1/91. nicorandil, a potassium channel opener, abolished torsades de pointes in a patient with complete atrioventricular block.TdP is a serious complication of AV block. We report a case of complete AV block with QT prolongation who had bouts of TdP resistant to lidocaine and isoproterenol. Temporary pacing could not be performed, because insertion of a pacing lead triggered TdP that deteriorated into ventricular fibrillation. nicorandil, a potassium channel opener, shortened the QT interval and abolished TdP. This may suggest that potassium channel opening drugs are clinically effective against TdP associated with bradycardia-dependent QT prolongation.- - - - - - - - - - ranking = 1keywords = drug (Clic here for more details about this article) |
2/91. meglumine antimoniate, amiodarone and torsades de pointes: a case report.Pentavalent antimonial drugs used for the treatment of leishmaniasis have been associated with sudden deaths, probably due to the development of ventricular tachyarrhythmias. Prolongation of the QT interval and ventricular tachyarrhymias have been described in patients on amiodarone therapy. We report a case of recurrent torsades de pointes following treatment with pentavalent antimonial drugs and amiodarone.- - - - - - - - - - ranking = 2keywords = drug (Clic here for more details about this article) |
3/91. 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.- - - - - - - - - - ranking = 2keywords = drug (Clic here for more details about this article) |
4/91. 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.- - - - - - - - - - ranking = 3keywords = drug (Clic here for more details about this article) |
5/91. clarithromycin associated with torsades de pointes.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.- - - - - - - - - - ranking = 1keywords = drug (Clic here for more details about this article) |
6/91. 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.- - - - - - - - - - ranking = 1keywords = drug (Clic here for more details about this article) |
7/91. Torsade de pointes induced by intravenous and long-term oral amiodarone therapy in a patient with dilated cardiomyopathy.A 70-year-old woman with dilated cardiomyopathy and ventricular tachyarrhythmia was initially treated in 1990 with intravenous amiodarone (240 mg). She developed a junctional escape rhythm (48 beats/min) with QT prolongation (QT: 0.68 s) and 8 h later developed torsade de pointes (TdP). Because other antiarrhythmic drugs did not suppress the arrhythmia, oral amiodarone (100 mg/day) was started in 1995, 7 weeks before she presented with congestive heart failure. The QT prolongation (QTc: 0.64) increased after administration of dopamine, and TdP again developed. This case suggests that amiodarone induces proarrhythmias by different mechanisms when administered intravenously or orally.- - - - - - - - - - ranking = 1keywords = drug (Clic here for more details about this article) |
8/91. fluconazole-induced torsade de pointes.OBJECTIVE: To present a case of fluconazole-associated torsade de pointes (TDP) and discuss fluconazole's role in causing TDP. CASE SUMMARY: A 68-year-old white woman with candida glabrata isolated from a presacral abscess developed TDP eight days after commencing oral fluconazole The patient had no other risk factors for TDP, including coronary artery disease, cardiomyopathy, congestive heart failure, and electrolyte abnormalities There was a temporal association between the initiation of fluconazole and TDP. The TDP resolved when fluconazole was discontinued; however, the patient continued to have premature ventricular contractions and nonsustained ventricular tachycardia (NSVT) until six days after drug cessation DISCUSSION: Use of the Naranjo probability scale indicates a probable relationship between the use of fluconazole and the development of TDP. The possible mechanism is depression of rapidly activating delayed rectifier potassium currents. In our patient, there was no other etiology identified that could explain QT prolongation or TDP The complete disappearance of NSVT and premature ventricular contractions followed by normalization of QT interval after the drug was stopped strongly suggests fluconazole as the etiology. CONCLUSIONS: Clinicians should be aware that fluconazole, even at low doses, may cause prolongation of the QT interval, leading to TDP. Serial electrocardiographic monitoring may be considered when fluconazole is administered in patients who are at risk for ventricular arrhythmias.- - - - - - - - - - ranking = 2keywords = drug (Clic here for more details about this article) |
9/91. torsades de pointes associated with chlorpromazine: case report and review of associated ventricular arrhythmias.PURPOSE: To present a case of chlorpromazine-associated torsades de pointes, review established cases of ventricular arrhythmias associated with chlorpromazine, and describe the proarrhythmic characteristics of this drug. DATA SOURCES: Articles identified through a search of medline and IDIS from January 1966-November 2000 and thorough review of the article bibliographies. Patient cases also were identified from a search of the food and Drug Administration's Adverse Event Reporting System database (November 1997-March 2001). Cases involving intentional overdoses of chlorpromazine were excluded. RESULTS: In addition to the case reported herein, 12 cases of documented, chlorpromazine-associated ventricular arrhythmias were identified; five had characteristic features of torsades de pointes. chlorpromazine delayed repolarization and produced electrocardiographic abnormalities; although, whether chlorpromazine induced torsades de pointes through a mechanism of early afterdepolarizations is unclear. Similar to other instances of drug-induced torsades de pointes, concurrent factors such as electrolyte deficiencies may place the patient at increased risk for arrhythmia. CONCLUSIONS: chlorpromazine can delay repolarization and produce electrocardiographic abnormalities. These can result infrequently in ventricular arrhythmias and torsades de pointes, particularly in patients with confounding factors.- - - - - - - - - - ranking = 2keywords = drug (Clic here for more details about this article) |
10/91. Torsade de pointes induced by ajmaline.ajmaline, a reserpine derivative, is an effective class I antiarrhythmic agent. Herein we report two cases of ajmaline-induced abnormal QT prolongation accompanied by polymorphic ventricular tachycardia of the torsade de pointes type. Since ajmaline is increasingly used for the acute termination of wide complex tachycardia and as a diagnostic tool after syncope and in patients with idiopathic ventricular tachyarrhythmias, our observations suggest that caution should be exercised with regard to the effects of the drug on the QT interval and its potency to induce proarrhythmia of the torsade de pointes type.- - - - - - - - - - ranking = 1keywords = drug (Clic here for more details about this article) |
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