Neefs J, van den Berg N W E, Limpens J, Berger W R, Boekholdt S M, Sanders P, de Groot J R
Department of Cardiology, Heart Center, and Medical Library, Academic Medical Center, Amsterdam, The Netherlands.
Centre for Heart Rhythm Disorders (CHRD), South Australian Health and Medical Research Institute (SAHMRI), University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia.
Int J Cardiol. 2017 Mar 15;231:155-161. doi: 10.1016/j.ijcard.2016.12.029. Epub 2016 Dec 23.
Despite advances in therapeutic interventions AF remains a progressive and symptomatic disease. Therefore, novel therapeutic interventions targeting the underlying arrhythmogenic substrate for AF is needed. Atrial fibrosis is an important component of the arrhythmogenic substrate of AF and may be initiated by aldosterone binding to the mineralocorticoid receptor. We hypothesized that aldosterone pathway blockade with mineralocorticoid receptor antagonists (MRA) reduces atrial fibrosis, and thus AF.
We searched OVID MEDLINE, OVID EMBASE and the Cochrane Central Register of Controlled Trials from inception to June 10th, 2016 for randomized controlled trials (RCT) and observational studies addressing MRA and providing information on AF occurrence. Two independent reviewers selected and appraised the data. We performed random-effects meta-analyses. Summary odds ratios (OR) with 95% confidence intervals (CI) were calculated.
We included 14 studies, 5 RCT and 9 observational cohorts, with a cumulative number of 5332 patients (male: 74.9%, age: 65.3years); 2397 (45.0%) received an MRA (spironolactone or eplerenone). During follow-up, 204 (8.5%) patients treated with MRAs, developed AF, compared to 547 (18.6%) patients, without MRA treatment. Meta-analyses showed a significant overall reduction of AF risk in MRA treated patients (OR: 0.48 CI: 0.38-0.60 p<0.001), including a reduction of new-onset AF (OR: 0.52 CI: 0.37-0.74 p<0.001) and recurrent AF (OR: 0.37 CI: 0.24-0.57 p<0.001), but not post-operative AF (POAF) (OR: 0.60 CI: 0.33-1.09 p=0.09).
MRAs significantly reduce new-onset AF and recurrent AF, but not POAF. MRA treatment can be considered an additive therapeutic strategy in AF.
尽管治疗干预取得了进展，但房颤仍然是一种进行性且有症状的疾病。因此，需要针对房颤潜在致心律失常基质的新型治疗干预措施。心房纤维化是房颤致心律失常基质的一个重要组成部分，可能由醛固酮与盐皮质激素受体结合引发。我们假设用盐皮质激素受体拮抗剂（MRA）阻断醛固酮途径可减少心房纤维化，从而减少房颤。
我们检索了从创刊至2016年6月10日的OVID MEDLINE、OVID EMBASE和Cochrane对照试验中央注册库，以查找涉及MRA并提供房颤发生信息的随机对照试验（RCT）和观察性研究。两名独立的评审员筛选并评估了数据。我们进行了随机效应荟萃分析。计算了95%置信区间（CI）的汇总比值比（OR）。
我们纳入了14项研究，5项RCT和9个观察性队列，累计患者5332例（男性：74.9%，年龄：65.3岁）；2397例（45.0%）接受了MRA（螺内酯或依普利酮）治疗。在随访期间，接受MRA治疗的患者中有204例（8.5%）发生房颤，未接受MRA治疗的患者中有547例（18.6%）发生房颤。荟萃分析显示，接受MRA治疗的患者房颤风险总体显著降低（OR：0.48，CI：0.38 - 0.60，p<0.001），包括新发房颤减少（OR：0.52，CI：0.37 - 0.74，p<0.001）和复发房颤减少（OR：0.37，CI：0.24 - 0.57，p<0.001），但术后房颤（POAF）未减少（OR：0.60，CI：0.33 - 1.09，p = 0.09）。
MRA可显著减少新发房颤和复发房颤，但不能减少POAF。MRA治疗可被视为房颤的一种辅助治疗策略。
