Moore Benjamin M, Cordina Rachael L, McGuire Mark A, Celermajer David S
Department of Cardiology, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia.
Sydney Medical School, University of Sydney, Camperdown, New South Wales, Australia.
Congenit Heart Dis. 2018 Nov;13(6):944-951. doi: 10.1111/chd.12657. Epub 2018 Sep 21.
Amiodarone is a highly effective antiarrhythmic therapy, however its toxicity profile often limits treatment. This is particularly relevant in adults with congenital heart disease (CHD), who are often young and in whom other antiarrhythmic agents commonly fail or are contraindicated. We sought to determine incidence and predictors of adverse effects caused by amiodarone in adult CHD (ACHD).
A retrospective review of patients with moderate to complex ACHD treated with amiodarone at our center between 2000 and 2017 was performed. Incidence and predictors of adverse effects were described. Efficacy of amiodarone therapy in controlling the clinical arrhythmia was assessed as complete, partial, or failed.
Amiodarone was prescribed in 57 patients of 902 ACHD patients reviewed (6%), for a mean duration of 2.7 ± 4.3 years. Significant adverse effects occurred in 56%, most commonly thyroid dysfunction, with amiodarone-induced thyrotoxicosis (AIT) in 30% and amiodarone-induced hypothyroidism in 14%. AIT frequently led to arrhythmia exacerbation and occurred most in those with Fontan anatomy. Severe dermatological effects were seen in 7% and bradycardia requiring pacing in 5%. Interstitial lung disease, peripheral neuropathy and alopecia were observed in single cases. Amiodarone toxicity led to discontinuation of the drug in 42%. Amiodarone was highly effective when tolerated, however, achieving complete arrhythmia control in 63%, partial control in 35%, with failure to control in only one patient.
Amiodarone therapy is effective in moderate to complex ACHD patients, but is frequently limited by adverse effects. ACHD patients seem especially vulnerable to thyroid dysfunction, with Fontan patients in particular at increased risk of AIT.
胺碘酮是一种高效的抗心律失常治疗药物，但其毒性特征常常限制了治疗。这在患有先天性心脏病（CHD）的成人中尤为相关，这些患者通常较为年轻，且其他抗心律失常药物通常无效或禁忌使用。我们试图确定胺碘酮在成人先天性心脏病（ACHD）患者中引起不良反应的发生率及预测因素。
对2000年至2017年间在我们中心接受胺碘酮治疗的中度至复杂ACHD患者进行回顾性研究。描述了不良反应的发生率及预测因素。评估胺碘酮治疗控制临床心律失常的疗效为完全控制、部分控制或未控制。
在902例接受评估的ACHD患者中，有57例（6%）使用了胺碘酮，平均用药时间为2.7±4.3年。56%的患者出现了显著的不良反应，最常见的是甲状腺功能障碍，其中胺碘酮诱发的甲状腺毒症（AIT）占30%，胺碘酮诱发的甲状腺功能减退占14%。AIT常导致心律失常加重，在采用Fontan术式的患者中最为常见。7%的患者出现严重皮肤反应，5%的患者出现需要起搏治疗的心动过缓。个别病例观察到间质性肺病、周围神经病变和脱发。胺碘酮毒性导致42%的患者停药。然而，胺碘酮在耐受时非常有效，63%的患者心律失常得到完全控制，35%的患者部分控制，仅1例患者未得到控制。
胺碘酮治疗对中度至复杂ACHD患者有效，但常受不良反应限制。ACHD患者似乎特别容易出现甲状腺功能障碍，尤其是采用Fontan术式的患者发生AIT的风险增加。
