Circulation. 2005;112:1519
(Circulation. 2005;112:1519.)
© 2005 American Heart Association, Inc.
Issue Highlights
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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 most important predictor
of all-cause and cardiovascular mortality as well as heart failure
events. This is one of the first studies in which the remodeling
process in a group of heart failure patients was directly associated
with outcomes, and it has implications for research on new therapeutics.
See p
1580.
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MOLECULAR PROFILING OF HEART ENDOTHELIAL CELLS, by Zhang et al.
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The identification of ligands that specifically target receptors
in the heart will aid in the discovery of new diagnostic and
therapeutic agents. Zhang et al combine 2 procedures to identify
novel heart-homing peptides and the receptors that bind to these
peptides. The first step involves screening a phage-display
peptide library for phage particles that specifically accumulate
in mouse heart. The second step uses these heart-homing peptides
as "bait" in a bacterial 2-hybridization procedure to identify
their binding partners. These procedures have led to the identification
of 5 heart-homing peptides and their corresponding receptors.
Independent methods confirmed that 4 of the receptors are preferentially
expressed in the heart vasculature. These heart-homing peptides
may have utility for the selective delivery of drugs or diagnostic
agents to the heart, and the receptors for these peptides may
become useful targets for drug discovery. See p
1601.
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Images in Cardiovascular Medicine
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Constrictive Pericarditis From a Severely Calcified Pericardium.
See p
e137.
Myocardial Infarction as a Rare Consequence of a Snakebite: Diagnosis With Novel Echocardiographic Tissue Doppler Techniques. See p e140.
Continuous Thrombus in the Right and Left Atria Penetrating the Patent Foramen Ovalis. See p e143.
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Correspondence
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See p
e145.
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