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Cardiovascular Research 2007 76(2):257-268; doi:10.1016/j.cardiores.2007.07.001
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Copyright © 2007, European Society of Cardiology

Enhanced heterogeneity of myocardial conduction and severe cardiac electrical instability in annexin A7-deficient mice

Jan W. Schrickela,*, Klara Brixiusb, Claudia Herrc, Christoph S. Clemenc, Philipp Sassed, Kathrin Reetzb, Christian Grohéa, Rainer Meyere, Klaus Tiemanna, Rolf Schröderf, Wilhelm Blochg, Georg Nickeniga, Bernd K. Fleischmannd, Angelika A. Noegelc, Robert H.G. Schwingerb,1 and Thorsten Lewaltera,1

aDepartment of Medicine-Cardiology, University of Bonn, Germany
bLaboratory of Muscle Research and Molecular Cardiology, Department of Internal Medicine III, University of Cologne, Germany
cInstitute of Biochemistry I and Center for Molecular Medicine Cologne, Medical Faculty, University of Cologne, Germany
dInstitute of Physiology I, Life and Brain Center, University of Bonn, Germany
eInstitute of Physiology II, University of Bonn, Germany
fInstitute of Neuropathology, University Erlangen-Nürnberg, Germany
gDepartment of Molecular and Cellular Sport Medicine, German Sport University Cologne, Germany

*Corresponding author. Tel.: +49 228 287 5507; fax: +49 228 287 4053. jan.schrickel{at}ukb.uni-bonn.de

Objectives Annexin A7 is involved in cardiomyocyte membrane organization and Ca2+-dependent signalling processes. We investigated the impact of annexin A7 on cardiac electrophysiological properties using an annexin A7-deficient mouse strain (annexin A7–/–).

Methods Nineteen adult annexin A7–/– and 14 wild-type mice were examined electrophysiologically in vivo by transvenous catheterization. Hearts were additionally perfused by the Langendorff method and epicardial activation mapping was performed.

Results The susceptibility to induction of atrial fibrillation was elevated in annexin A7–/– mice. Ten deficient animals showed atrial fibrillation (AF) episodes ≥ min and sustained AF ≥30 min was observed in 4 annexin A7–/– mice, but in none of the wild-type mice. The incidence of ventricular tachycardia (VT) was higher in annexin A7–/– mice and VT duration was prolonged. Epicardial mapping showed elevated anisotropy and inhomogeneity of conduction, leading to conduction blocks in the deficient mice. Besides alterations of intracellular calcium homeostasis, electron microscopy showed a homogeneous, electron-dense material that filled the myocardial intercellular compartments and accumulated at the basement membranes. This led to expansion of the extracellular spaces, which was the most probable substrate factor responsible for the disturbances of electrical communication.

Conclusions Annexin A7 deficiency causes severe electrical instability in the murine heart, including conduction disturbances and anisotropy of impulse propagation, which is accompanied by disturbed calcium handling and intercellular deposits.

KEYWORDS Arrhythmia (mechanisms); Cell communication; Conduction; Extracellular matrix; Annexin A7

1 Both senior authors contributed equally to this work.


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