Articles: qt-prolongation.
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Multicenter Study Observational Study
Racial susceptibility for QT prolongation in acute drug overdoses.
QT prolongation independently predicts adverse cardiovascular events in suspected poisoning. We aimed to evaluate the association between race and drug-induced QT prolongation for patients with acute overdose. ⋯ We found significant racial susceptibility to drug-induced QT prolongation in this large urban study of acute overdoses.
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Status epilepticus has been increasingly associated with cardiac injury in both clinical and animal studies. Our group has previously shown that excitotoxic seizure induction results in the formation of ischaemic myocardial infarcts and loss of cardiac haemodynamic function. We hypothesised that attenuation of cardiac sympathetic/parasympathetic balance with a central presynaptic α₂ agonist, clonidine, can reduce the development of interictal ECG and ventricular morphological changes resulting from kainic acid (KA; 10mg/kg) induced status epilepticus in a conscious rat model. ⋯ These results demonstrate that KA-induced seizures are associated with altered ECG activity and cardiac structural pathology. We suggest that pharmacological modulation of sympathetic/parasympathetic activity in status epilepticus provides a promising therapeutic approach to reduce seizure-induced cardiomyopathy.
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Congenital heart disease · Jan 2014
Case ReportsLong QT syndrome unmasked by dexmedetomidine: a case report.
Dexmedetomidine is a selective alpha-2 adrenergic agonist that is used frequently for short-term sedation in children. It has been noted to cause hypertension, hypotension, bradycardia, and sinus pauses; however, QTc prolongation has not been reported with dexmedetomidine administration. We describe a case of marked QT prolongation with use of dexmedetomidine in a pediatric critical care setting. Clinicians should be vigilant about potential QT prolongation in patients on dexmedetomidine, particularly in those receiving multiple other medications.
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Cerebrogenic ECG abnormalities, especially prominent T wave inversions and prolongation of the QT(U) interval, are well-described. Brady- and tachyarrhythmias, including polymorphic VT, have been also described in the setting of neurologic injury. ⋯ Serial ECG findings included marked ventricular repolarization prolongation with bursts of torsade de pointes, diffuse ST elevations simulating extensive myocardial ischemia or infarction, as well as a Brugada-like pattern. To our knowledge, this case is the first reported with the combination of such findings in a patient with a catastrophic neurologic syndrome.
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Drug Healthc Patient Saf · Jan 2012
Clinical use of antidepressant therapy and associated cardiovascular risk.
A number of different psychotropic agents have been associated with an increased risk of cardiovascular disease, and these relationships have been difficult to interpret due to the presence of confounding factors. Recently, there has been renewed interest in the potential for certain antidepressants to cause QT prolongation, which is a predisposing factor for arrhythmia. However, the optimum means of determining QT remains contentious due to discrepancies between methods that may be readily applied in a clinical setting versus more detailed techniques during regulatory assessment. ⋯ Pre-existing cardiac disease and other factors that independently predispose to arrhythmia are important considerations. Therefore, clinical judgment is needed to evaluate the overall risk or benefit of a particular antidepressant in any patient. Close monitoring should be considered for those at greatest risk of QT prolongation and arrhythmia.