11/230. Transient QT prolongation with torsades de pointes tachycardia after ablation of permanent junctional reciprocating tachycardia. INTRODUCTION: catheter ablation with radiofrequency energy is a curative therapy in patients with permanent junctional reciprocating tachycardia (PJRT). methods AND RESULTS: For the first time, we report a case of transient QT prolongation with torsades de pointes tachycardia 18 hours after successful radiofrequency energy ablation of PJRT in a 25-year-old woman with tachycardia-induced cardiomyopathy. Of note, the torsades de pointes occurred in the absence of bradycardia, electrolyte disturbances, or QT-prolonging drugs. This patient initially was thought to have a hereditary long qt syndrome that was unmasked by PJRT ablation. Therefore, the patient received an implantable defibrillator in addition to beta-blocker therapy, which was discontinued 6 months later. Surprisingly, the QT interval completely normalized within 1 week after PJRT ablation, and the patient remained free of arrhythmias during a follow-up period of 4.5 years. CONCLUSION: patients with incessant tachyarrhythmias should undergo ECG monitoring for at least 24 hours following successful radiofrequency catheter ablation because transient QT prolongation with torsades de pointes may occur even in the absence of bradycardia, QT-prolonging drugs, or electrolyte disturbances. ( info) |
12/230. torsades de pointes secondary to intravenous haloperidol after coronary bypass grafting surgery. PURPOSE: Postoperative delirium occurs in about 2% of patients undergoing major cardiac surgery including coronary artery bypass grafting surgery (CABG). haloperidol (Sabex, Boucherville, canada) is a drug commonly used in the intensive care unit for the treatment of delirium and is usually considered safe even at high doses and is rarely implicated in the development of malignant ventricular arrhythmias such as torsades de pointes. The purpose of this study is to report such a complication of use of haloperidol after myocardial revascularization. CLINICAL FEATURES: The patient reported underwent uneventful triple bypass surgery. Administration of large intravenous doses of haloperidol was necessary for control of psychomotor agitation due to delirium. torsades de pointes occurred in the absence of QT prolongation on the third postoperative day following use of the drug with no other obvious etiological factor. CONCLUSION: awareness of this rare complication is key to judicious use of this drug in the post CABG patient in whom such an arrhythmia may have very deleterious consequences because of the underlying cardiac condition. ( info) |
13/230. Torsade de pointes associated with hypokalemia after anthracycline treatment in a patient with acute lymphocytic leukemia. Severe dose-dependent anthracycline cardiotoxicity is reported to cause myocardial damage resulting in congestive heart failure. However, torsade de pointes, a life-threatening arrhythmia caused by chronic anthracycline cardiotoxicity, has not been reported previously. A 16-year-old girl who developed torsade de pointes after 6 months of chemotherapy for acute lymphocytic leukemia (French-American-British classification L2) is described. When the patient was readmitted to the hospital because of syncope, peripheral blood and bone marrow analysis indicated a relapse. In addition, the patient was hypokalemic. Twenty-four-hour ambulatory electrocardiographic monitoring demonstrated QT prolongation and an episode of torsade de pointes. The electrocardiographic changes and arrhythmia improved after correction of the hypokalemia. An inverse correlation between leukocyte count and hypokalemia was observed. The patient died from pulmonary hemorrhage. autopsy examination demonstrated myocardial degeneration consistent with damage induced by antineoplastic antibiotics. The cumulative dose of anthracycline and anthraquinone was less than the conventional dose limit associated with chronic cardiotoxicity, even for children who are more sensitive to anthracyclines. Torsade de pointes can occur in the setting of chronic anthracycline cardiotoxicity. Therefore, children or young adults who are more sensitive to anthracycline need careful observation that includes electrolyte monitoring, especially for potassium. ( info) |
14/230. Torsade de pointes associated with encephalitis. Torsade de pointes is a polymorphic ventricular tachycardia. Causes of torsade de pointes are well described. Although intracranial disease can produce dramatic electrocardiographic (ECG) changes, we are not aware of previous cases with torsade de pointes and encephalitis. We report a case with encephalitis who developed torsade de pointes, and was treated with temporary ventricular pacing and magnesium infusion. ( info) |
| A patient with long qt syndrome and a history of palpitations underwent electrophysiologic study. Runs of polymorphic self-terminating atrial tachyarrhythmias were easily induced and occurred spontaneously several times. Atrial monophasic action potential (MAP) durations were prolonged at short pacing cycle lengths. Premature high right atrial extrastimuli prolonged MAP durations in the low right atrium, resulting in an inverse electrical restitution curve, and increased dispersion of repolarization. MAP morphology showed gradually increasing early afterdepolarizations. When the arrhythmia was initiated, a new action potential reproducibly emerged from these afterdepolarizations. To the knowledge of the authors, this is the first reported case of "atrial torsades de pointes" in a patient. ( info) |
| Two cases of QT prolongation and torsades de pointes (TdP) are presented. The patients had been taking clarithromycin (400 mg/day) for respiratory disease. Although erythromycin is reportedly associated with TdP, this is the first report of clarithromycin associated with TdP in the absence of other drugs already known to produce QT prolongation. ( info) |
17/230. hypokalemia-induced long qt syndrome with an underlying novel missense mutation in S4-S5 linker of KCNQ1. Congenital long qt syndrome (LQTS) is caused by mutations in at least five genes coding for cardiac potassium or sodium channels that regulate the duration of ventricular action potentials. Acquired LQTS often is associated with drugs or metabolic abnormalities. A 47-year-old woman who presented with marked QT prolongation (QTc = 620 msec(1/2)) and repeated episodes of torsades de pointes associated with hypokalemia (2.6 mEq/L) was screened for mutations in LQTS genes using polymerase chain reaction/single-strand conformation polymorphism (PCR/SSCP). We identified a novel missense mutation in the intracellular linker of S4-S5 domains of KCNQ1, resulting in an amino acid substitution of cysteine for arginine at position 259 (R259C). Whole cell, patch clamp experiments were conducted on COS7 cells transfected with wild-type and/or R259C KCNQ1 with or without KCNE1. Functional analyses of the mutant KCNQ1 subunit on COS7 cells revealed its functional channels in the homozygous state, producing a significantly smaller current than the KCNQ1 channels and a less severe dominant-negative effect on I(Ks). The novel KCNQ1 mutation R259C is the molecular basis for I(Ks) dysfunction underlying an apparently sporadic case of hypokalemia-induced LQTS, consistent with a mild mutation likely to disclose the clinical manifestation of LQTS in a context of severe hypokalemia. Our findings suggest that gene carriers with such mild mutations might not be so rare as commonly expected in patients with acquired LQTS, and stress the importance of mutational analysis for detecting either "silent" forms of congenital LQTS or de novo mutations. ( info) |
18/230. Polymorphic ventricular tachycardia due to renal artery stenosis--a case report. Atherosclerotic renal artery disease is common among patients with hypertension over the age 50 years who are resistant to medical treatment. In this case report, the authors present a 55-year-old woman with unilateral renal artery stenosis with a history of cardiac arrest. QT prolongation and evident hypokalemia were the main clinical findings of the patient. The patient also had an episode of polymorphic ventricular tachycardia during hospitalization that degenerated into ventricular fibrillation. After successful balloon dilation of the stenotic renal artery, the patient stayed normotensive and normokalemic without medication, and no arrhythmia was observed during the 6-month follow-up period. ( info) |
19/230. Torsade de pointes in a child with acute rheumatic fever. Ventricular arrhythmias are uncommon in acute rheumatic carditis. We report the case of a child who presented with rheumatic carditis, prolonged corrected QT interval, and torsade de pointes. The episodes of torsade were controlled with beta-blockade and cardiac pacing. The child subsequently died as a result of brain injury; the autopsy revealed classic findings of acute rheumatic carditis. ( info) |
| Arsenic trioxide is used in clinical trials in the treatment of relapsed and resistant cases of acute promyelocytic leukemia. Adverse effects from arsenic in these studies have been multisystemic. Arsenic is known to cause corrected QT-interval prolongation and T-wave changes, but the potential for serious ventricular arrhythmias is less well understood. torsades de pointes, a form of ventricular tachycardia, has been reported with arsenic poisoning but not at therapeutic doses used in protocols for hematologic malignancies. We describe 3 patients in whom this arrhythmia developed while they were treated with arsenic trioxide. Early recognition of the arrhythmia or correction of contributory factors is important because arsenic induced ventricular arrhythmias are known to be resistant to most chemical methods and electrical cardioversion. ( info) |