A 62-year-old woman was admitted to our hospital due to cardiopulmonary arrest. She had been prescribed flecainide 200 mg a day for paroxysmal atrial fibrillation for 5 years, and garenoxacin 400 mg a day was added because of infectious enteritis. Initially, her monitor electrocardiogram in the ambulance showed a sine-wave-pattern ventricular tachycardia with a cycle length of 320 ms (Panel A), which required cardiopulmonary resuscitation, then, it turned into tachycardic atrial fibrillation with a significant intraventricular conduction delay, showing a QRS duration of 180 ms (Panel B). Blood chemistry on admission showed no electrolyte concentration abnormalities, no kidney or liver function disturbances, and acute coronary syndrome was ruled out by an immediate coronary angiogram. An endomyocardial biopsy of the left ventricle (LV) demonstrated no inflammatory cell infiltration, however, electron microscopy examination later revealed significant phospholipidosis, demonstrating intracellular accumulation of phospholipids with lysosomes appearing as lamellar bodies (Panel C, area surrounded by yellow asterisks, and Panel D). Administration of flecainide was stopped, and her congestive heart failure and 21% LV ejection fraction spontaneously ameliorated. Sinus rhythm was maintained until hospital discharge. Her medical history indicated flecainide intoxication exacerbated by quinolone antibiotics. A similar finding of phospholipidosis demonstrated by electron microscopy was reported in hepatocytes injured by long-term amiodarone treatment. Flecainide is a cationic amphiphilic drug with a cationic pyridine group and hydrophobic trifluoromethyl groups. Cationic amphiphilic drugs bind to phospholipid on the membrane of lamellar bodies causing intracellular digestion, thus, marked phospholipidosis in our patient’s LV cardiomyocytes coincided with flecainide intoxication.

中文翻译：

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氟卡尼中毒的心肌细胞中的磷脂血症

一名62岁的妇女因心肺骤停而入院。她被告知每天服用200mg氟卡尼用于阵发性心房颤动，为期5年，由于感染性肠炎，每天加加雷沙星400mg。最初，她在救护车上的监护器心电图显示正弦波型室性心动过速，周期长度为320 ms（图A），需要进行心肺复苏，然后变为心动过速，心室传导延迟明显，显示出心动过速。 QRS持续时间为180毫秒（面板B）。入院时的血液化学检查没有发现电解质浓度异常，没有肾脏或肝功能障碍，并且通过立即的冠状动脉造影检查排除了急性冠状动脉综合征。左心室（LV）的心肌内膜活检未见炎性细胞浸润，但是，随后的电子显微镜检查显示，磷脂显着磷脂化，表明磷脂在细胞内蓄积，溶酶体以层状体形式出现（图C，黄色星号包围的区域，图D）。 ）。停用氟卡尼特，其充血性心力衰竭和21％左室射血分数自发改善。保持窦性心律直至出院。她的病史表明喹诺酮类抗生素加剧了氟卡尼中毒。在长期胺碘酮治疗后受损的肝细胞中，也报道了通过电子显微镜观察到的类似磷脂质发现。氟卡尼是具有阳离子吡啶基和疏水性三氟甲基的阳离子两亲药物。阳离子两亲药物与片状体膜上的磷脂结合，引起细胞内消化，因此，在我们患者的LV心肌细胞中明显的磷脂酰化与氟卡尼中毒同时发生。