Potpara Tatjana S, Jokic Vera, Dagres Nikolaos, Marin Francisco, Prostran Milica S, Blomstrom-Lundqvist Carina, Lip Gregory Y H
Cardiology Clinic, Clinical Centre of Serbia, School of Medicine, University of Belgrade, Serbia, Visegradska 26, 11000 Belgrade, Serbia.
Curr Med Chem. 2016;23(19):2070-83. doi: 10.2174/0929867323666160309114246.
The kidney has numerous complex interactions with the heart, including shared risk factors (e.g., hypertension, dyslipidemia, etc.) and mutual amplification of morbidity and mortality. Both cardiovascular diseases and chronic kidney disease (CKD) may cause various alterations in cardiovascular system, metabolic homeostasis and autonomic nervous system that may facilitate the occurrence of cardiac arrhythmias. Also, pre-existent or incident cardiac arrhythmias such as atrial fibrillation (AF) may accelerate the progression of CKD. Patients with CKD may experience various cardiac rhythm disturbances including sudden cardiac death. Contemporary management of cardiac arrhythmias includes the use of antiarrhythmic drugs (AADs), catheter ablation and cardiac implantable electronic devices (CIEDs). Importantly, AADs are not used only as the principal treatment strategy, but also as an adjunct therapy in combination with CIEDs, to facilitate their effects or to minimize inappropriate device activation in selected patients. Along with their principal antiarrhythmic effect, AADs may also induce cardiac arrhythmias and the risk for such proarrhythmic effect(s) is particularly increased in patients with reduced left ventricular systolic function or in the setting of electrolyte imbalance. Moreover, CKD itself can induce profound alterations in the pharmacokinetics and pharmacodynamics of many drugs including AADs, thus facilitating the drug accumulation and increased exposure. Hence, the use of AADs in patients with CKD may be challenging. In this review article, we provide an overview of the characteristics of arrhythmogenesis in patients with CKD with special emphasis on the complexity of pharmacokinetics and risk for proarrhythmias when using AADs in patients with cardiac arrhythmias and CKD.
肾脏与心脏存在众多复杂的相互作用，包括共同的危险因素（如高血压、血脂异常等）以及发病率和死亡率的相互加剧。心血管疾病和慢性肾脏病（CKD）均可导致心血管系统、代谢稳态和自主神经系统发生各种改变，这些改变可能促使心律失常的发生。此外，既往存在的或新发的心律失常，如心房颤动（AF），可能加速CKD的进展。CKD患者可能会经历各种心律失常，包括心源性猝死。当代心律失常的治疗方法包括使用抗心律失常药物（AADs）、导管消融和心脏植入式电子设备（CIEDs）。重要的是，AADs不仅用作主要治疗策略，还作为与CIEDs联合使用的辅助治疗，以增强其效果或减少特定患者中设备的不适当激活。除了其主要的抗心律失常作用外，AADs还可能诱发心律失常，在左心室收缩功能降低的患者或存在电解质失衡的情况下，这种促心律失常作用的风险尤其增加。此外，CKD本身可导致包括AADs在内的许多药物的药代动力学和药效学发生深刻改变，从而促进药物蓄积和暴露增加。因此，在CKD患者中使用AADs可能具有挑战性。在这篇综述文章中，我们概述了CKD患者心律失常发生的特征，特别强调了在心律失常合并CKD患者中使用AADs时药代动力学的复杂性和促心律失常的风险。
