Zaidi Syed Arsalan Akhter, Shaikh Danial, Saad Muhammad, Vittorio Timothy J
Department of Medicine, BronxCare Health System, New York, NY, USA.
Department of Cardiology, BronxCare Health System, New York, NY, USA.
Case Rep Med. 2019 Dec 31;2019:2740617. doi: 10.1155/2019/2740617. eCollection 2019.
Ranolazine is a well-known antianginal drug, that was first licensed for use in the United States in 2006. It was objectively shown to improve exercise capacity and to lengthen the time to symptom onset in patients with coronary artery disease. The most commonly reported side effects of ranolazine include dizziness, headache, constipation, and nausea. Here, we describe a case of bradycardia, hyperkalemia, and acute renal injury in the setting of ranolazine use. Our patient is an 88-year-old female who presented with abdominal pain, nausea, and vomiting. Her medical comorbidities included hypertension, diabetes, CAD, heart failure with preserved ejection fraction, paroxysmal atrial fibrillation, hypothyroidism, and a history of cerebrovascular accident without any residual deficits. Her prescription regimen included amlodipine, furosemide, isosorbide mononitrate, levothyroxine, metformin, omeprazole, and ranolazine. Physical examination was remarkable for bradycardia and decreased breath sounds in the left lower lung field. Laboratory studies were significant for a serum potassium level of 6.8 mEq/L and a serum creatinine level of 1.6 mg/dL. She was given insulin with dextrose, sodium polystyrene, and calcium gluconate in addition to fluids. Her bradycardia and renal function worsened over the next 24 hours. Ranolazine was discontinued. Metabolic derangements were treated appropriately. After 48 hours from presentation, potassium and renal function returned to baseline and her heart rate improved to a range of 60-100 bpm. She was discharged with an outpatient cardiology follow-up. Ranolazine treatment was not continued upon discharge. In summary, our case illustrates an association between ranolazine and renal failure induced hyperkalemia, leading to conduction delays in the myocardium. Though further studies are warranted, we suspect that this is a variant of the recently described BRASH syndrome. We propose that in cases such as ours, along with treatment of the hyperkalemia, medication review and removal of any offending agent should be considered.
雷诺嗪是一种知名的抗心绞痛药物,于2006年在美国首次获得许可使用。客观证据表明,它能提高冠心病患者的运动能力,并延长症状出现的时间。雷诺嗪最常报告的副作用包括头晕、头痛、便秘和恶心。在此,我们描述一例在使用雷诺嗪过程中出现心动过缓、高钾血症和急性肾损伤的病例。我们的患者是一位88岁女性,出现腹痛、恶心和呕吐。她的内科合并症包括高血压、糖尿病、冠心病、射血分数保留的心力衰竭、阵发性心房颤动、甲状腺功能减退以及有脑血管意外病史但无任何残留缺陷。她的处方用药包括氨氯地平、呋塞米、单硝酸异山梨酯、左甲状腺素、二甲双胍、奥美拉唑和雷诺嗪。体格检查发现心动过缓,左下肺野呼吸音减弱。实验室检查显示血清钾水平为6.8 mEq/L,血清肌酐水平为1.6 mg/dL。除了补液外,还给予了胰岛素加葡萄糖、聚苯乙烯磺酸钠和葡萄糖酸钙。在接下来的24小时内,她的心动过缓和肾功能恶化。停用了雷诺嗪。代谢紊乱得到了适当治疗。就诊48小时后,钾水平和肾功能恢复到基线,心率改善至60 - 100次/分的范围。她出院时安排了门诊心脏病学随访。出院后未继续使用雷诺嗪治疗。总之,我们的病例说明了雷诺嗪与肾衰竭诱发的高钾血症之间的关联,导致心肌传导延迟。尽管有必要进行进一步研究,但我们怀疑这是最近描述的BRASH综合征的一种变体。我们建议在像我们这样的病例中,除了治疗高钾血症外,还应考虑药物审查并停用任何有问题的药物。