超聲預(yù)測心房顫動導管消融術(shù)后復發(fā)的研究現(xiàn)狀

吳曉宇 周根青 劉少穩(wěn)

隨著對心房顫動(簡稱房顫)發(fā)生機制認識的逐漸深入以及導管消融技術(shù)水平的不斷進步，導管消融治療房顫的新模式已被廣泛運用于臨床。導管消融在改善心悸癥狀、提高生活質(zhì)量和減少房顫再發(fā)等方面均優(yōu)于抗心律失常藥物治療[1]，但仍有38.9%的陣發(fā)性房顫和58.4%的非陣發(fā)性房顫患者在三年內(nèi)出現(xiàn)房顫復發(fā)[2]。導管消融術(shù)后的高復發(fā)率成了臨床工作中的一個難題，如何降低房顫患者導管消融術(shù)后的復發(fā)率是臨床研究工作的重要部分。隨著超聲技術(shù)的發(fā)展，多種超聲檢測的特異性預(yù)測因子被用來評估房顫復發(fā)。筆者將圍繞房顫導管消融術(shù)后復發(fā)的超聲預(yù)測因子的研究現(xiàn)狀進行綜述。

1 超聲預(yù)測消融術(shù)后房顫復發(fā)的理論基礎(chǔ)

在山羊的房顫模型中發(fā)現(xiàn)，纖維化和心肌細胞肥大等心房的結(jié)構(gòu)性重構(gòu)是引起顫動波傳導方式改變和房顫穩(wěn)定性增加的潛在機制[3]。細胞外基質(zhì)中膠原合成，包繞在心房肌纖維周圍形成結(jié)締組織間隔，引起心房縱向肌束電分離[4]。房顫又引起心臟功能障礙和電重構(gòu)，這些改變與房顫互為因果并造成惡性循環(huán)[5]，心肌重構(gòu)加重，房顫也趨于穩(wěn)定，甚至能從陣發(fā)性房顫進展為持續(xù)性或永久性房顫[3]。消融術(shù)后肺靜脈傳導恢復、非肺靜脈異位灶的存在是房顫復發(fā)的重要原因[6-8]，而消融引起的局部、全身炎癥反應(yīng)和自主神經(jīng)功能改變是術(shù)后早期復發(fā)房顫的可能原因[9-10]。可見,術(shù)前的左房基質(zhì)影響了術(shù)后房顫的復發(fā)，復發(fā)率與疾病本身的病理生理機制有關(guān)。通過超聲檢測房顫患者心房的結(jié)構(gòu)和功能改變，就能幫助對消融術(shù)后房顫復發(fā)情況進行評估。

2 結(jié)構(gòu)性預(yù)測因子

2.1術(shù)前左房直徑(left atrial diameter, LAD) 正常的心肌在心力衰竭、心室壁增厚或心臟增大后更容易發(fā)生房顫等心律失常[5]。早期的幾項研究檢測房顫發(fā)生前后超聲心動圖上左房大小，發(fā)現(xiàn)左房增大是房顫發(fā)作的獨立預(yù)測因子[11-13]。目前臨床多采用胸骨旁心臟長軸觀來測量術(shù)前LAD，這種方法因操作簡便被廣泛運用于評價左房的大小。Gerede等[14]在51例陣發(fā)性房顫患者的研究中發(fā)現(xiàn)，復發(fā)組術(shù)前LAD明顯大于未復發(fā)組[( 41 ± 5 ) mm vs ( 34 ± 5 ) mm，P<0.000 1],并且界定術(shù)前LAD > 40 mm是房顫復發(fā)的預(yù)測因子。McCready等[15]發(fā)現(xiàn)，術(shù)前LAD < 43 mm是房顫消融術(shù)后房顫長期緩解的預(yù)測因子(敏感性92%，特異性52%)。Miyazaki等[16]對474例藥物治療無效的陣發(fā)性房顫患者進行了更加細致的分析,發(fā)現(xiàn)LAD每增加1mm，消融術(shù)后復發(fā)率就上升7.2%。另外，與正常直徑相比，左房中度擴張(LAD: 40 ～ 50 mm)和重度擴張(LAD > 50 mm)的房顫患者術(shù)后復發(fā)率分別增加1.30和2.14倍[16]。D′Ascenzo等[17]進行了一項大樣本的研究，包含4 357例陣發(fā)性房顫和1 777例持續(xù)性房顫患者，發(fā)現(xiàn)LAD > 50 mm是消融術(shù)后房顫復發(fā)的一個強有力的預(yù)測因子。Tzou等[18]、Montserrat等[19]和 Lo等[20]的研究均有類似發(fā)現(xiàn)，LAD越大，術(shù)后房顫復發(fā)率可能越高。

另外，考慮到左房大小與體形存在明顯關(guān)系，有研究在測得LAD后除以體表面積得到左房直徑指數(shù)(left atrial diameter index,LADI)。Shin等[21]選取消融術(shù)前左房前后徑(胸骨旁長軸觀)、左房上下徑(心尖四腔觀)，計算得到LADI，發(fā)現(xiàn)消融術(shù)后房顫復發(fā)組和未復發(fā)組左房前后LADI、上下LADI都具有統(tǒng)計學差異[(25.9 ± 4.4 )mm/m2vs ( 22.5 ± 2.9 ) mm/m2、 ( 34.0 ± 5.2 )mm/m2vs ( 29.3 ± 3.3 ) mm/m2,P均= 0.01]。

可見，LAD是房顫復發(fā)理想的預(yù)測因子。而LADI進一步減弱了不同體形對LAD基礎(chǔ)值的影響，其預(yù)測效益可能更高。

2.2左房容積(left atrial volume ,LAV) 由于左房形狀不規(guī)則，單個切面上的直徑不能充分反映整個心房重構(gòu)的程度。LAV預(yù)測消融術(shù)后房顫復發(fā)的效益可能優(yōu)于LAD。另外，超聲檢查中心尖四腔觀能完全暴露整個左房，此切面評價LAV優(yōu)于胸骨旁兩腔觀[22]。Montserrat等[19]對154例房顫病人的研究中，發(fā)現(xiàn)LAV > 82.35 ml是首次消融術(shù)后房顫復發(fā)的預(yù)測因子(特異性 96% )。以研究對象中位數(shù)年齡(54歲)分組，年齡≤54歲的房顫未復發(fā)組和復發(fā)組間LAV具有統(tǒng)計學差異[(50.7 ± 12.9 ) ml vs ( 67.7 ±24.1 ) ml，P=0.04]，而年齡>54歲兩組間LAV無顯著差異[(52.0 ± 6.2 ) ml vs ( 54.2 ± 17.4 ) ml，P=0.82]，說明復發(fā)組與未復發(fā)組間的LAV在年輕患者中差異更明顯。

與LAD相同，LAV也與體形相關(guān)。有研究在測得LAV后除以體表面積得到左房容積指數(shù)(left atrial volume index ,LAVI)。Shin等[21]發(fā)現(xiàn)術(shù)前LAVI > 34 ml/m2是消融術(shù)后房顫復發(fā)的預(yù)測因子(敏感性70% ，特異性91%)。Kohari等[22]認為LAVI > 26 ml/m2是房顫復發(fā)的預(yù)測因子。den Uijl等[23]發(fā)現(xiàn)消融術(shù)后房顫復發(fā)組的LAVI明顯大于未復發(fā)組[ ( 46.06 ± 16.9 ) ml/m2vs ( 40.26 ± 14.1 ) ml/m2，P=0.016]。

2.3結(jié)構(gòu)性預(yù)測因子的研究存在分歧 最近有幾項研究認為，導管消融術(shù)后房顫復發(fā)組與未復發(fā)組的LAD或LAV無差異[24-26]。多種原因可能引起這種分歧。上述Montserrat等[19]對房顫復發(fā)組與未復發(fā)組術(shù)前LAV的研究中，不同年齡分層兩組間的LAV差異性不同，表明研究對象的年齡異質(zhì)性可能會對研究結(jié)果產(chǎn)生影響。此外，上述研究房顫類型、消融術(shù)式和隨訪時間均存在差異，都可能影響預(yù)測效益。同時，超聲在檢測結(jié)構(gòu)性預(yù)測因子時誤差較大：左房不規(guī)則的形狀使LAD評價左房大小存在缺陷；拖帶效應(yīng)(即周圍組織牽拉)和角度偏差降低了檢測指標的可靠性[27]。即便如此，也不能完全否定結(jié)構(gòu)性預(yù)測因子對消融術(shù)后房顫復發(fā)的預(yù)測效益。

3 功能性預(yù)測因子引起廣泛的關(guān)注

與房顫相關(guān)的心臟結(jié)構(gòu)改變是一個歷時較長的過程[3, 28]。山羊的動物模型中，在心房結(jié)構(gòu)性重構(gòu)能被檢測之前，房顫的性質(zhì)早已穩(wěn)定[3]。因此，用左房結(jié)構(gòu)來預(yù)測房顫復發(fā)就顯得相對滯后，對房顫復發(fā)的二級預(yù)防意義不大。而心房超微結(jié)構(gòu)的改變相對較早發(fā)生，這種改變由心肌細胞能量的產(chǎn)生和利用出現(xiàn)缺陷引起，包括心肌細胞內(nèi)糖原累積、收縮結(jié)構(gòu)消失和線粒體外形變異[29]。在陣發(fā)性房顫患者的早期病程中，左房的結(jié)構(gòu)性重構(gòu)還未能被監(jiān)測到，功能性重構(gòu)的預(yù)測因子此時就體現(xiàn)出了優(yōu)越性[30]。而且，在組織多普勒成像基礎(chǔ)上發(fā)展的新技術(shù)如應(yīng)變率成像、二維斑點追蹤成像、實時三維超聲心動圖等在評價左房功能時能有效減少檢測過程中的誤差[31-33]。因此，左房的功能性重構(gòu)與房顫復發(fā)的關(guān)系引起廣泛關(guān)注。

3.1左心耳血流速度(left atrial appendage flow velocity ,LAAV) LAAV可作為左房儲存器功能和收縮功能的評估指標[34]。心房纖維化時，左心耳通過其自身的伸展性來調(diào)節(jié)左房壓力-容量關(guān)系，以增強血流動力學功能[35]。Gerede等[14]在51例陣發(fā)性房顫患者消融術(shù)后1年的隨訪中發(fā)現(xiàn)，房顫復發(fā)組的LAAV小于未復發(fā)組[(25.00 ± 9.16 )cm/s vs ( 56.00 ± 26.72 ) cm/s,P< 0.000 ]，LAAV ≤ 30 cm/s是消融術(shù)后房顫復發(fā)的預(yù)測因子(敏感性85%，特異性95%)。其他的研究還報道了LAAV > 28 cm/s(敏感性62%，特異性69%)[36]，> 30 cm/s (敏感性77.8%，特異性72.8%)[37],> 31 cm/s(敏感性約40%，特異性約80%)[38],> 40 cm/s(敏感性56%，特異性80%)[39]是消融成功的獨立性預(yù)測因子，但后兩項研究的結(jié)果的敏感性相對較低。

3.2左房和左室血流速度 多普勒超聲測得的心腔中血流速度，如E、e′、A等(E：舒張早期最大峰值流速，e′：舒張早期跨二尖瓣環(huán)流速，A：舒張晚期最大峰值流速)，可以反應(yīng)左房和左室中的壓力梯度[40]。左房、左室血流速度的下降提示左室舒張功能障礙，左室順應(yīng)性降低，使左房長時間處于壓力過載的情況下，促進房顫的發(fā)生和維持[41]。Chung等[42]對66例房顫消融術(shù)后患者隨訪中，發(fā)現(xiàn)E/e′值> 9.15是消融術(shù)后房顫復發(fā)的預(yù)測因子(敏感性75%，特異性73.1%)。

另外，有最新的研究引入Sa(收縮期跨二尖瓣環(huán)流速)、Aa(舒張晚期跨二尖瓣環(huán)流速)，Sa與左心室收縮功能有關(guān)[43]，所以 E/( e′*Sa)和Ea/(Aa*Sa)的值就能同時反應(yīng)左心室的收縮和舒張功能。在對73例消融術(shù)后房顫患者的隨訪中發(fā)現(xiàn)，E/( e′×Sa)和Ea/(Aa×Sa)比E/e′值預(yù)測消融術(shù)后房顫復發(fā)更敏感[44]。

3.3左房射血分數(shù)(left atrial emptying fraction ,LAEF) LAEF=(左房最大容積-左房最小容積) / 左房最大容積×100%。LAEF是公認的左房儲存功能和管道功能的代表因子，檢測方法相對簡單可行[45]。Kim等[45]在130例房顫消融術(shù)后患者2年的隨訪中發(fā)現(xiàn)，房顫復發(fā)組的LAEF低于未復發(fā)組[ (28.1 ± 7.7 ) % vs ( 31.4 ± 9.4 ) %,P=0.034]，LAEF < 20%是消融術(shù)后房顫復發(fā)的預(yù)測因子(敏感性69%，特異性84%)。在Lim等[46]的研究中，定義LAEFactive = 100 ×(心電圖上p波出現(xiàn)時的左房容積-左房最小容積)/ 心電圖p波出現(xiàn)時的左房容積，發(fā)現(xiàn)LAEFactive < 23.5% 是消融術(shù)后房顫復發(fā)的預(yù)測因子(敏感性66.7%，特異性63.6%)。

3.4左房應(yīng)變(left atrial strain ,LAS) LAS(左房內(nèi)徑的變化值占原內(nèi)徑的百分比)是基于左房形變的功能參數(shù)，反應(yīng)了心肌的生理力學特性[47-48]，其結(jié)果不受心臟整體運動和拖帶效應(yīng)的影響，測值相對準確而客觀[31]。Hong等[49]發(fā)現(xiàn)LAS降低是消融術(shù)后3個月房顫復發(fā)的唯一預(yù)測因子。另外，LAS在區(qū)分孤立性房顫患者和健康人的效能優(yōu)于LAV，因此LAS比LAV更有效地反應(yīng)左房重構(gòu)[49]。其他類似的研究在消融術(shù)后的隨訪中發(fā)現(xiàn)術(shù)前LAS > 20%(敏感性86%，特異性70%)[26]、LAS > 23.2%(敏感性76%，特異性66%)[50]是房顫患者保持竇性心律的預(yù)測因子。Ma等[51]匯總了8項關(guān)于LAS與消融術(shù)后房顫復發(fā)關(guān)系的研究，總樣本量高達686例，發(fā)現(xiàn)消融術(shù)后房顫復發(fā)組的LAS小于未復發(fā)組，LAS≤22.8%為消融術(shù)后房顫復發(fā)的預(yù)測因子(敏感性78%，特異性75%)。

左房側(cè)壁不受右房和肺靜脈影響，左房側(cè)壁的應(yīng)變能最真實地反應(yīng)左房肌肉的收縮能力和左房的功能[30]。Yasuda等[30]對100名房顫患者1年的隨訪中，發(fā)現(xiàn)以左房側(cè)壁的應(yīng)變(left atrial lateral strain ,LA-LS=心室收縮時左房側(cè)壁的應(yīng)變—心房收縮時左房側(cè)壁的應(yīng)變)<25.27%作為消融術(shù)后房顫復發(fā)的預(yù)測因子(敏感性81%，特異性82%)，其預(yù)測效益優(yōu)于LAS。

3.5估計肺動脈楔壓(estimated pulmonary capillary wedge Pressure , ePCWP) ePCWP[10.8-12.4×log10(AEFactive / LAVImin)]是采用斑點追蹤超聲監(jiān)測動力學追蹤指數(shù)來估算的指標，它結(jié)合了房顫復發(fā)的功能性預(yù)測因子(LAEF)和結(jié)構(gòu)性預(yù)測因子(LAVI)，比單獨使用左房功能或結(jié)構(gòu)因子來評估消融預(yù)后效益高。Kawasaki等[52]發(fā)現(xiàn)ePCWP< 13 mmHg是消融術(shù)后房顫復發(fā)的預(yù)測因子(敏感性73%，特異性77%)。

消融術(shù)后房顫復發(fā)的功能性預(yù)測因子種類較多、各有特點，綜合分析其敏感性和特異性大多具有較準確的預(yù)測價值。并且其在預(yù)測效益上較結(jié)構(gòu)性預(yù)測因子具有優(yōu)越性，臨床上可以參考這些超聲參數(shù)篩選適合消融手術(shù)的房顫患者。

4 結(jié)論

超聲監(jiān)測的結(jié)構(gòu)性預(yù)測因子雖然得到廣泛認可，但受多種因素影響、檢測誤差大、缺乏統(tǒng)一的標準等限制，不應(yīng)該作為預(yù)測消融結(jié)果的唯一因素。隨著新型超聲設(shè)備的使用，功能性參數(shù)能為左房狀態(tài)提供額外的信息，并且都被證明是消融術(shù)后房顫復發(fā)的獨立預(yù)測因子。這些檢測在臨床上方便可行，檢測結(jié)果可信度高，可被廣泛運用以指導臨床治療策略，使房顫患者獲益。

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