gms | German Medical Science

33. Internationale Konferenz für Elektrokardiographie

Internationale Konferenz für Elektrokardiographie

Age-Related Changes In Ventricular Activation In Rat Heart

Meeting Abstract

  • corresponding author presenting/speaker S. Rossi - Università degli Studi, Parma, Italy
  • S. Baruffi - Università degli Studi, Parma, Italy
  • A. Bertuzzi - Università degli Studi, Parma, Italy
  • D. Corradi - Università degli Studi, Parma, Italy
  • E. Musso - Università degli Studi, Parma, Italy
  • E. Macchi - Università degli Studi, Parma, Italy

33rd International Congress on Electrocardiology. Cologne, 28.06.-01.07.2006. Düsseldorf, Köln: German Medical Science; 2007. Doc06ice025

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Veröffentlicht: 8. Februar 2007

© 2007 Rossi et al.
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Question: It is not known why aged hearts are more vulnerable to arrhythmias. To clarify this point we identified basic electrophysiological parameters and ventricular activation patterns in in vivo aged rat hearts.

Method Used: Unipolar epicardial potentials were recorded by means of 1 mm resolution uniform electrode arrays (8x8) during sinus rhythm (SR) and point stimulation in normal (10 months, n=4) and aged hearts (22 months, n=10). Electrical data were related to the histologically reconstructed fiber architecture of the underlying tissue.

Results: P wave, PQ interval, QRS complex and RR interval increased significantly in aged rats. Conduction velocity slightly decreased along but was unaltered across fibers. In adult hearts SR ventricular activation patterns were always stable and normally displayed one breakthrough point (BTP) in the area explored followed by isochrones synchronized by the conduction system, in agreement with previous findings. The presence of a BTP usually relates to an underlying Purkinje-ventricular junction (PVJ). In aged rats 70% of the hearts displayed abnormal and unstable SR ventricular activation patterns characterized by single, multiple or no BTPs in the area explored followed by isochrones which were similar to paced activations. This activation pattern, unsynchronized by the conduction system, was likely due to non uniform PVJ latency change occasionally resulting in functional conduction block; thus, some BTPs could disappear and new ones emerge in different regions. Spontaneous non-sustained ventricular tachycardia was also observed in some of the aged hearts.

Conclusion: The abnormal and unstable ventricular activation patterns and the altered electrophysiological parameters observed in aged hearts are consistent with conduction system impairment, most critically at the PVJs, and enhanced susceptibility to ventricular arrhythmia.