Cases reported "Long QT Syndrome"

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1/9. Fatal case of delayed repolarization due to cocaine abuse and global ischemia.

    When a previously healthy, middle-aged patient presents with apparent seizures, what should alert the physician to the possibility of underlying cardiac disease? This report describes a case of long qt syndrome, initially presenting as seizures, which expressed itself at an atypically advanced age as a result of cocaine use, global myocardial ischemia, and ventricular tachycardia.
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2/9. The romano-ward syndrome: a case presenting as near drowning with a clinical review.

    patients with the romano-ward syndrome, a form of congenital long Q-T syndrome (LQTS), present with syncopal episodes and are at risk for sudden death. patients with LQTS may be misdiagnosed if the physician is unaware of this entity. The risk of sudden death makes recognition important so that appropriate therapy can be initiated. A case is discussed in which the patient presented following a near-drowning episode. family history revealed a familial "seizure disorder." After analysis of the patient's and father's ECGs, the diagnosis of romano-ward syndrome was made. A review of the literature was done, concentrating on presentation, pathophysiology, electrocardiographic findings, etiology, diagnosis, prognosis, and treatment of congenital LQTS. This paper is presented to emphasize the importance of physician awareness of LQTS because of the risk of sudden death. Proper diagnosis can lead to treatment that is effective in reducing mortality by more than 90%.
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3/9. QTc prolongation associated with combination therapy of levofloxacin, imipramine, and fluoxetine.

    OBJECTIVE: To report QTc interval prolongation associated with combination therapy including levofloxacin, imipramine, and fluoxetine. CASE SUMMARY: A 49-year-old white female presented to the emergency department with fever, aches, and pains for the past 3 days. She was diagnosed and treated for pyelonephritis in the hospital. Therapy included intravenous levofloxacin 500 mg every 24 hours and ceftriaxone 2 g every 24 hours, along with her medications upon admission, including imipramine 50 mg at bedtime and fluoxetine 10 mg/day. She was discharged after 5 days and returned the next day with chest tightness and shortness of breath. Upon the second admission, a 12-lead electrocardiogram showed a QTc interval of 509 msec. levofloxacin was discontinued and the QTc interval fell to 403 msec. The patient was discharged 3 days later and instructed to consult with her primary care physician about discontinuing imipramine. DISCUSSION: This adverse drug reaction is thought to be a pharmacodynamic additive effect among fluoxetine, imipramine, and levofloxacin. fluoxetine is a potent inhibitor of CYP2D6, and imipramine is metabolized by CYP2D6. Therefore, fluoxetine is able to increase the plasma concentrations of imipramine, leading to QT interval prolongation. Taken with imipramine, levofloxacin can lead to even greater prolongation of the QT interval. Based on the Naranjo probability scale, levofloxacin was possibly associated with cardiac arrhythmias in our patient. CONCLUSIONS: The use of levofloxacin alone, or more often in concomitant therapy with other medications that are known to prolong the QT interval, may cause QT interval prolongation; however, additional studies/case reports are needed to validate this conclusion.
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4/9. Acquired QT prolongation associated with esophagitis and acute weight loss: how to evaluate a prolonged QT interval.

    When the physician is confronted with a patient having significant QT prolongation, it is critical to determine whether the patient harbors a genetic defect and a transmissible form of long qt syndrome (LQTS) or whether the QT prolongation has an acquired cause. The distinction has profound ramifications for the type of care provided to the patient and family. We report the case of a previously healthy 14-year-old boy who presented with a 10-day history of painful swallowing, a 10-lb weight loss, and chest pain. A 12-lead electrocardiogram (ECG) showed marked QT prolongation. endoscopy and culture identified a herpes simplex esophageal ulcer. After treatment with acyclovir, the patient recovered completely. Three weeks after the resolution of his symptoms and recovery from his acute weight loss, a follow-up ECG showed complete normalization of the QT interval. This case illustrates yet another potential mechanism for acquired QT prolongation. We also provide a diagnostic algorithm for the careful evaluation of a prolonged QT interval.
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5/9. A twist on torsade: a prolonged QT interval on methadone.

    A woman developed a prolonged QT interval and torsade de pointes while on methadone treatment for heroin addiction. We think methadone, or its impaired metabolism, was the major cause for her prolonged QT interval and progression to torsade. However, torsade is often multifactorial, as was likely so in this case. We advise physicians treating patients taking methadone to obtain careful medication and drug-use histories, screen for risk factors associated with long qt syndrome, counsel patients about potential drug interactions, and measure the QT interval before and during methadone treatment in high-risk patients.
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6/9. A new form of long qt syndrome associated with syndactyly.

    OBJECTIVES. The purpose of this study was to characterize a possible association between long qt syndrome and syndactyly. BACKGROUND. long qt syndrome causes syncope and sudden death from ventricular arrhythmias. syndactyly is a developmental disorder that causes webbing of the hands and feet. Both disorders can be inherited as isolated, autosomal dominant traits, but an association between them has not been established. methods. We identified three children with long qt syndrome, atrioventricular (AV) block and simple syndactyly. Phenotypic and laboratory data were obtained from families, attending physicians and medical records. RESULTS. All patients had bilateral cutaneous syndactyly and were diagnosed with long qt syndrome within the 1st 2 years of life. Structural heart disease, particularly a patent ductus arteriosus, was present in all three patients. Analysis of electrocardiograms showed marked prolongation of the QT intervals with rate-corrected QT intervals of 633, 628 and 680 ms, respectively. Transient AV block was also noted. Two of the three children died suddenly despite treatment with beta-adrenergic blocking agents and permanent pacing. CONCLUSIONS. We postulate that these children have a new form of long qt syndrome associated with syndactyly and a high risk of sudden death. The association of syndactyly with long qt syndrome may provide insight into the mechanisms underlying both disorders. patients with syndactyly should be evaluated for the presence of long qt syndrome, and if it is found, aggressive treatment may be warranted.
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7/9. seizures and the long-QT syndrome.

    We describe a case of idiopathic long-QT syndrome in a 4-year-old Hispanic girl. She had been seen previously at an outside hospital for possible new-onset seizure disorder but was brought to our emergency department after sustaining an unwitnessed fall. Her ECG was significant for changes consistent with long-QT syndrome. Emergency physicians should understand the necessity of electrocardiography in all pediatric patients who present with multiple spontaneous falls, episodes of dizziness, new-onset seizure activity and syncopal episodes.
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8/9. The long qt syndrome.

    The LQTS is no longer the rare "zebra" whose purpose is to ensure that trainees recall that deafness and sudden cardiac death may be related (Jervell and Lange-Nielsen syndrome). Over the past 10 to 20 years, the number of cases of inherited LQTS (romano-ward syndrome) has increased dramatically. It is doubtful that this reflects a true increase in incidence of disease due to a greater rate of sporadic gene mutations occurring in the heart or because of a rising incidence of consanguinity. Rather, the "incidence" of LQTS has risen because of the emerging awareness of and respect for this electrical malady in the heart. Understanding the principal elements of the LQTS, knowing the types of presentations, and being able to identify its presence electrocardiographically will allow the astute physician to expose this silent killer.
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9/9. Q-T interval prolongation and pleomorphic ventricular tachyarrhythmia ('Torsade de pointes') in organophosphate poisoning: report of a case.

    1. A 63-year-old woman presented with drowsy consciousness and dyspnea, followed by respiratory failure, after taking a bottle of parathion for suicide. 2. Sinus tachycardia was noted initially by ECG and Q-T interval prolongation with pleomorphic ventricular tachyarrhythmia ('Torsade de pointes') occurred on the third day of admission. 3. Torsade de pointes was relieved by magnesium sulfate and atropine sulfate intravenously. Q-T interval returned to normal on the fifth day of admission. 4. Practicing physicians should be aware of this uncommon type of cardiac toxicity caused by organophosphate poisoning, Q-T interval prolongation and pleomorphic ventricular tachyarrhythmia.
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