What is the clinical evidence from this study?

Study design: Other. Population: Chronic left atrial dilatation (CDLA) and Atrial Fibrillation (n=16). Intervention: Creation of mitral regurgitation (CDLA model) vs. Control dogs. Primary outcome: Conduction velocity at the left atrial posterior wall (m/s) (p=<0.01).

January 1, 2007Open Access

Alterations in Electrophysiology and Tissue Structure of the Left Atrial Posterior Wall in a Canine Model of Atrial Fibrillation Caused by Chronic Atrial Dilatation

Q: What are the key findings of this study?

In a canine model of chronic left atrial dilatation, conduction velocity in the left atrial posterior wall was significantly decreased (0.87 vs 1.06 m/s, p<0.01) and associated with increased interstitial fibrosis and atrial fibrillation inducibility.

Key Result

In a canine model of chronic left atrial dilatation, conduction velocity in the left atrial posterior wall was significantly decreased (0.87 vs 1.06 m/s, p<0.01) and associated with increased interstitial fibrosis and atrial fibrillation inducibility.

PICO

Population

Chronic left atrial dilatation (CDLA) and Atrial Fibrillation (n=16)

Intervention / Comparator

Creation of mitral regurgitation (CDLA model) vs Control dogs

Primary Outcome

Conduction velocity at the left atrial posterior wall (m/s), p=<0.01

Main Result

Absolute Event Rate: 0.87% vs 1.06%

p-value: p=<0.01

Limitations

Analysis of conduction between the pulmonary veins and left atrium was not performed.
Did not investigate other factors like dominant frequencies or direction-dependent abnormal conduction.
Care should be taken in extrapolating the mechanism to other models of atrial fibrillation.

Abstract

BACKGROUND: Chronic left atrial dilatation (CDLA) is associated with an increased incidence of atrial fibrillation (AF). The electrophysiological functions of the left atrial posterior wall (LAPW) are not well understood. METHODS AND RESULTS: Eight control dogs and 8 with CDLA (developed 6 months after partial mitral valve avulsion) were studied. An electrophysiological study was performed using the noncontact mapping system. The conduction velocity was significantly decreased in the LAPW in the CDLA group. During atrial extrastimulation, a sharp curvature in the activation wavefront became apparent in the LAPW of 6 CDLA dogs, with unidirectional block in 1 dog. The effective refractory periods increased homogeneously throughout the atrium in the CDLA group. AF was much more easily inducible in the CDLA dogs than in the controls. After the onset of AF, the LAPW exhibited the earliest disorganized activity as compared with other sites in the left atrial. In the CDLA dogs, the most extensive interstitial fibrosis was observed in the LAPW. CONCLUSIONS: Alterations in the electrophysiologic properties and tissue structure of the LAPW were observed in the CDLA dogs. This study supports the idea that the LAPW may play a role in the mechanism of AF induced by CDLA.

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Cite This Study

Tang et al. (Mon,) conducted a other in Chronic left atrial dilatation (CDLA) and Atrial Fibrillation (n=16). Creation of mitral regurgitation (CDLA model) vs. Control dogs was evaluated on Conduction velocity at the left atrial posterior wall (m/s) (p=<0.01). In a canine model of chronic left atrial dilatation, conduction velocity in the left atrial posterior wall was significantly decreased (0.87 vs 1.06 m/s, p<0.01) and associated with increased interstitial fibrosis and atrial fibrillation inducibility.

synapsesocial.com/papers/6a0f03b22eca052da64804c5 https://doi.org/https://doi.org/10.1253/circj.71.1636