Impact of Medical Castration on Malignant Arrhythmias in Patients With Prostate Cancer.
Impact of Medical Castration on Malignant Arrhythmias in Patients With Prostate Cancer.
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DOI：
10.1161/jaha.120.017267
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发表时间：
2021-03
影响因子：
5.4
通讯作者：
Tada H
中科院分区：
文献类型：
--
作者：
Hasegawa K;Ito H;Kaseno K;Miyazaki S;Shiomi Y;Tama N;Ikeda H;Ishida K;Uzui H;Ohno S;Horie M;Yokoyama O;Tada H
药物去势、促性腺激素释放激素激动剂和抗雄激素已被广泛应用于前列腺癌的治疗。性类固醇激素影响心脏离子通道。然而，很少有研究探讨药物去势的promammic属性。本研究纳入了149例使用促性腺激素释放激素联合/不联合抗雄激素治疗前列腺癌的药物去势患者。观察治疗过程中心电图的变化及其与恶性心律失常的关系。治疗期间QT间期和校正QT间期（QTc）较基线延长（QT，394±32至406±39 ms [P<0.001]; QTc，416±27至439±31 ms [P<0.001]）。119例（79.9%）患者治疗期间QTc间期较基线延长。2例（1.3%）无器质性心脏病的患者在开始治疗后≥6个月发生尖端扭转型室性心动过速（TdP）和室颤（VF）。在TdP/VF患者中，QTc间期较治疗前值增加>80 ms。然而，在无TdP/VF的患者中，QTc间期较治疗前值增加>50 ms的患病率为11%，仅在4例（3%）患者中发现QTc间期较治疗前值增加>80 ms。药物去势使大多数前列腺癌患者的QT/QTc间期延长，即使在治疗前没有QT间期延长风险的患者中，药物去势也可引起TdP/VF。QTc间期较治疗前值增加>50 ms可能成为TdP/VF的预测因素。在药物去势的各个阶段都应注意QTc间期的变化，以预防恶性心律失常的发生。
Medical castration, gonadotropin‐releasing hormone agonists, and antiandrogens have been widely applied as a treatment for prostate cancer. Sex steroid hormones influence cardiac ion channels. However, few studies have examined the proarrhythmic properties of medical castration. This study included 149 patients who underwent medical castration using gonadotropin‐releasing hormones with/without antiandrogen for prostate cancer. The changes in the ECG findings during the therapy and associations of the electrocardiographic findings with malignant arrhythmias were studied. The QT and corrected QT (QTc) intervals prolonged during the therapy compared with baseline (QT, 394±32 to 406±39 ms [P<0.001]; QTc, 416±27 to 439±31 ms [P<0.001]). The QTc interval was prolonged in 119 (79.9%) patients during the therapy compared with baseline. In 2 (1.3%) patients who had no structural heart disease, torsade de pointes (TdP) and ventricular fibrillation (VF) occurred ≥6 months after starting the therapy. In patients with TdP/VF, the increase in the QTc interval from the pretreatment value was >80 ms. However, in patients without TdP/VF, the prevalence of an increase in the QTc interval from the pretreatment value of >50 ms was 11%, and an increase in the QTc interval from the pretreatment value >80 ms was found in only 4 (3%) patients. Medical castration prolongs the QT/QTc intervals in most patients with prostate cancer, and it could cause TdP/VFs even in patients with no risk of QT prolongation before the therapy. An increase in the QTc interval from the pretreatment value >50 ms might become a predictor of TdP/VF. Much attention should be paid to the QTc interval throughout all periods of medical castration to prevent malignant arrhythmias.