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. 2003 May 27;107(20):2615-22.
doi: 10.1161/01.CIR.0000066915.15187.51. Epub 2003 May 5.

Alterations in atrial electrophysiology and tissue structure in a canine model of chronic atrial dilatation due to mitral regurgitation

Sander Verheule  1 , Emily Wilson, Thomas Everett 4th, Sujata Shanbhag, Catherine Golden, Jeffrey Olgin
Affiliations
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Alterations in atrial electrophysiology and tissue structure in a canine model of chronic atrial dilatation due to mitral regurgitation

Sander Verheule et al. Circulation. .
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Abstract

Background: Clinically, chronic atrial dilatation is associated with an increased incidence of atrial fibrillation (AF), but the underlying mechanism is not clear. We have investigated atrial electrophysiology and tissue structure in a canine model of chronic atrial dilatation due to mitral regurgitation (MR).

Methods and results: Thirteen control and 19 MR dogs (1 month after partial mitral valve avulsion) were studied. Dogs in the MR group were monitored using echocardiography and Holter recording. In open-chest follow-up experiments, electrode arrays were placed on the atria to investigate conduction patterns, effective refractory periods, and inducibility of AF. Alterations in tissue structure and ultrastructure were assessed in atrial tissue samples. At follow-up, left atrial length in MR dogs was 4.09+/-0.45 cm, compared with 3.25+/-0.28 at baseline (P<0.01), corresponding to a volume of 205+/-61% of baseline. At follow-up, no differences in atrial conduction pattern and conduction velocities were noted between control and MR dogs. Effective refractory periods were increased homogeneously throughout the left and right atrium. Sustained AF (>1 hour) was inducible in 10 of 19 MR dogs and none of 13 control dogs (P<0.01). In the dilated MR left atrium, areas of increased interstitial fibrosis and chronic inflammation were accompanied by increased glycogen ultrastructurally.

Conclusions: Chronic atrial dilatation in the absence of overt heart failure leads to an increased vulnerability to AF that is not based on a decrease in wavelength.

Figures

Figure 1
Figure 1
Creation of MR. TEE images from the transgastric view 5 minutes after partial avulsion of the mitral valve. A, Color Doppler revealed a large regurgitant jet (Ao indicates aorta). B, Continuous-wave Doppler at the level of the mitral valve showed high-velocity holosystolic regurgitant flow.
Figure 2
Figure 2
Time course of LA dilatation and LV fractional shortening. A, LA length as percent of baseline (bsln) was significantly increased in the first week after creation of MR (P<0.01, n=16). B, LV fractional shortening showed a nonsignificant increasing trend after the procedure (n=16).
Figure 3
Figure 3
AF inducibility in open-chest studies. A, Longest observed AF episode duration in control and MR dogs. B, Relationship between the longest observed AF episode duration in individual MR dogs and LA dilatation (% increase in LA length with respect to baseline).
Figure 4
Figure 4
Atrial conduction patterns in control and MR dogs. A, Control RA and LA; B, MR RA and LA. Maps for the RA and LA were acquired separately; color scales for RA and LA are independent.
Figure 5
Figure 5
Effect of LA dilatation on ERP and CV. ERP (A), CV (B), and wavelength (C) as a function of BCL in the LA (left) and RA (right). Control, n=8; MR, n=10; data are mean±SEM.
Figure 6
Figure 6
Regional distribution of ERP and CV. A, Schematic representation of the atria indicating the regions in which the ERP was measured. ERP (B), CV (C), and wavelength (D) at the sites indicated in panel A, determined at a BCL of 300 ms. LLW indicates low lateral wall; HLW, high lateral wall; BB, Bachmann’s bundle; RAA, RA appendage; PW, posterior wall; and IW, inferior wall. Data are mean±SEM; control, n=8; MR, n=10.
Figure 7
Figure 7
Tissue structure in control LA and MR LA. H&E; staining of control LA at ×100 (A) and ×400 (B) magnification and MR LA at ×100 (C) and ×400 (D) magnification. Sirius red staining of control LA (E) and MR LA (F), both at ×400 magnification. Masson’s trichrome staining of control LA at ×100 (G) and ×400 (H) magnification and MR LA at ×100 (I) and ×400 (J) magnification.
Figure 8
Figure 8
Myocardial ultrastructure. A, Control LA; B, MR LA, both at ×4125 original magnification. C, Control LA; D, MR LA, both at ×28 750 original magnification. At high magnification in D, the MR LA showed extensive glycogen accumulation, visible as small black granules (arrows).
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