Beta blockers, potassium supplements, and implantable defibrillators have been used for treatment of long QT syndrome. Unfortunately, not all persons with long QT syndrome have premonitory symptoms or identifiable electrocardiographic abnormalities, and they may first present with sudden death. Long QT syndrome should be suspected in patients with recurrent syncope during exertion and those with family histories of sudden, unexpected death. Torsades de pointes and ventricular fibrillation are the usual fatal arrhythmias. Most cardiac events are precipitated by vigorous exercise or emotional stress, but they also can occur during sleep. In addition to a prolonged QT interval, which occurs in some but not all persons with long QT syndrome, another characteristic electrocardiographic abnormality is the so-called Brugada sign (an upward deflection of the terminal portion of the QRS complex). The median age of persons who die of long QT syndrome is 32 years men are predominately affected. Some of the highest rates of inherited long QT syndrome occur in Southeast Asian and Pacific Rim countries. Recently, attention has focused on a group of inherited gene mutations in cardiac ion channels that cause long QT syndrome and carry an increased risk for sudden death. A number of drugs are known to cause QT prolongation (e.g., terfenadine), as are hypokalemia, hypomagnesemia, myocarditis, and endocrine and nutritional disorders. A prolonged QT interval is a common thread among the various entities associated with sudden arrhythmia death syndrome. Some cases are caused by sudden arrhythmia death syndrome. In approximately 5 percent of sudden cardiac deaths, no demonstrable anatomic abnormality is found.
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