Cases reported "Long QT Syndrome"

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1/7. Laser surgery in a patient with Romano-Ward (long QT) syndrome and an automatic implantable cardioverter defibrillator.

    A 48-year-old woman with romano-ward syndrome (a hereditary long qt syndrome), asthma and an automatic implantable cardioverter defibrillator presented for laser surgery for debulking of a massive nasopharyngeal tumour prior to radiotherapy. Automatic implantable cardioverter defibrillators have only relatively recently been used to treat patients with the long qt syndrome and are indicated for the high-risk individual when conventional treatment has failed or when beta-blockers are contraindicated. If surgery requires the use of surgical diathermy, a cardiac technician must be present to deactivate the defibrillator and external pacing electrodes are sited on the chest until the defibrillator can be reactivated. radiotherapy requires both deactivation and shielding of the device.
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2/7. Familial hypertrophic cardiomyopathy associated with prolongation of the QT interval.

    In a 61 year old female patient who suffered from atypical chest pain we diagnosed long qt syndrome by QTc duration of 467 ms, macroscopic T wave alternans and notched T waves in three leads and hypertrophic cardiomyopathy with asymmetric thickening of basal parts of the septum (2.0 cm) without relevant outflow tract obstruction by echocardiography. coronary angiography could exclude coronary artery disease. In a systematic family screening two sons of the patient could also be diagnosed as having long qt syndrome with QTc durations of 472 and 496 ms and asymmetric septal thickening (1.8 and 2.1 cm, respectively). One of these two sons suffered from pre-syncope, the other was asymptomatic despite maximum sports activity. In the third son, LQTS and hypertrophic cardiomyopathy could be excluded.
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3/7. 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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4/7. long qt syndrome and torsade de pointes in transient left ventricular apical ballooning syndrome.

    A recently reported cardiac syndrome of reversible left ventricular apical ballooning, also called takotsubo cardiomyopathy or ampulla cardiomyopathy, clinically resembles acute myocardial infarction and presents with chest pain, anterior electrocardiographic changes and minimal elevation of cardiac enzymes in absence of myocardial ischemia or injury. Left ventricular function recovers completely in days to weeks. This syndrome is likely a non-ischemic, metabolic-dependent syndrome caused by stress-induced activation of the cardiac adrenoceptors, and results in markedly abnormal ventricular repolarization. Reported here is a case of left ventricular apical ballooning syndrome with QT interval prolongation in a young man who developed torsade de pointes and experienced aborted sudden cardiac death. Patient had a complete recovery of cardiac function and normalization of QT interval in a few days. The syndrome of transient left ventricular apical ballooning could be considered among the causes of long qt syndrome and torsade de pointes.
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5/7. 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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6/7. anorexia nervosa and myocardial infarction.

    A 39-year-old woman with long-standing anorexia nervosa was admitted to our hospital because of extreme weakness and cachexia. During a hyperalimentation therapy, she developed chest pain, revealing the electrocardiogram and cardiac enzymes a myocardial infarction of the inferior wall. We suggest that anorexia nervosa does not 'protect' against coronary atherosclerosis, and that some of the cases of sudden death could be related to myocardial ischemia.
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7/7. T wave alternans in idiopathic long-QT syndrome: insight from body surface mapping.

    Body surface mapping was recorded during T wave alternans in two patients with idiopathic long qt syndrome. Eighty-seven lead ECGs of two consecutive beats during T wave alternans demonstrated that alternating changes in the morphology and polarity of the T wave existed mainly in the left frontal chest. The QRST isointegral maps of the same two consecutive beats showed alternation of a large negative area appearing mainly in the left frontal chest. These results indicate that T wave alternans in the two patients were related to alternate heterogeneous prolongation of the action potential duration in this region.
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