Vomiting, electrolyte disturbance, and medications; the perfect storm for acquired long QT syndrome and cardiac arrest: a case report

Background Acquired long QT syndrome is an important and preventable cause of cardiac arrest. Certain medications and electrolyte disturbance are common contributors, and often coexist. In this case, we report five contributors to cardiac arrest. Case presentation This case is of a 51-year-old Caucasian female patient who presented with vomiting associated with hypokalemia and hypomagnesemia. She subsequently received ondansetron and metoclopramide, on the background of chronic treatment with fluoxetine. She then suffered an in-hospital monitored cardiac arrest, with features of long QT and torsades de pointes retrospectively noted on her prearrest electrocardiogram. She was diagnosed with acquired long QT syndrome, and her QT interval later normalized after removal of offending causes. Conclusions This case highlights the importance of proper consideration prior to prescribing QT prolonging medications, especially in patients who have other risk factors for prolonged QT, such as electrolyte disturbances and pretreatment with QT prolonging medications.

Transient Hypogonadism Is Associated With Heart Rate–Corrected QT Prolongation and Torsades de Pointes Risk During Active Systemic Inflammation in Men

Background Systemic inflammation and male hypogonadism are 2 increasingly recognized “nonconventional” risk factors for long‐QT syndrome and torsades de pointes (TdP). Specifically, inflammatory cytokines prolong, while testosterone shortens the heart rate–corrected QT interval (QTc) via direct electrophysiological effects on cardiomyocytes. Moreover, several studies demonstrated important interplays between inflammation and reduced gonad function in men. We hypothesized that, during inflammatory activation in men, testosterone levels decrease and that this enhances TdP risk by contributing to the overall prolonging effect of inflammation on QTc. Methods and Results We investigated (1) the levels of sex hormones and their relationship with inflammatory markers and QTc in male patients with different types of inflammatory diseases, during active phase and recovery; and (2) the association between inflammatory markers and sex hormones in a cohort of male patients who developed extreme QTc prolongation and TdP, consecutively collected over 10 years. In men with active inflammatory diseases, testosterone levels were significantly reduced, but promptly normalized in association with the decrease in C‐reactive protein and interleukin‐6 levels. Reduction of testosterone levels, which also inversely correlated with 17‐β estradiol over time, significantly contributed to inflammation‐induced QTc prolongation. In men with TdP, both active systemic inflammation and hypogonadism were frequently present, with significant correlations between C‐reactive protein, testosterone, and 17‐β estradiol levels; in these patients, increased C‐reactive protein and reduced testosterone were associated with a worse short‐term outcome of the arrhythmia. Conclusions During systemic inflammatory activation, interleukin‐6 elevation is associated with reduced testosterone levels in males, possibly deriving from an enhanced androgen‐to‐estrogen conversion. While transient, inflammatory hypotestosteronemia is significantly associated with an increased long‐QT syndrome/TdP risk in men.

Torsades de pointes in the PACU after outpatient endoscopy: a case report

Background This case demonstrates the severe electrolyte derangements that may present after a common therapy such as a bowel preparation for an outpatient procedure and the rare yet potential detrimental outcomes of those abnormalities. It also highlights the implications of long QT syndrome regarding pharmacology and treatment. Case presentation We present a case of 48 year-old female with severe electrolyte derangements and long QT syndrome (LQTS) leading to Torsades de Pointes (TdP), pulseless ventricular fibrillation, and unsynchronized defibrillation in the post anesthesia care unit (PACU) after uneventful upper and lower endoscopy. This led to an unanticipated intensive care unit admission for aggressive electrolyte repletion, cardiology consultation, and implantable cardioverter defibrillator (ICD) placement. Conclusions This is a rare presentation after an outpatient procedure that would have had a detrimental outcome if not promptly diagnosed and treated appropriately. Therefore, we aim to provide further insight into the diagnosis and treatment of severe hypokalemia and long QT syndrome resulting in Torsades de Pointes and ventricular fibrillation.

Peripartum Management of Patient with Long QT3 after Successful ICD Device Discharge Resulting in Device Failure: A Case Report

Background Long QT3 syndrome (LQT3) is a gain of function mutation of the SCN5A gene that is inherited in an autosomal dominant fashion. LQT3 results in an increase in arrhythmic events during rest, sleep, and bradycardia by extending the QT interval and inducing Torsades de pointes and sudden cardiac death. Attempting to block the sodium channel with Class I anti-arrhythmics or blocking adrenergic tone with beta blockers especially in women, have shown to be beneficial. There have been few large-scale studies on treating patients with LQT3 due to its lethality and underreported number of cases. Specifically, the safety and efficacy of pharmacologic treatment in pregnant LQT3 patients is unknown. Case summary This case demonstrates the safe use of Mexiletine and Propranolol in a third trimester pregnant LQT3 patient after a presumed ventricular arrhythmia and device-lead electrical short from therapy rendered her Implantable Cardioverter Defibrillator (ICD) inoperable in a VVI mode. With appropriate medications, the patient was safely monitored through the remainder of her pregnancy and safely delivered at 36 weeks of pregnancy a healthy baby girl. The daughter, heterozygous for LQT3, showed no evidence of intrauterine growth restriction or other side effects from the medications. Discussion There are many variants of the SCN5A gene mutations that can lead to different phenotypes and not all mutations are responsive to the same medications. In this case, Mexiletine and Propranolol, both of which have only recently shown to benefit certain variants or LQT3 respectively, were safely started during the third trimester of pregnancy without harming the fetus.

Abiraterone Induced Refractory Hypokalemia and Torsades de Pointes in a Patient with Metastatic Castration-Resistant Prostate Carcinoma: A Case Report

Background Abiraterone, an androgen deprivation therapy (ADT), has been used in the treatment of metastatic castration-resistant prostate cancer (mCRPC). It has been associated with increased risks of hypokalemia and cardiac disorders. We report a case of torsades de pointes (TdP) associated with abiraterone use and refractory hypokalemia in a man with mCRPC. Case summary A 78-year-old man with mCRPC presented to the emergency room for generalized weakness. Laboratory results revealed a potassium level of 2.2 mmol/L (3.5-5.0), magnesium level of 2.4 mg/dl (1.6-2.5), and normal kidney and hepatic functions. Initial EKG showed atrial fibrillation with rapid ventricular rate of 106 b.p.m., frequent premature ventricular contractions (PVCs), and a QTc of 634 ms. The patient had multiple episodes of TdP, became pulseless and underwent advanced cardiac life support, including defibrillation. Despite a total of 220 mEq of intravenous potassium chloride, his potassium level only improved to 2.8 mmol/L. He received spironolactone and amiloride to promote urinary potassium reabsorption in addition to hydrocortisone, in an effort to reduce abiraterone’s effect on increasing mineralocorticoid synthesis. Discussion Abiraterone has been widely used in mCRPC since its approval by the FDA in 2011. Regulatory guidelines and standardized close QTc and electrolyte monitoring in patients may help prevent fatal arrhythmias associated with abiraterone.

Successful treatment of bepridil-induced intraoperative torsades de pointes by isoproterenol infusion

Background Several types of antiarrhythmic drugs are known to induce QT prolongation and torsades de pointes. Case presentation An 84-year-old man was scheduled for open gastrectomy for residual cancer. He had been prescribed bepridil for atrial fibrillation that converted to sinus rhythm with prolonged QT interval in the operating room. After the surgery was initiated under general and epidural anesthesia, the patient’s heart rate decreased to 50/min and multifocal premature ventricular contractions appeared, followed by several episodes of torsades de pointes, each lasting for 5 to 15 s. Infusion of isoproterenol was started (0.01 μg/kg/min), and the heart rate was maintained at around 80/min. Premature ventricular contractions disappeared, and torsades de pointes did not recur during the surgery. The operation was completed uneventfully. The serum bepridil concentration was found to be extremely high postoperatively. Conclusions Bepridil-induced intraoperative episodes of torsades de pointes were successfully treated by increasing the heart rate with isoproterenol.

Cardiac Arrest Related to Torsades de Pointes in a Patient Recovering from Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is an acute complication related to severe hyperglycemia. While the mortality rate for DKA is low with appropriate therapy, several complications may lead to deterioration of the clinical course. Here, we report a case of a 23-year-old patient with DKA who suffered from a rare but hemodynamically unstable cardiac arrhythmia, polymorphic ventricular tachycardia with prolonged QT interval, or Torsades de Pointes. During the recovery phase of DKA, three episodes of Torsades de Pointes suddenly occurred, and were recovered by immediate defibrillation. The patient did not have structural heart disease or a genetic predisposition. To the best of our knowledge, this is the first report of an adult with DKA complicated with QT prolongation related to Torsades de Points after correction of ketosis. To manage DKA, more attention may be needed on changes in the QT interval as well as risk factors for Torsades de Points.