医线心声|心律失常引起的心肌病:心房纤颤诱发的心肌病

小雁的记事本 2024-08-05 08:12:43

泰达国际心血管病医院 郑 刚

长期以来,心律失常一直被认为是心力衰竭(HF)和心肌病(CM)临床表现的一部分。然而,单独的室上性或室性快速性心律失常可导致或触发可逆的非缺血性心肌病。最近,尽管有足够的心率控制,但心房颤动(房颤,AF)以及室性早搏(PVC)已被认为是非缺血性扩张型心肌病的独特病因[1-3]。因此,出现了一个更具包容性的心律失常诱导心肌病(AiCM)术语,包括心动过速诱导心肌病(T-CM)、房颤诱导心肌病(AF-CM)和PVC心肌病(PVC-CM)。然而,该术语不包括最近因传导异常/不同步而识别的心肌病,如慢性右心室起搏、左束支传导阻滞和预激[1,4]。

1 心动过速诱发的心肌病(T-CM)

1.1定义和患病率 T-CM是指仅由于心室率增加而出现的可逆性左心室功能障碍,而与心动过速的起源无关。发展为T-CM的风险不仅取决于心动过速的类型,还取决于心动过速的持续时间和速率。T-CM的总体患病率和发病率尚不清楚,可能被低估。

一项研究报告,2.7%的患者接受射频消融术(RFA)治疗,但也包括接受PVC消融术治疗的患者[10]。据报道,10%的心房性心动过速(AT)患者出现T-CM[11],持续性AT患者高达37%。此外,永久性交界性往复心动过速(PJRT)似乎与T-CM的相关性最高(20%~50%),因为它经常表现为持续性室上性心动过快(SVT)[12]。尽管房颤是最常见的心律失常,但没有关于该人群中T-CM患病率的明确数据。只有一项研究报告了4%的肺静脉隔离转诊患者的T-CM[13],然而,这些数据被选择和转诊偏差所混淆。儿童也容易发生T-CM,最常见的是AT(59%)、PJRT(23%)和室性心动过速(7%)[12]。

1.2 病因 T-CM可表现为持续性或阵发性心动过速,如果没有发现左心室功能障碍的其他原因,则应予以怀疑。当心动过速使已知心肌病恶化时,一个常见的挑战是识别叠加的T-CM。据报道,T-CM在心动过速发作后数周或数月至数年出现[14]。

室上性心律失常是最常见的病因,即房颤和具有快速心室反应的房扑。尽管很罕见,但其他心律失常也可能是其原因,如持续或非常频繁的阵发性AT、持续性房室折返性心动过速(AVRT)和房室结折返性心动过速(AVNRT)、持续性窦性心动过过速、频繁的室性心动过快(特发性、束支和束支)和起搏器介导的心动过速。一般来说,尽管没有研究支持这一假设,但人们怀疑更快的心动过速和室性心律失常会导致更严重的T-CM[1]。

1.3 病理生理学与机制 动物模型是了解T-CM病理生理学和机制的关键。与人类类似,使用连续快速心房或心室起搏暴露于持续性心动过速的动物会出现心力衰竭症状、左心室收缩功能障碍和扩张、左心室dP/dt max和心肌血流量减少以及左心室壁应力和舒张末期压力和容积增加[9,15-16]。扩张倾向于双心室,伴有轻度变薄或无相关肥大或心脏质量变化[9,15]。这些生理变化的进展包括全身血压下降、左心室和肺动脉压升高,在1周时趋于平稳,而心输出量、射血分数和容量在接下来的4周内继续恶化,在2~3周内出现症状性心衰[9]。T-CM以心肌结构和功能变化为特征。与人类研究类似,T-CM模型也证明了电重构和异常钙稳态被认为是兴奋-收缩耦合受损和舒张功能障碍的原因[9,16-18]。只有总钙循环、钙通道抑制和基础ATP酶活性与左心室射血分数(LVEF)的降低具有统计学相关性[17]。

停止快速起搏可使右心房和动脉压正常化,LVEF和心输出量在48 h内显著恢复,1~2周后完全正常[9]。然而,在心动过速消退一周后,左心室质量增加26%,左心室仍扩张,肌细胞继续表现出收缩功能障碍[15]。此外,在停止快速起搏4周后,只有Ca循环(Ca摄取和Ca释放的总和)、Ca摄取和肌酸激酶(CK)活性显著正常化[17]。重要的是,尽管心动过速消失,左心室功能正常化,但一些变化(如纤维化)似乎仍持续存在[16,19]。

1.4 临床表现、诊断和影像学特征 临床研究发现,从心律失常症状发作到T-CM发展的时间各不相同,从3~120天不等,总LVEF为32%[14]。无论快速性心律失常如何,在较高的心动过速率下[1,9,16],心力衰竭症状都会更早出现,例如持续性房扑患者或心率大于150 bpm的2:1 房室传导的心动过缓患者。最近一项临床研究发现,与扩张型和炎症型心肌病(LVEF分别为32.1±10.2%和41.9±12.9%;P<0.001)相比,T-CM的左心室功能障碍(LVEF为29.3±6.6%)更严重[18]。

主要症状包括心悸(29%)、心衰的纽约心功能分级(NYHA)III-IV级(47%)和晕厥/黑蒙(12%),其余可能没有症状[10]。心脏性猝死并不常见,但据报道,尽管心肌病得到了治疗和缓解,但仍有高达8~12%的患者死亡[14,20]。左心室功能障碍和既往或持续或频繁发作性心动过速且无明显病因的患者应怀疑T-CM。如果存在心动过速,尽管存在潜在的继发性心肌病(缺血性、浸润性或毒性/药物相关),但应考虑叠加性T-CM。因此,至少2周的动态心电图监护仪是确认或排除T-CM的关键。

超声心动图或心脏磁共振可帮助排除其他病因。T-CM的特征是扩张型心肌病(左心室舒张末期大小和面积增加),伴有中度至重度双心室收缩功能障碍,左心室间隔和后壁厚度正常(无肥大)。二尖瓣功能不全可能是由于左心室和二尖瓣环扩张而缺乏小叶接合[16]。神经激素标志物,如脑钠肽(BNP)和N末端脑钠肽前体(NT-proBNP),通常会根据心衰和心肌病的程度升高[11,21]。此外,在心动过速消除后一周内,NT-proBNP的突然下降有助于T-CM[21]。然而,只有在快速性心律失常消除后1~6个月内左心室收缩功能恢复或改善后,才能确认T-CM的最终诊断。

1.5治疗 T-CM的一个主要特点是其在心动过速消除后的可逆性。因此,主要治疗方法是用抗心律失常药(AADs)和/或RFA抑制基于罪犯心律失常的心动过速。然而,T-CM的初始治疗应包括启动和优化心衰和左心室收缩功能障碍的药物治疗(β受体阻滞剂、血管紧张素转换酶抑制剂[ACEI]或血管紧张素受体阻滞剂[ARB]、利尿剂和醛固酮阻滞剂),以优化逆转重塑。在大多数患者中,消除快速性心律失常不仅能在4~12周内解决左心室功能,而且还能通过至少一种NYHA级别改善心衰症状[9,14,16]。多因素分析表明,年龄、心动过速率、基线LVEF和左心室舒张末直径(LVEDD)是儿科人群康复的预测因素[12]。不幸的是,T-CM的恢复并不总完全。组织病理学异常,舒张尽管LVEF正常,功能障碍和心室扩张伴肥厚反应仍可能持续[15-16,18-19]。在存在叠加T-CM的情况下,快速性心律失常治疗后左心室功能不太可能完全可逆。尽管如此,治疗不应气馁,因为它可能有微小但显著的益处。

1.6 既往T-CM病史中的心动过速复发 研究表明,与最初表现相比,心律失常复发后的T-CM复发和心衰症状更快,且严重程度至少相同[14,20]。据推测,如果心律失常复发,从最初表现开始持续存在潜在的组织病理学异常可能是导致更快速、更严重表现的原因[16,19]。然而,随着新发或复发性心动过速的消除,左心室功能障碍恢复到先前或正常水平。因此,对于成功率或治愈率高的心律失常,如心房扑动、房室结折返性心动过速、房室传导阻滞和AT,应特别考虑采用消融治疗等永久性治疗方法。

2 房颤诱发的心肌病(AF-CM)

房颤通常被认为是T-CM的主要原因。有限的证据表明,房颤期间的心室率不能预测心肌病的可逆性[22]。这就提出了一个问题,即房颤持续时间和/或不规则性是否预示左心室功能障碍,而不是心室率。最近,在心衰中进行的房颤消融试验对目前的建议提出了质疑,即对阵发性/持续性房颤和相关心肌病/心衰患者单独进行心率控制是合适的[3,23]。这是因为与药物治疗相比,房颤消融后左心室功能和心衰症状显著改善,支持尽管进行了适当的心率控制,但单独的房颤仍会导致心肌病的前提。

AF-CM被定义为阵发性或持续性房颤患者的左心室收缩功能障碍,尽管有适当的心率控制。因此,动态心电图监护仪是排除心率控制不良和T-CM的关键。尽管房颤是最常见的心律失常,但房颤的发生率和易发或预防房颤的因素尚不清楚。一个常见的临床挑战是识别房颤是否是由心衰和心肌病引起,反之亦然。

AF-CM的机制尚不清楚。据信,AF-CM的触发部分是由于①心律不规则,钙处理不当[1,24]和②与交感神经激活相关的心房收缩/排空损失,导致心室充盈受限和充盈压力增加,功能性二尖瓣反流和舒张功能障碍[2,25]。不幸的是,没有AF-CM动物模型可更好地了解其发病机制中的因果关系、风险因素和/或机制。AF-CM是一种排除性诊断,应主要怀疑非缺血性心肌病和持续性房颤患者在适当的药物治疗和心率控制后没有改善。由于与T-CM的重叠和缺乏动物模型,尚不清楚AF-CM和T-CM之间的时间进程、临床、实验室或成像特征有何不同只有在消除房颤后左心室收缩功能改善或正常时,才能证实最终的AF-CM诊断。

如果怀疑AF-CM,应考虑窦性心律的恢复。据报道,在患有心衰和心肌病的阵发性和持续性房颤患者中,房颤消融可实现50%~88%的窦性心律[2-3,23,26]。虽然房颤消融的并发症发生率较低(2%~3%),但经常需要进行第二次消融。相反,AADs在因副作用而频繁停药的情况下,维持窦性心律的总成功率为30%~50%[2,26]。进一步证据表明,在AF-CM中,房颤消融术可能优于AADs[2]。

AADs的标志性房颤试验未能证明结果益处,包括心衰或心肌病患者和非心衰患者的心衰入院[2,27-28]。这与随机临床研究相反,随机临床研究将房颤消融术作为一种节律控制策略与心率控制策略进行了比较,报告称,在随机接受消融术的房颤和心肌病患者中,60%~70%的LVEF绝对增加8%~18%[2,12,23,29]。唯一一项比较房颤和心肌病患者心律控制策略(消融与胺碘酮)的试验表明,在2年随访后,消融通过改善房颤发生(70%对34%)、生活质量、心衰入院率(31%对57%)和死亡率(8%对18%)而具有优势[26]。最后,CAMERA-MRI研究支持使用晚期钆增强的心脏MRI作为消融前预测心肌病可逆性的筛查工具。无心室瘢痕或瘢痕负荷<10%可预测AF-CM的可逆性[23]。

小结

心律失常诱导的心肌病是一种可逆性心肌病,其表现形式多种多样,从无症状到严重心衰症状。即使在病因明显的患者中,临床医生也应该对叠加AiCM有很高的怀疑。对于阵发性或持续性室上性心动过速患者,主要是房颤/扑动、房性心动过快和心率超过100 bpm的持续性交界性往复心动过速,应强烈考虑T-CM。即使有适当的心率控制,非缺血性心肌病和阵发性、持续性或永久性房颤患者也应怀疑AF-CM。AiCM的适当诊断和治疗不仅可逆转左心室功能障碍及其相关的发病率、死亡率和医疗支出,而且最重要的是可改善生活质量和长期预后。

专家简介

郑刚 教授

现任泰达国际心血管病医院特聘专家,济兴医院副院长

中国高血压联盟理事,中国心力衰竭学会委员,中国老年医学会高血压分会天津工作组副组长,中国医疗保健国际交流促进会高血压分会委员

天津医学会心血管病专业委员会委员,天津医学会老年病专业委员会常委,天津市医师协会高血压专业委员会常委,天津市医师协会老年病专业委员会委员,天津市医师协会心力衰竭专业委员,天津市医师协会心血管内科医师分会双心专业委员会委员,天津市心脏学会理事,天津市心律学会第一届委员会委员,天津市房颤中心联盟常委,天津市医药学专家协会第一届心血管专业委员会委员,天津市药理学会临床心血管药理专业委员会常委,天津市中西医结合学会心血管疾病专业委员会常委

《中华临床医师杂志(电子版)》特邀审稿专家,《中华诊断学电子杂志》《心血管外科杂志(电子版)》审稿专家,《华夏医学》副主编,《中国心血管杂志》常务编委,《中国心血管病研究》杂志第四届编委,《中华老年心脑血管病杂志》《世界临床药物》《医学综述》《中国医药导报》《中国现代医生》编委

本人在专业期刊和心血管网发表文章979篇,其中第一作者790篇,参加著书11部。获天津市2005年度“五一劳动奖章和奖状”和“天津市卫生行业第二届人民满意的好医生”称号

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29. Chen MS, Marrouche NF, Khaykin Y et al. Pulmonary vein isolation for the treatment of atrial fibrillation in patients with impaired systolic function. J Am Coll Cardiol 2004;43:1004–9.

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26. Di Biase L, Mohanty P, Mohanty S et al. Ablation Versus Amiodarone for Treatment of Persistent Atrial Fibrillation in Patients With Congestive Heart Failure and an Implanted Device: Results From the AATAC Multicenter Randomized Trial. Circulation 2016;133:1637–44.

27. Al-Khatib SM, Shaw LK, Lee KL, O’Connor C, Califf RM. Is rhythm control superior to rate control in patients with atrial fibrillation and congestive heart failure? Am J Cardiol 2004;94:797–800.

28. Roy D, Talajic M, Nattel S et al. Rhythm control versus rate control for atrial fibrillation and heart failure. N Engl J Med 2008;358:2667–77.

29. Chen MS, Marrouche NF, Khaykin Y et al. Pulmonary vein isolation for the treatment of atrial fibrillation in patients with impaired systolic function. J Am Coll Cardiol 2004;43:1004–9.

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