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A systematic review was conducted for all published case reports on drug-induced torsade de pointes (TdP) in elderly (≥80 years) patients to study if the administration of the offending agent was reckless. Overall, 61 reports on drug-induced TdP in patients aged 80-97 years were included in the analysis. Non-modifiable risk factors for drug-induced TdP (e.g. acute coronary syndrome, female gender and congestive heart failure), modifiable risk factors (e.g. hypokalemia, severe hypomagnesemia and digitalis toxicity) and reckless administration of a QT interval-prolonging agent (e.g. despite a known QT interval prolongation or a history of TdP, together with other QT interval prolonging agents in higher than recommended doses) were recorded in each case. Overall, 54 (88.5%) patients had non-modifiable risk factors for drug-induced TdP and 21 (34.4%) patients had modifiable risk factors. The administration of the offending agent was reckless in one half (n = 31; 50.8%) of the patients. The most prevalent reckless administration of a QT interval-prolonging agent was together with other QT interval-prolonging agents (n = 16; 51.6%) or despite QT interval prolongation (n = 8; 25.8%). In conclusion, although risk factors for drug-induced TdP are prevalent in elderly patients with drug-induced TdP, in approximately 50% of patients it appeared following a reckless administration of a QT interval-prolonging agent. In this population physicians should particularly avoid administration of two or more QT interval-prolonging agents simultaneously or administration of a QT interval-prolonging agent despite QT interval prolongation.

Objectives: QT interval prolongation is prevalent among patients with Takotsubo cardiomyopathy (TC), whereas torsades de pointes (TdP) has rarely been reported in these patients. We studied all peer-reviewed reports on TC-associated QT interval prolongation and all peer-reviewed reports on TC-associated TdP to characterize the clinical circumstances leading to TdP in patients with TC., Methods: The literature search yielded 14 reports on TC-associated TdP and 26 reports on TC-associated QT interval prolongation. Overall, 15 patients with TC-associated TdP and 86 patients with TC-associated QT interval prolongation were reported. We systematically reviewed each report and recorded the risk factors for TdP as well as the clinical circumstances of TC., Results: The prevalence of the male sex was higher among patients with TC-associated TdP relative to patients with TC-associated QT interval prolongation (26.7% vs 5.8%; P = .01). There was a trend in the mean maximal corrected QT interval being longer among patients with TC-associated TdP relative to patients with TC-associated QT interval prolongation (679.9 +/- 230.6 vs 555.9 +/- 63.8 milliseconds; P = .06). There were no differences between patients with TC-associated TdP and patients with TC-associated QT interval prolongation in mean age, maximal troponin levels, and lowest ejection fraction. Overall, 12 (80.0%) patients with TC-associated TdP had risk factors for TdP other than the female sex and systolic dysfunction, including suspicion of congenital long QT syndrome, bradycardia, hypokalemia, recent conversion from atrial fibrillation to sinus rhythm, and using QT prolonging agents., Conclusions: Men with TC-associated QT interval prolongation are at risk for TdP. Most patients with TC-associated TdP have risk factors for TdP other than the female sex and systolic dysfunction.

Objective: We studied all English-written peer-reviewed reports on drug-induced torsades de pointes (TdP) in patients aged 80 years or more in order to characterize the clinical circumstances leading to this serious complication., Methods: Our literature search yielded 24 reports on 25 patients aged 80-95 years with drug-induced TdP. We systematically reviewed each report and recorded the non-modifiable risk factors for drug-induced TdP (i.e., female sex and structural heart disease) as well as preventable clinical circumstances, which might have been associated with drug-induced TdP., Results: The most prevalent risk factors for drug-induced TdP were non-modifiable risk factors: 22 (88%) patients were female patients and 19 (76%) patients had structural heart disease. Overall, 16 (64%) patients were female patients with structural heart disease. The literature did not report any elderly male patients without structural heart disease. Among the preventable clinical circumstances, which might have been associated with drug-induced TdP, the most prevalent were: administrating QT prolonging agents despite long QT interval (n=11; 44%) and co-administration of two or more QT prolonging agents (n=9; 36%). The most prevalent QT prolonging agents found to trigger TdP were macrolides and quinolones (n=9; 36%). All but three patients had at least one or more preventable clinical circumstances, which might have been associated with drug-induced TdP., Conclusion: Physicians should be more aware of the risk for drug-induced TdP in patients aged 80 years or more while administrating QT prolonging agents despite long QT interval and co- administrating two or more QT prolonging agents, specifically in elderly female patients with structural heart disease.

Anthracyclines reduce myocardial repolarization reserve and might increase the risk for Torsades de Pointes a long time after treatment. We studied all the publications concerning Torsades de Pointes in patients previously treated with anthracyclines to investigate the clinical circumstances leading to this rare life-threatening complication. Our literature search yielded nine reports of 11 patients who had developed Torsades de Pointes anywhere from weeks to years following treatment with anthracyclines. One of the patients was hospitalized in our medical center. Risk factors and triggers for Torsades de Pointes, among other clinical aspects, were analyzed in each report. Most patients (n=10; 90.9%) were previously treated with anthracyclines owing to acute leukemias: acute myelogenous leukemia (n=5), acute lymphocytic leukemia (n=3) and acute promyelocytic leukemia (n=2). One patient was previously treated with anthracyclines owing to Hodgkin's lymphoma. Most patients were women (n=9; 81.8%). The most prevalent triggers for Torsades de Pointes were the administration of a QT-prolonging agent (n=10; 90.9%) and hypokalemia (n=9; 81.8%). Azole derivatives were the most prevalent of the QT-prolonging agents that triggered Torsades de Pointes (n=5; 45.5%). Although four patients suffered from anthracycline-induced left ventricular dysfunction and five other patients had only one or two questionable triggers for Torsades de Pointes, in only two of these cases the authors considered previous treatment with anthracyclines as a risk factor for Torsades de Pointes. Previous treatment with anthracycline is an underestimated risk factor for Torsades de Pointes. Possible triggers includes azole derivatives, other QT-prolonging agents and hypokalemia. Women patients are particularly at risk.

Objectives: The purpose of this study was to define the electrocardiographic (ECG) predictors of torsade de pointes (TdP) during acquired bradyarrhythmias., Background: Complete atrioventricular block (CAVB) might lead to downregulation of potassium channels, QT interval prolongation, and TdP. Because potassium-channel malfunction causes characteristic T-wave abnormalities in the congenital long QT syndrome (LQTS), we reasoned that T-wave abnormalities like those described in the congenital LQTS would identify patients at risk for TdP during acquired bradyarrhythmias., Methods: In a case-control study, we compared 30 cases of bradyarrhythmias complicated by TdP with 113 cases of uncomplicated bradyarrhythmias. On the basis of the criteria used for the congenital LQTS, T waves were defined as LQT1-like (long QT interval with broad T waves), LQT2-like (notched T waves), and LQT3-like (small and late) T waves., Results: Neither the ventricular rate nor the QRS width at the time of worst bradyarrhythmia predicted the risk of TdP. However, the QT, corrected QT (QTc), and T(peak)-T(end) intervals correlated with the risk of TdP. The best single discriminator was a T(peak)-T(end) of 117 ms. LQT1-like and LQT3-like morphologies were rare during bradyarrhythmias. In contrast, LQT2-like "notched T waves" were observed in 55% of patients with TdP but in only 3% of patients with uncomplicated bradyarrhythmias (p < 0.001). A 2-step model based on QT duration and the presence of LQT2-like T waves identified patients at risk for TdP with a positive predictive value of 84%., Conclusions: Prolonged QT interval, QTc interval, and T(peak)-T(end) correlate with increased risk for TdP during acquired bradyarrhythmias, particularly when accompanied by LQT2-like notched T waves.

Numerous medications not intended for cardiac use (including antibiotics, histamine blockers, and antipsychotic medications) incidentally block potassium channels in myocardial cells, prolong the QT interval, and may trigger malignant arrhythmias. Although the odds for a given patient for developing arrhythmias are small, the number of patients receiving such drugs is enormous. Most patients developing proarrhythmia have additional risk factors that could be easily identified from their medical history. The list of risk factors includes female gender, organic heart disease, hypokalemia, and a history of long QT or drug-induced arrhythmias. Patients without risk factors are at very low risk. For these patients, it is neither practical nor necessary to record an electrocardiogram before therapy is initiated and the most important preventive measure is to avoid concurrent administration of 2 or more drugs that prolong the QT interval or administration of a medication that impairs the metabolism of a QT-prolonging drug. We performed a computerized literature search using the key words "long QT," "torsade," "drug-adverse effects," and "drug-ventricular arrhythmias," searching for published reports of drug-induced torsade de pointes. The references in each of these reports also were reviewed to identify additional publications. In addition, we reviewed the published reviews and the Internet sites dealing with drug-induced arrhythmias. All the original articles quoted in these reviews and Web sites were examined critically., (Copyright 2003, Elsevier Science (USA). All rights reserved.)