling in heart cells. While calcium spark frequency remains unchanged, their duration and width increase, alongside more frequent calcium waves in AF patients.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Physiology

Background:

  • Atrial fibrillation (AF) is linked to altered sarcoplasmic reticulum Ca(2+) handling proteins in atrial myocytes.
  • The functional impact of these protein alterations on Ca(2+) handling in AF remains largely unknown.

Purpose of the Study:

  • To investigate if ryanodine receptor (RyR)-mediated intracellular Ca(2+) events are affected by protein alterations in AF atrial myocytes.
  • To analyze spontaneous Ca(2+) sparks and Ca(2+) waves in atrial myocytes from AF and normal sinus rhythm (NSR) patients.

Main Methods:

  • Laser scanning confocal microscopy was used to examine intact and permeabilized atrial myocytes.
  • Compared Ca(2+) spark and wave properties between AF patients (n=21) and NSR patients (n=22).

Main Results:

  • Ca(2+) spark frequency, amplitude, and rise time were similar between AF and NSR groups.
  • AF atrial myocytes showed significantly increased full width and full duration at half maximum intensity for Ca(2+) sparks.
  • The frequency of both small and global Ca(2+) waves increased in AF atrial myocytes.

Conclusions:

  • Spatiotemporal properties, not frequency, of Ca(2+) sparks are affected in AF atrial myocytes.
  • Increased frequency of Ca(2+) waves was observed in AF atrial myocytes.
  • The observed alterations in RyR-mediated Ca(2+) events differ from previous studies, warranting further investigation into underlying mechanisms.

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