A QTc risk score in patients with obstructive sleep apnea.

INTRODUCTION: Patients with obstructive sleep apnea (OSA) are at risk for QTc prolongation, a known risk factor for increased mortality. The pro-QTc score can help identify individuals at increased risk for mortality associated with increased QTc however, it has not been evaluated in patients with OSA. The goal of this study was to evaluate the pro-QTc score in patients with OSA. METHODS: Medical records of patients undergoing a sleep study at our sleep center from February 2012 to August 2020 were analyzed. Presence or absence of OSA was determined by polysomnography. The pro-QTc score was calculated with 1 point assigned for each of the following: female sex, QT-prolonging diagnoses and conditions, QT-prolonging electrolyte abnormalities, and medications with known risk for QT-prolongation. Mortality was determined from the electronic medical record of an integrated healthcare system. RESULTS: There were 2246 patients (age 58 ± 15 years, 54% male, 82 dead) with OSA and 421 patients (age 54 ± 18 years, 43% male, 18 dead) without OSA. Of those with OSA, 1628 (72.5%) had at least one risk factor for QTc prolongation. A higher pro-QTc score was associated with greater mortality in patients with OSA (HR 1.48 per pro-QTc score, p < 0.001, 95% CI 1.3-1.7) but not in patients without OSA (HR 1.25 per pro-QTc score, p = 0.30, 95% CI 0.82-1.9), after adjusting for age, body mass index (BMI), and smoking status. CONCLUSION: In patients with OSA, a higher pro-QTc score was associated with greater mortality.

Right ventricular epicardial arrhythmogenic substrate in long-QT syndrome patients at risk of sudden death.

AIMS: The long-QT syndrome (LQTS) represents a leading cause of sudden cardiac death (SCD). The aim of this study was to assess the presence of an underlying electroanatomical arrhythmogenic substrate in high-risk LQTS patients. METHODS AND RESULTS: The present study enrolled 11 consecutive LQTS patients who had experienced frequent implantable cardioverter-defibrillator (ICD discharges triggered by ventricular fibrillation (VF). We acquired electroanatomical biventricular maps of both endo and epicardial regions for all patients and analyzed electrograms sampled from several myocardial regions. Abnormal electrical activities were targeted and eliminated by the means of radiofrequency catheter ablation. VF episodes caused a median of four ICD discharges in eleven patients (6 male, 54.5%; mean age 44.0 ± 7.8 years, range 22-53) prior to our mapping and ablation procedures. The average QTc interval was 500.0 ± 30.2 ms. Endo-epicardial biventricular maps displayed abnormally fragmented, low-voltage (0.9 ± 0.2 mV) and prolonged electrograms (89.9 ± 24.1 ms) exclusively localized in the right ventricular epicardium. We found electrical abnormalities extending over a mean epicardial area of 15.7 ± 3.1 cm2. Catheter ablation of the abnormal epicardial area completely suppressed malignant arrhythmias over a mean 12 months of follow-up (median VF episodes before vs. after ablation, 4 vs. 0; P = 0.003). After the procedure, the QTc interval measured in a 12-lead ECG analysis shortened to a mean of 461.8 ± 23.6 ms (P = 0.004). CONCLUSION: This study reveals that, among high-risk LQTS patients, regions localized in the epicardium of the right ventricle harbour structural electrophysiological abnormalities. Elimination of these abnormal electrical activities successfully prevented malignant ventricular arrhythmia recurrences.

Impact of Dietary Factors on Brugada Syndrome and Long QT Syndrome.

A healthy regime is fundamental for the prevention of cardiovascular diseases (CVD). In inherited channelopathies, such as Brugada syndrome (BrS) and Long QT syndrome (LQTS), unfortunately, sudden cardiac death could be the first sign for patients affected by these syndromes. Several known factors are used to stratify the risk of developing cardiac arrhythmias, although none are determinative. The risk factors can be affected by adjusting lifestyle habits, such as a particular diet, impacting the risk of arrhythmogenic events and mortality. To date, the importance of understanding the relationship between diet and inherited channelopathies has been underrated. Therefore, we describe herein the effects of dietary factors on the development of arrhythmia in patients affected by BrS and LQTS. Modifying the diet might not be enough to fully prevent arrhythmias, but it can help lower the risk.

Unique ECG presentations and clinical management of a symptomatic LQT2 female carrying a novel de novo KCNH2 mutation.

A 26-year-old woman, 12 days in postpartum, developed recurrent syncope and cardiac arrest. Her ECG revealed QT-prolongation associated with LQT2-specific T-U wave patterns, T wave alternans, long QT-dependent torsade de pointes (TdP) and ventricular fibrillation (VF). She also had intermittent LBBB (80bpm) on alternate beats and RBBB at sinus tachycardia (113bpm). Family genotyping revealed a novel de novo missense mutation G604C of KCNH2. Propranolol slowed heart rate and further prolonged QT interval (610ms) that caused TdP recurrence. Mexiletine combined with magnesium and potassium supplements prevented TdP/VF recurrence. This patient has remained event-free after 9-month follow-up.

Quality of life after videoscopic left cardiac sympathetic denervation in patients with potentially life-threatening cardiac channelopathies/cardiomyopathies.

BACKGROUND: Left cardiac sympathetic denervation (LCSD) provides an additive or potentially alternative treatment option for patients with life-threatening cardiac channelopathies/cardiomyopathies. OBJECTIVE: We sought to examine the effects of LCSD on quality of life (QOL). METHODS: From November 2005 to May 2013, 109 patients who underwent LCSD were subsequently sent postoperative QOL surveys. RESULTS: Of 109 patients, 8 (7%) could not be contacted. Of the remaining 101 patients, 62 returned surveys (response rate 61%). There were an average of 4.1 ± 1.8 self-reported side effects immediately after LCSD. The most common anticipated side effects included unilateral hand dryness, color or temperature variance between sides of the face, and abnormal sweating. Although parent-reported pediatric physical QOL scores were lower than national norms, there were no differences in psychosocial QOL or disability scores (P = .09 and .33, respectively). QOL scores for adult patients were not significantly different from a US normative sample. Adult LCSD patients reported less disability than a US normative sample (P < .01). There was no correlation between QOL scores and the presence of anticipated side effects. However, among the subset of pediatric patients who continued to receive ventricular fibrillation-terminating implantable cardioverter-defibrillator shocks after LCSD, there was a correlation between their disability scores and the number of reported shocks (Spearman correlation = 0.56). The majority of patients/parents reported that they were very or somewhat satisfied with their surgery (or their child's surgery) and would definitely or probably recommend LCSD to another patient. CONCLUSION: Despite the anticipated side effects associated with LCSD, patients are satisfied with their surgery and indicate that they would recommend the surgery to another patient.

Hyperbaric oxygen therapy reduces the risk of QTc interval prolongation in patients with diabetes and hard-to-heal foot ulcers.

AIMS: Heart rate corrected QT (QTc) interval prolongation is a risk factor associated with increased mortality. Hyperbaric oxygen therapy (HBO) has previously been shown to have acute beneficial effects on QTc dispersion. The aim of this study was to evaluate long-term effects of HBO on QTc time in diabetic patients with hard-to-heal foot ulcers. METHODS: In a prospective, double-blinded placebo-controlled study, patients were randomized to 40 treatment sessions with either HBO or air (placebo), at 2.5 ATA. Patients fulfilling >35 completed treatment sessions were included in the evaluation. RESULTS: Of the initial 75 patients (38 HBO/37 placebo), two were excluded due to pacemaker use. Baseline characteristics were similar between groups. At the 2-year follow-up, QTc time was significantly shorter in the HBO compared to the placebo group (438 vs. 453ms, p<0.05). Further, fewer HBO treated patients had a QTc time >450ms (22 vs. 53 %, p<0.02). This difference seemed to be caused by a significant prolongation of the QTc interval in the placebo group (427 (419-459) at baseline vs. 456ms (424-469) after 2years), whereas no significant change was seen in HBO treated patients. CONCLUSIONS: HBO treatment might protect against QTc prolongation in this high-risk diabetic population.

KN-93, A CaMKII inhibitor, suppresses ventricular arrhythmia induced by LQT2 without decreasing TDR.

Abnormal enhanced transmural dispersion of repolarization (TDR) plays an important role in the maintaining of the severe ventricular arrhythmias such as torsades de pointes (TDP) which can be induced in long-QT (LQT) syndrome. Taking advantage of an in vitro rabbit model of LQT2, we detected the effects of KN-93, a CaM-dependent kinase (CaMK) II inhibitor on repolarization heterogeneity of ventricular myocardium. Using the monophasic action potential recording technique, the action potentials of epicardium and endocardium were recorded in rabbit cardiac wedge infused with hypokalemic, hypomagnesaemic Tyrode's solution. At a basic length (BCL) of 2000 ms, LQT2 model was successfully mimicked with the perfusion of 0.5 µmol/L E-4031, QT intervals and the interval from the peak of T wave to the end of T wave (Tp-e) were prolonged, and Tp-e/QT increased. Besides, TDR was increased and the occurrence rate of arrhythmias like EAD, R-on-T extrasystole, and TDP increased under the above condition. Pretreatment with KN-93 (0.5 µmol/L) could inhibit EAD, R-on-T extrasystole, and TDP induced by E-4031 without affecting QT interval, Tp-e, and Tp-e/QT. This study demonstrated KN-93, a CaMKII inhibitor, can inhibit EADs which are the triggers of TDP, resulting in the suppression of TDP induced by LQT2 without affecting TDR.

Perioperative management of hereditary arrhythmogenic syndromes.

Patients with inherited cardiac channel disorders are at high risk of perioperative lethal arrhythmias. Preoperative control of symptoms and a multidisciplinary approach are required for a well-planned management. Good haemodynamic monitoring, adequate anaesthesia and analgesia, perioperative maintenance of normocarbia, normothermia, and normovolaemia are important. In congenital long QT syndrome, torsades de pointes should be prevented with magnesium sulphate infusion and avoidance of drugs such as droperidol, succinylcholine, ketamine, and ondansetron. Propofol and epidural anaesthesia represent safe choices, while caution is needed with volatile agents. In Brugada syndrome, ß-blockers, α-agonists, and cholinergic drugs should be avoided, while isoproterenol reverses the ECG changes. Propofol, thiopental, and volatiles have been used uneventfully. In congenital sick sinus syndrome, severe bradycardia resistant to atropine may require isoproterenol or epinephrine. Anaesthetics with vagolytic properties are preferable, while propofol and vecuronium should be given with caution due to risk of inducing bradyarrhythmias. Neuraxial anaesthesia should produce the least autonomic imbalance. Arrhythmogenic right ventricular dysplasia/cardiomyopathy induces ventricular tachyarrhythmias, which should be treated with ß-blockers. Generally, ß-adrenergic stimulation and catecholamine release should be avoided. Halothane and pancuronium are contraindicated, while large doses of local anaesthetics and epinephrine should be avoided in neuraxial blocks. In catecholaminergic polymorphic ventricular tachycardia, ß-blocker treatment should be continued perioperatively. Catecholamine release and ß-agonists, such as isoproterenol, should be avoided. Propofol and remifentanil are probably safe, while halothane and pancuronium are contraindicated. Regional anaesthesia, without epinephrine, is relatively safe. In suspicious cardiac deaths, postmortem examination and familial screening are recommended.

Ranolazine stabilizes cardiac ryanodine receptors: a novel mechanism for the suppression of early afterdepolarization and torsades de pointes in long QT type 2.

BACKGROUND: Ranolazine (Ran) is known to inhibit multiple targets, including the late Na(+)current, the rapid delayed rectifying K(+)current, the L-type Ca(2+)current, and fatty acid metabolism. Functionally, Ran suppresses early afterdepolarization (EADs) and torsades de pointes (TdP) in drug-induced long QT type 2 (LQT2) presumably by decreasing intracellular [Na(+)](i) and Ca(2+)overload. However, simulations of EADs in LQT2 failed to predict their suppression by Ran. OBJECTIVE: To elucidate the mechanism(s) whereby Ran alters cardiac action potentials (APs) and cytosolic Ca(2+)transients and suppresses EADs and TdP in LQT2. METHODS: The known effects of Ran were included in simulations (Shannon and Mahajan models) of rabbit ventricular APs and Ca(2+)transients in control and LQT2 models and compared with experimental optical mapping data from Langendorff rabbit hearts treated with E4031 (0.5 µM) to block the rapid delayed rectifying K(+)current. Direct effects of Ran on cardiac ryanodine receptors (RyR2) were investigated in single channels and changes in Ca(2+)-dependent high-affinity ryanodine binding. RESULTS: Ran (10 µM) alone prolonged action potential durations (206 ± 4.6 to 240 ± 7.8 ms; P <0.05); E4031 prolonged action potential durations (204 ± 6 to 546 ± 35 ms; P <0.05) and elicited EADs and TdP that were suppressed by Ran (10 µM; n = 7 of 7 hearts). Simulations (Shannon but not Mahajan model) closely reproduced experimental data except for EAD suppression by Ran. Ran reduced open probability (P(o)) of RyR2 (half maximal inhibitory concentration = 10 ± 3 µM; n = 7) in bilayers and shifted half maximal effective concentration for Ca(2+)-dependent ryanodine binding from 0.42 ± 0.02 to 0.64 ± 0.02 µM with 30 µM Ran. CONCLUSIONS: Ran reduces P(o) of RyR2, desensitizes Ca(2+)-dependent RyR2 activation, and inhibits Ca(i) oscillations, which represents a novel mechanism for its suppression of EADs and TdP.

[Clinical characteristics of 52 patients with torsade de points associated with acquired QT prolongation].

OBJECTIVE: Risk factors, ECG characteristics and treatment options of patients with Torsade de Points associated with acquired QT prolongation are summarized in this study. METHOD: Using "torsade de points" and "QT prolongation" as the keywords to search the inpatients database from 1990 - 2010 of Fuwai hospital, 52 eligible patients were included in this analysis. RESULTS: Structural heart diseases were found in 67.3% and electrolyte disorders in 59.6% patients, 36.5% patients received diuretic therapy and 28.8% received antiarrhythmic drugs which might induce prolonged QT interval. The mean QTc was (571 ± 93) ms and (456 ± 50) ms before and after treatment. All patients received potassium and magnesium supplement. Isoproterenol was used in 32.7% patients. 13.5% patients received temporary pacing therapy. CONCLUSIONS: Torsade de points and acquired QT interval prolongation was often associated with electrolyte disorders and drugs causing QT prolongation. ECG and QTc should be intensively monitored for high risk patients. Early awareness of the warning signs might contribute to early recognition and proper treatment of patients with Torsade de Points associated with acquired QT prolongation.

[Clinical characteristics and outcome of 32 patients with long-QT syndrome accompanied with torsade de pointes].

OBJECTIVE: To summarize the clinical characteristics and outcome of patients with long-QT syndrome (LQTs) accompanied with torsade de pointes. METHODS: Thirty-two eligible patients were included in this study. Clinical and electrocardiographic data were analyzed and telephone or out-patient follow-up were made in all patients. RESULTS: There were 15 patients with inherited LQTs (h-LQTs) and 17 patients with acquired LQTs (a-LQTs). There are more women (n = 24) than men (n = 8). ß blockers, potassium and magnesium supplement were the basic therapy for h-LQTs patients, bivent pacemaker was implanted in 2 patients and implantable cardioverter defibrillator was implanted in 5 patients. Ventricular tachyarrhythmias and syncope occurred in 4 patients during (39.4 ± 25.1) months follow-up. In 17 a-LQTs patients, one patient with dilated cardiomyopathy died suddenly and another patient with implanted cardioverter defibrillator experienced one ventricular tachycardia during (30.9 ± 13.3) months follow-up. CONCLUSIONS: The prognosis in h-LQTs and a-LQTs patients with structure heart disease is poor. ICD or CRT-D therapy is suggestive for a-LQTs patients with structure heart disease.

Canais iônicos de potássio associados à sindrome do QT longo adquirido: [revisão] / Potassium ion channels associated with acquired long QT syndrome: [review]

Intervalo QT é um parâmetro mensurado pelo eletrocardiograma de superfície que corresponde ao período que vai desde o início da despolarização até o final da repolarização ventricular. Devido à dependência da frequência cardíaca instantânea, o intervalo QT é corrigido pela frequência cardíaca. O intervalo QT corrigido é então empregado na prática clínica, por meio de valores de normalidade. Valores superiores aos recomendados pela literatura revelam o prolongamento significativo do intervalo QT - a síndrome do QT longo - uma desordem da condução elétrica do miocárdio que altera a repolarização ventricular e, consequentemente, aumenta a vulnerabilidade para o desenvolvimento de taquiarritmias ventriculares do tipo torsades de pointes e morte súbita. Esta síndrome pode apresentar origem congênita ou adquirida, com alterações nas propriedades dos canais iônicos de potássio, seja na sua cinética de ativação e inativação seja na densidade da corrente iônica ou mesmo em sua estrutura, resultando no prolongamento do tempo de repolarização ventricular. Assim, o objetivo deste trabalho foi revisar a literatura quanto à descrição ou à caracterização eletrofisiológica dos canais de potássio, em condições normais e relacionadas à síndrome do QT longo.

Un caso de QT largo y torsades de pointes por ciprofloxacino / No disponible

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A sweet tooth as the root cause of cardiac arrest.

A 71-year-old woman was admitted with hypotension and bradycardia. An electrocardiogram showed flattened T waves and increased U wave prominence, resulting in a long QT(U) syndrome. Her initial serum potassium level was 1.6 mmol/L (all other electrolytes, including magnesium, were normal). She suffered recurrent ventricular tachycardia and ventricular fibrillation arrest requiring direct current cardioversion and high-dose intravenous potassium chloride replacement. Systematic enquiry revealed that she had been constipated for a number of months and had resorted to consuming large quantities of liquorice on a daily basis for its laxative effects. Endocrinology review identified no primary abnormality of the renin- angiotensin- aldosterone axis, and the patient was diagnosed with hypokalemia secondary to liquorice overindulgence. Liquorice has a mineralocorticoid effect. If chronically consumed in large quantities, this effect may lead to severe depletion of whole-body potassium stores. The present case highlights a rare but important cause of hypokalemic cardiac arrest of which all acute care physicians should be aware.

Drug induced shortening of the QT/QTc interval: an emerging safety issue warranting further modelling and evaluation in drug research and development?

INTRODUCTION: A session dedicated to the issue of drug-induced QT and/or QTc interval (QT/QTc) shortening of the electrocardiogram (ECG) was held at the 2007 Safety Pharmacology Society (SPS) meeting in Edinburgh. METHODS: The session included a presentation on the results of a cross company survey on QT/QTc-shortening, a podium debate with speakers arguing "for" and "against" QT/QTc shortening being a safety issue and a panel discussion with the audience. RESULTS: Compared to QT/QTc prolongation, relatively little is known about the relevance to safety of drug-induced QT/QTc shortening. As with QT/QTc prolongation, there are genetic syndromes and pharmaceutical agents which cause shortening of QT/QTc. The potential safety issue of QT/QTc shortening and its suitability as a biomarker of drug-induced cardiac arrhythmias, are unclear, however, the type of arrhythmia associated with prolongation and shortening are thought to differ. Prolongation is associated with torsades de pointes, whereas, shortening of QT/QTc is proposed to be associated with the more severe arrhythmia, ventricular fibrillation (VF). The industry-wide survey (53 total responses representing 45 different companies) indicates that the number of compounds that induce QT/QTc shortening has increased over the past 5 years with 51% of responses reporting QT/QTc shortening in pre-clinical studies and 22% reporting a corresponding clinical experience. The reason for the increase is not clear but there is a clear business impact with 13% (7/56) of these compounds being discontinued in the pre-clinical phase due to QT/QTc shortening. The majority of companies with clinical experience of QT/QTc shortening have engaged with the regulatory agencies and these experiences will be valuable in shaping how the pharmaceutical industry and the agencies view drug-induced QT/QTc shortening in the future. DISCUSSION: Currently it is not clear how much shortening of QT/QTc is required before it might be considered a safety issue and indeed, whether QT/QTc shortening is a suitable biomarker for cardiac arrhythmias. It is clear, however, that with our current understanding, compounds which shorten QT/QTc will attract close regulatory scrutiny and carry a business risk. The need to better understand this potential cardiac safety issue points to further research including; model development to determine the mechanism(s) of action of drug-induced QT/QTc shortening and the translation between the non-clinical and clinical situation.

QT interval prolongation, torsade de pointes and renal disease.

Torsade de pointes is a form of polymorphic ventricular tachycardia occurring in a setting of prolonged QT interval on surface electrocardiogram. Several non-antiarrhythmic drugs including antibiotic and antipsychotic agents have been shown to prolong cardiac repolarization predisposing to torsade de pointes ventricular tachycardia. Blockade of the delayed rectifier (repolarising) potassium current and drug interactions with inhibitors of the cytochromes P450 (CYP)-mediated metabolism are the most common underlying mechanisms. Many antiarrhythmic drugs have been also implicated in prolonging QT interval and triggering torsades de pointes, especially during chronic therapy or in case of acute high dose toxicity. Progressive renal disease is associated from the earliest stages with increased QT interval and dispersal and with an increased risk of cardiovascular death, specifically sudden death. It has also been reported that cCorrected QT (QTc) interval prolongation and torsade de pointes are associated with end-stage renal disease (ESRD) and that they can be a cause of sudden death in ESRD. We present a case of torsade de pointes in a 82-year-old Italian woman with chronic renal failure.

Fever accentuates transmural dispersion of repolarization and facilitates development of early afterdepolarizations and torsade de pointes under long-QT Conditions.

BACKGROUND: The arrhythmogenic effects of hyperthermia have been highlighted in the Brugada syndrome but remain largely unexplored in other arrhythmic syndromes. The present study examines the effect of hyperthermia on transmural dispersion of action potential duration (TD-APD), early afterdepolarization (EAD) activity, and torsade de pointes (TdP) under long-QT conditions. METHODS AND RESULTS: Standard and floating glass microelectrodes were used to record action potentials from epicardial, M cell, and endocardial regions of the arterially perfused left ventricle wedge, from tissue slices isolated from these regions, and from isolated Purkinje fibers. A transmural ECG was simultaneously recorded across the wedge. Under baseline conditions and in the presence of I(Ks) block (chromanol 293B), hyperthermia (39 degrees C to 40 degrees C) abbreviated APD in tissue slices from all 3 regions. In the presence of I(Kr) block (E-4031), hyperthermia prolonged APD and induced or augmented EADs in M cell and Purkinje preparations at pacing cycle lengths > or = 800 ms but abbreviated APD in epicardium and endocardium, resulting in a marked accentuation of TD-APD. Ryanodine prevented the hyperthermia- induced EAD. In perfused wedge preparations, hyperthermia abbreviated APD throughout both in the absence or presence of I(Kr) or I(Ks) block and did not induce EADs or TdP. Combined I(Kr) and I(Ks) block increased TD-APD and induced EADs (4/12) and spontaneous TdP (3/12) at 36 degrees C to 37 degrees C; hyperthermia (39 degrees C to 40 degrees C) further accentuated TD-APD and facilitated the development of EAD activity (9/12) and TdP (6/12). CONCLUSIONS: Our findings suggest that hyperthermia can be associated with an increased arrhythmic risk when the repolarization reserve of the myocardium is compromised.

Acquired long QT syndrome and elective anesthesia in children.

We present the case of a child who had had a previous episode of torsades de pointes (TdP) and who was scheduled for elective surgery under general anesthesia. The pathophysiology of this condition and the anesthesia concerns are discussed. An 8-year-old male with a history of osteogenic sarcoma had undergone an uneventful limb salvage procedure 2 years earlier. During a subsequent admission to the hospital, he had had a cardiopulmonary arrest with complete recovery. Telemetry electrocardiogram (ECG) rhythm recordings obtained during the event showed TdP that degenerated into ventricular fibrillation, which then terminated spontaneously. On a subsequent ECG, the QTc interval was 694 ms. The prolonged QT interval was attributed to homeopathic use of cesium chloride supplements and the QT interval normalized after cesium was stopped. He presented for an elective procedure and, with an anesthetic plan that emphasized medications without known effect on the QT interval, had an uneventful perioperative course. The optimal anesthesia plan for patients with prolonged QT or those suspected to be at risk for prolongation of the QT interval has not been well described. Available evidence suggests that using total intravenous anesthesia with propofol may be the safest and was used uneventfully in this case. Additionally, this case emphasizes the need to inquire about the use of supplements and naturopathic medications, even in children, that may have life-threatening side effects or interactions with anesthetic agents.

Role of invasive and noninvasive testing in risk stratification of sudden cardiac death in children and young adults: an electrophysiologic perspective.

Sudden cardiac death is a rare, but devastating, event in the young population. Arrhythmia is the mechanism of death in many cases. In addition to clinical history, noninvasive and invasive tests can be used to identify patients who are at risk. Although these tools are not perfect, they can prove valuable if used in proper clinical circumstances. An overview of these tests is presented.

Acquired long QT syndrome and monomorphic ventricular tachycardia after alternative treatment with cesium chloride for brain cancer.

Individuals searching for symptomatic relief or a potential cure are increasingly seeking and using nontraditional therapies for their various diseases. Little is known about the potential adverse effects that patients may encounter while undergoing these alternative treatments. Cesium chloride is an unregulated agent that has been reported to have antineoplastic properties. Cesium chloride is advertised as an alternative agent for many different types of cancers and can be purchased easily on the Internet. Recently, QT prolongation and polymorphic ventricular tachycardia were reported in several patients taking cesium chloride as alternative treatment for cancer. We report acquired QT prolongation and sustained monomorphic ventricular tachycardia in a patient who self-initiated and completed a course of cesium chloride as adjunctive treatment for brain cancer.