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Atrial apoptosis and fibrosis adversely affect atrial conduit, reservoir and contractile functions

Chronic atrial volume overload and atrial fibrillation (AF) induce structural changes within atrial myocardium. The aim of this study was to evaluate the effect of adverse cellular remodelling on echocardiographic strain rate (SR) deformation indices of atrial contractile, conduit and reservoir functions. Forty-four consecutive patients with organic mitral regurgitation were analysed. Twenty-eight patients had long-standing persistent AF (AF group), while 16 were in normal sinus rhythm (NSR group). Left atrial (LA) samples were harvested from all the patients for histological analysis. Postoperative echocardiographic data acquisition was performed exclusively during organized atrial electrical activity in order to assess the contractile reserve of patients from both groups. RESULTS: Fibrotic atria had inferior conduit (SR-E: r = -0.36, P = 0.017), reservoir (SR-S: r = -0.31, P = 0.041) and contractile functions (SR-A: r = -0.33, P = 0.027). Analogously, atria with greater apoptotic burdens showed a negative correlation with multiple indices of left atrial functions (SR-E: r = -0.38, P = 0.010 ; SR-S: r = -0.33, P = 0.028 ; SR-A: r = -0.28, P = 0.067). The efficiency of atrial contractility was significantly reduced among AF-group patients after conversion to sinus rhythm, when compared with patients in the NSR group (LA active emptying fraction: 20 ± 12 vs 30 ± 10%, P = 0.004 ; SR-A: 1.1 ± 1.0 vs 2.8 ± 1.9 s(-1), P < 0.001). Superior strain-rate indices of atrial conduit and reservoir functions were noted in the NSR group (SR-E: 3.5 ± 2.3 vs 1.3 ± 1.0 s(-1), P < 0.001 ; LA expansion index: 86 ± 31 vs 60 ± 42%, P = 0.004). Fibrosis was evident in 7.2 [3.3 ; 9.4]% of the LA tissue sample in the AF group, while it accounted for 3.4 [1.2 ; 8.1]% of atrial tissue in the NSR group (P = 0.054). Apoptosis was documented in 13 (46%) patients in the AF group, whereas none of the patients in the NSR group exhibited signs of programmed cell death (P = 0.001). Myocyte degeneration was more prevalent in the AF group (odds ratio: 7.0, 95% confidence interval: 1.3-36.7, P = 0.021). Age showed a positive correlation with worsening degrees of atrial fibrosis and apoptosis (r = 0.41, P = 0.006 ; r = 0.49, P = 0.001, respectively). Multiple regression analysis identified SR-S (β = -1.263, P = 0.036) and age (β = 0.144, P = 0.057) as independent predictors of fibrosis. Independent determinants of apoptosis were preoperative AF (β = 4.539, P = 0.007), age (β = 0.188, P = 0.009) and SR-S (β = -1.780, P = 0.002). Atria exhibiting greater fibrotic and apoptotic burdens had impaired conduit, reservoir and contractile function, as evaluated by deformation imaging. Among patients with chronic LA volume overload, exposure to long-standing persistent AF induced more pronounced degrees of adverse atrial cellular remodelling. Strain-rate descriptors of atrial reservoir function harboured potential to predict atrial fibrosis and apoptosis.

Apoptosis; Atrial fibrillation; Atrial function; Atrial remodelling; Fibrosis

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