房颤射频消融术后复发的影响因素

作者:许翔[1] 蔡尚郎[1] 
单位:青岛大学医学院附属医院[1]

   房颤是最常见的心律失常,据统计报道,2010年全球约有3亿多的房颤患者,在过去的20多年间,房颤的患病率和发病率都显著增加[1]。目前认为,多子波折返机制与局灶激动机制是参与房颤发生和维持的两种重要机制,同时心房重构及自主神经、体液因子等诸多因素亦参与其中[2]。近年来大量国内外文献表明房颤的射频消融治疗(RFA)能够明显改善房颤患者的预后,已被推荐作为阵发性房颤的一线治疗手段。然而,射频消融术后的房颤复发率仍然不让人满意,文献报道其约为15%~50%[3][4],所以探明射频术后复发的影响因素,降低复发率是目前研究的热点问题。
1  左房压力(LAP)与房颤射频消融复发的关系
   近年来新的研究进展显示,左房压力是房颤射频消融复发的独立预测因素。Park等[5] 术中测量454名房颤射频病人 (71.8%为阵发性房颤)的左房压,随后进行13.1±6.0个月随访,结果显示LAP最大值≥19mmHg的患者,其复发率明显超过LAP最大值≤19mmHg的患者(22.3 vs.12.3%, P=0.004)。并且LAP最大值≥19mmHg的患者左房容积指数更大(P﹤o .001),左房电压更低 (P﹤0.007),因此认为高左房压力与房颤患者心房的电解剖重构有关,并且是射频消融复发的独立预测因素。与之相似,Bergau等[6]研究发现,LAP最大值≥18mmHg对预测射频消融术后复发的敏感度为77%,特异度为60%。而Linhart[7]等的研究虽然也认同LAP平均是预测房颤射频后复发的因素,但是研究者根据“左房大小”将患者分成两组后,发现LAP平均仅在“小心房”组具有预测价值。在这一组中,LAP平均每升高1mmHg,复发率就增加11%。另一方面,Hirai[8]等通过测量心超E/e’比值间接验证了左房压力对房颤射频消融术后复发的预测价值。Hirai的研究指出,高左房压力组的患者(平均E/e’>13)的术后复发率更高(67% vs. 35%,OR=3.70, p <0.05),并认为E/e’比值是反应左房压力的一种简便易行的非侵入式测量指标,今后对于房颤射频患者可能具有更大的实用价值。
   左房压力的升高影响射频术后复发的机制尚不完全明确。左房压力的大小本身受多种因素的影响,包括心室的功能及舒张末期压力,心房的节律及收缩功能和对容量状态的顺应性等[9-13]。目前的研究认为左房压力反应了左房的牵张程度,而这种牵张状态能引起心房电重构和解剖重构,促发异位和折返活动。高压力状态下的心房通过机械电反馈途径提高钾离子通道基因的表达,导致了动作电位时程的时限缩短,有效不应期延长且离散度增大,出现早期后除极,引起起源于上肺静脉处异位激动数量明显增多,进而诱发心律失常[14,15]。同时,心房的牵张状态诱导细胞肥大、去分化以及心房纤维化并影响缝隙链接的调控,引起心房的重构[16,17]。这些变化使得心房传导减慢,传导异质性增加,为回旋波的折返提供条件[18,19]。此外,心房的牵张也参与维持左房后壁及肺静脉高频转子的稳定[20],以上这些变化共同参与了房颤的发生及维持。
2  基础指标与房颤射频消融复发的关系
2.1  年龄
   年龄与AF复发之间的关系目前存在争议。 Kusmnoto等[21]按年龄将240例房颤患者分成小于65岁、65—75岁和大于75岁3个组,进行12个月随访,结果显示复发者在大于75岁组占的比例明显高于其他两组(24%、34%、66%)。而Zado E等[22]的研究中同样的分组中却未见统计学意义。
2.2  体重
   目前绝大多数研究认为超重和肥胖是AF复发的危险因素之一。Tang RB等[23]按体重指数BMI>25.0 kg/m2作为超重和肥胖的诊断标准,经多因素分析显示超重和肥胖是房颤复发的独立危险因。LIU等[24]通过Meta发现BMI指数的升高与房颤射频术后复发有密切关系。研究表明肥胖与心房扩大有关[25-27],同时Letsas等[28]和Korantzopolos等[29]发现肥胖与慢性炎症反应和氧化应激也有联系。 因此,推测超重或肥胖可能通过炎症反应、氧化应激等多个因素影响心颤的复发。
3 临床特征与房颤射频消融复发的关系
3.1  房颤的类型与病程
   Bergau等[6]研究认为阵发性房颤比持续性房颤拥有更佳的预后。近年来一些房颤射频消融中心的统计也证实持续性房颤常需多次消融且术式也较复杂[30]。另一方面,Takigawa 等[31]发现房颤的持续时间是房颤复发的显著预测因子 ( [HR]1.03; P<0.0001)。刘旭等人对房颤病程与复发的关系做了更细致的研究,其将患者根据病程长短分5组,结果也提示房颤病程为消融术后复发的预测指标( P =0.012; OR 1.055,95% CI 1.001~1.111,P =0.045)。目前认为,慢性房颤中心房电解剖重构是其发生和维持的主要因素,房颤的持续导致心房基质重构,而重构又诱发促进房颤维持发展,二者形成“房颤致房颤”的恶性循环。
3.2  合并器质性心脏病
   Anselmino[32]等借助Meta分析,发现没有器质性心脏病的患者复发率较低(P=0.003)。Gertz[33]等研究认为二尖瓣反流与房颤术后复发有关系。上述研究提示合并器质性心脏病的患者更易出现术后复发。但是Estner[34]等和Seow等[35]的研究中合并结构性心脏病与术后复发并无关系。故目前器质性心脏病是否为房颤术后复发的危险因素尚不确定,需要进一步深入研究。
3.3  代谢综合征
   多项研究显示代谢综合征是房颤导管消融复发的独立预测因素,Chang等[36]发现无论对于阵发性房颤还是非阵发性房颤,代谢综合征均是房颤导管消融复发的独立危险因素。而Mohanty等[37]认为代谢综合征仅增加非阵发性房颤消融术后的复发,不影响阵发性房颤导管消融的成功率。Chang[36]认为代谢综合征引发房颤复发是以肺静脉外机制为主,而Tang[38]等的研究认为肺静脉-左心房传导恢复是阵发性房颤导管消融复发的主要机制之一。
3.4  睡眠呼吸暂停综合征
   阻塞性睡眠呼吸暂停综合征(OSA)与房颤消融术后复发的关系是近年研究的热点。Ng 等[39]对3995名病人进行Meta分析,发现OSA病人术后复发危险更高(RR1.25, p = 0.003)。Matiello等[40]也认为房颤患者中存在严重的OSA是手术复发的独立危险因素。其机制可能为低氧血症、交感激活、胸腔负压动荡导致心脏架构的变化[41],造成左心房重构扩大,另外在动物试验[42]及人类临床试验[43]中发现自主神经机制也参与其中。
3.5  肾功能
   Li等[44]的Meta分析发现慢性肾功能不全(CKD)与房颤射频术后的高复发率有关(HR = 1.96, 95% CI 1.35-2.85, p = 0.0004)。Tokuda等[45]发现房颤复发组的肾小球滤过率比无复发组更低。Naruse[46]等的研究发现CKD是房颤射频术后的独立预测因子,并认为房颤的复发是CKD导致左房扩大等因素造成的。
4  心脏解剖结构与房颤射频消融复发的关系
4.1  左房大小和容积
   心房扩大造成心房内不同部位的非均质性电活动,导致折返形成,诱发或加重房颤的发生。目前认为,左房的扩大和房颤射频消融术后的复发有明确的关系。现在临床上常用左房内径(LAD)与左房容积(LAV)来表示左房的大小。Zhuang等[47]的Meta分析认为LAD扩大显著增加复发的风险,特别是随着随访时间延长,这种趋势更加明显。Shin等[48]则发现左房容积可以提示术后复发的风险。von [49]等利用非侵入性的CT及磁共振技术发现LAV >95 ml的病人有明显更高的复发风险(24% vs. 8%, p = 0.02)。
4.2  左心房纤维化及疲痕
   心房纤维化是心房损伤及炎症的后遗症之一,心房纤维化会加重传导阻滞,促进折返形成和局部激动的触发。相似的,左房疤痕组织也可以改变心房内的传导和增加心房的有效不应期,导致房颤的形成和维持,故左心房纤维化及疲痕是术后复发的一个重要危险因素。Den等[50]以左房超声反射率作为左房纤维化的代替指标,测量随访170名手术病人后认为左房超声反射率是房颤射频术后复发的预测因子。而Verma等[51]对左房瘢痕(LAS)进行了研究,发现LAS的病人复发率较无瘢痕病人显著升高(57% vs.19%, p = 0.003)。
4.3  心包脂肪组织
   Nagashima等[52]通过心脏三维重建显示心外脂肪组织,发现心房颤动患者的心包脂肪组织明显增加。心包脂肪组织能分泌众多炎症因子[53],引起心房结构重塑。同时其内包含大量神经节[54],这也可能和消融术后复发有关。另外一点值得注意的是,心包脂肪组织包绕左心房的部位与高主频点相似[55],分布在肺静脉前庭、左房耳、二尖瓣环以及左房顶部等部位,而高主频点已被认为是引发或维持心房颤动的重要区域,故两者之间是否存在联系有待进一步的研究。
4.4  多异住灶AF起源及肺静脉外起源
   目前认为异位灶数目愈多射频成功率愈低。Ma等[56]研究结果显示,多异位灶起源是一个射频术后复发的强预测 (OR=3.7)因子。Haissagurre等[57]研究也表明单灶起源者消融成功率远高于多灶起源。除肺静脉外,上腔静脉、界嵴、右房室交界和左心房上部,均可触发房颤的发生。Chang等[58]发现起源于上腔静脉的阵发性房颤患者,单次消融后有73%五年未复发,故单纯SVC消融可用于治疗起源于上腔静脉的房颤。
5  神经体液因素
5.1  炎症
   炎症与房颤的关系是近年研究的热点之一。C-反应蛋白(CRP) 作为重要的炎症标志物,可能与房颤的发生和维持有关。Sotomi等[59]认为异常升高的CRP是晚期复发的独立预测因子(HR 4.9, 95% CI 2.3-10.7, P < 0.0001)。Kimura等[60]则发现 MMP-2和 TNF-α可能会对房颤射频的复发有预测价值。Wu等[61]等也通过meta分析发现, CRP和IL-6等循环炎症因子水平的升高与射频术后的复发有关。
5.2  肾素一血管紧张素—醛固酮系统
   现有研究显示,RAAS系统激活是心房间质纤维化的可能原因。在AF患者中,心房组织血管紧张素转换酶增高,使心肌细胞内钙负荷增加,钙超载导致AF患者心房电重构。Ishikawa[62]等发现RAAS系统拮抗剂可抑制房颤射频术后的复发,据此推测RAAS系统和房颤射频消融复发有密切联系。
5.3  B型钠尿肽:
   Hussein[63]等研究BNP与孤立性房颤射频术后复发的关系,发现BNP水平不论单因素(HR 2.32; 95%CI 2.11-2.74; P<0.001)还是多因素分析(HR2.13; 95% CI 2.06-2.38; P<0.001)时都与复发相关。Solheim E等[64]认为与基线相比NTpro-BNP下降>25%是射频成功的标志。可能的机制为神经内分泌反应:正常心功能患者的BNP水平增高多来源于心房肌细胞的分泌[65],房颤患者左房容量或压力负荷的增高,心房肌张力增加,引起心房增大以及心房重构,导致负荷状态的心房肌细胞分泌BNP水平增高。
5.4  自主神经
   有大量证据显示迷走神经张力与房颤复发有关。Scherlag 等[66]报道肺静脉前庭电隔离加自主神经节消融可以提高手术成功率,并认为心脏自主神经节对房颤的发生和维持起到至关重要的作用。而Pappone 等[67]认为导管消融术中发生迷走反射并去迷走反射化的患者复发率明显降低。故现在自主神经节消融术也成为一种房颤射频的术式。现认为人类肺静脉壁中含有神经节细胞,有大量乙酰胆碱类神经传出纤维,乙酰胆碱可通过早期后除极导致局部心房肌触发活动,从而产生高频电位,进而诱发房颤。
6  结语
   房颤是临床上最常见的心律失常,其形成机制复杂,预测射频复发的因素也很多。本文阐述了左房压力、年龄体重等基础指标、病人临床特征、心脏解剖结构、神经体液等因素对射频复发的影响,但是目前许多研究结果存有争议,相关机制尚不完全清楚,还有许多潜在的因素尚未发现和探明,需要进一步研究。
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