Atrial apoptosis and fibrosis adversely affect atrial conduit, reservoir and contractile functions
Atrial apoptosis and fibrosis adversely affect atrial conduit, reservoir and contractile functions
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DOI：
10.1093/icvts/ivu095
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发表时间：
2014-08-01
影响因子：
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通讯作者：
Biocina, Bojan
中科院分区：
文献类型：
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作者：
Gasparovic, Hrvoje;Cikes, Maja;Biocina, Bojan
结论：慢性心房容量超负荷和心房颤动（AF）诱导心房心肌内的结构变化。本研究的目的是评估不利的细胞重塑对超声心动图应变率（SR）变形指标的心房收缩，管道和水库functions.METHODS：四十四个连续的有机二尖瓣返流患者进行了分析。28例患者有长期持续性AF（AF组），而16例患者处于正常窦性心律（NSR组）。所有患者均采集左心房（LA）样本进行组织学分析。术后超声心动图数据采集仅在有组织的心房电活动期间进行，以评估两组患者的收缩储备。（SR-E：r =-0.36，P = 0.017）、储库（SR-S：r =-0.31，P = 0.041）和收缩功能（SR-A：r =-0.33，P = 0.027）。类似地，具有较大凋亡负荷的心房与多个左心房功能指标呈负相关（SR-E：r =-0.38，P = 0.010; SR-S：r =-0.33，P = 0.028; SR-A：r =-0.28，P = 0.067）。与NSR组患者相比，AF组患者转为窦性心律后心房收缩效率显著降低（LA主动排空分数：20 +/- 12 vs 30 +/-10%，P = 0.004; SR-A：1.1 +/- 1.0 vs 2.8 +/- 1.9 s（-1），P < 0.001）。在NSR组中观察到心房导管和储血器功能的上级应变率指数（SR-E：3.5 +/- 2.3 vs 1.3 +/- 1.0 s（-1），P < 0.001; LA扩张指数：86 +/- 31 vs 60 +/-42%，P = 0.004）。AF组中7.2 [3.3; 9.4]%的LA组织样本中纤维化明显，而NSR组中纤维化占心房组织的3.4 [1.2; 8.1]%（P = 0.054）。AF组中13例（46%）患者记录到细胞凋亡，而NSR组中无患者显示程序性细胞死亡迹象（P = 0.001）。AF组的肌细胞变性更普遍（比值比：7.0，95%置信区间：1.3-36.7，P = 0.021）。年龄与心房纤维化和细胞凋亡的恶化程度呈正相关（分别为r = 0.41，P = 0.006; r = 0.49，P = 0.001）。多元回归分析确定SR-S（β =-1.263，P = 0.036）和年龄（β = 0.144，P = 0.057）为纤维化的独立预测因子。凋亡的独立决定因素是术前AF（β = 4.539，P = 0.007）、年龄（β = 0.188，P = 0.009）和SR-S（β =-1.780，P = 0.002）。结论：通过变形成像评估，显示更大纤维化和凋亡负荷的心房具有受损的管道、储库和收缩功能。在慢性左心房容量超负荷的患者中，暴露于长期持续性AF会诱导更明显程度的不良心房细胞重构。心房储血功能的应变率描述符具有预测心房纤维化和细胞凋亡的潜力。
OBJECTIVES: 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.METHODS: 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 (beta = -1.263, P = 0.036) and age (beta = 0.144, P = 0.057) as independent predictors of fibrosis. Independent determinants of apoptosis were preoperative AF (beta = 4.539, P = 0.007), age (beta = 0.188, P = 0.009) and SR-S (beta = -1.780, P = 0.002).CONCLUSIONS: 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.