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Medline ® Abstracts for References 5,6

of 'Acquired long QT syndrome'

5
TI
Polymorphic ventricular tachycardia, long Q-T syndrome, and torsades de pointes.
AU
Passman R, Kadish A
SO
Med Clin North Am. 2001;85(2):321.
 
PMVT is an uncommon arrhythmia with multiple causes. Classification and management are based on the Q-T interval. Torsades de pointes denotes PMVT in the setting of a prolonged Q-T interval and usually is iatrogenic in origin, although congenital LQTS is being recognized more frequently. Therapy of PMVT focuses on the establishment of hemodynamic stability, the removal or correction of precipitants, and the acute and long-term inhibition of subsequent episodes. Evaluation of these patients should include a thorough history and physical examination and an assessment for underlying heart disease and known [figure: see text]eliciting factors. Long-term management must be tailored to the individual and the underlying cause and should be conducted by an experienced cardiac electrophysiologist.
AD
Departments of Medicine and Preventive Medicine, Cardiac Electrophysiology, Northwestern University Medical School, Chicago, Illinois, USA. r-passman@nwu.edu
PMID
6
TI
Long QT syndrome: diagnosis and management.
AU
Khan IA
SO
Am Heart J. 2002;143(1):7.
 
BACKGROUND: Long QT syndrome (LQT) is characterized by prolongation of the QT interval, causing torsade de pointes and sudden cardiac death. The LQT is a disorder of cardiac repolarization caused by alterations in the transmembrane potassium and sodium currents. Congenital LQT is a disease of transmembrane ion-channel proteins. Six genetic loci of the disease have been identified. Sporadic cases of the disease occur as a result of spontaneous mutations. The acquired causes of LQT include drugs, electrolyte imbalance, marked bradycardia, cocaine, organophosphorus compounds, subarachnoid hemorrhage, myocardial ischemia, protein sparing fasting, autonomic neuropathy, and human immunodeficiency virus disease.
METHODS: Data on the diagnosis and management of LQT were thoroughly reviewed.
RESULTS AND CONCLUSIONS: The diagnosis of LQT primarily rests on clinical and electrocardiographic features and family history. The clinical presentations range from dizziness to syncope and sudden death. Genetic screening is available primarily as a research tool. Short-term treatment of LQT is aimed at preventing the recurrences of torsades and includes intravenous magnesium and potassium administration, temporary cardiacpacing, withdrawal of the offending agent, correction of electrolyte imbalance, and, rarely, intravenous isoproterenol administration. The long-term treatment is aimed at reducing the QT-interval duration and preventing the torsades and sudden death and includes use of oral beta-adrenergic blockers, implantation of permanent pacemaker/cardioverter-defibrillator, and left thoracic sympathectomy. Sodium channel blockers are promising agents under investigation. Electrocardiograms are recorded for screening of family members. The data favor treating asymptomatic patients, if<40 years old at the time of diagnosis, with beta-adrenergic blockers.
AD
Division of Cardiology, Department of Medicine, Creighton University School of Medicine, Omaha, Neb, USA. ikhan@cardiac.creighton.edu
PMID