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(Circulation. 2005;112:1519.)
© 2005 American Heart Association, Inc.
Issue Highlights
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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UNMASKING OF BRUGADA SYNDROME BY LITHIUM, by Darbar et al. |
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Antiarrhythmic drugs and agents from many other classes, including some used for psychiatric illness, can cause marked QT prolongation and torsades de pointes. Similarly, the distinctive Brugada syndrome ECG pattern (and occasionally ventricular fibrillation) can be provoked by sodium channel–blocking antiarrhythmic drugs like flecainide, procainamide, and ajmaline. Unlike in the long-QT syndrome, however, only a few nonantiarrhythmic drugs, notably tricyclic antidepressants and possibly cocaine, are known to block sodium channels and precipitate the Brugada syndrome ECG. The present report adds the widely used agent lithium to that list. Pharmacoepidemiological studies have suggested that drugs used in psychiatric therapy can increase risk for sudden death, and this study thus suggests that Brugada syndrome–related ventricular fibrillation may contribute. Practical mechanisms to identify patients at risk in psychiatric or other settings are not well established. Notably, both patients in this study reported a personal history of syncope as well as sudden death in young family members. See p 1527.
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LEFT VENTRICULAR REVERSE REMODELING BUT NOT CLINICAL IMPROVEMENT PREDICTS LONG-TERM SURVIVAL AFTER CARDIAC RESYNCHRONIZATION THERAPY, by Yu et al. |
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Unfavorable left ventricular remodeling is considered an important pathophysiological factor of the heart failure syndrome and has been used as a surrogate end point in early studies of new heart failure therapies. This concept is based in large part on substudies of selected patients from larger clinical trials. In this issue of Circulation, Yu and colleagues report on a group of patients with advanced heart failure who had evaluations of left ventricular volumes before and serially after pacemaker resynchronization therapy. In a Cox regression analysis model, the change in end-systolic volume was the
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