Circulation. 2008;117:1909
doi: 10.1161/CIRCULATIONAHA.107.189186
(Circulation. 2008;117:1909.)
© 2008 American Heart Association, Inc.
Clinical Summaries
An extract of the first 250 words of the full text is provided, because this article has no abstract.
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Death Without Prior Appropriate Implantable Cardioverter-Defibrillator Therapy: A Competing Risk Study
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Implantable cardioverter-defibrillators (ICDs) improve survival
in selected patients in randomized controlled trials. The contemporary
ICD population, however, is older and has a higher comorbidity
burden than the selected populations of randomized controlled
trials. It is therefore of interest to study the extent to which
patients die before appropriate ICD therapy for ventricular
tachyarrhythmia in a "real-world" ICD population. Such "prior
deaths" are referred to as competing risks and need to be taken
into account when we build models to predict which patients
will and which patients will not use their devices. The present
study indicates that in our routine-care population, about half
of the patients receive appropriate ICD therapy for ventricular
tachycardia or ventricular fibrillation. Eleven percent died
without ever using their devices. Focusing on ventricular fibrillation
only shows that 13% experienced ventricular fibrillation and
23% died before experiencing ventricular fibrillation. In competing
risk models, patients most likely to receive appropriate ICD
therapy were those with a secondary prevention indication, higher
age, or reduced ejection fraction. At the same time, patients
who needed diuretic treatment for congestive heart failure had
a 4-fold increased risk of dying before device use. Future risk
stratification tools should aim to optimize device implantation
and replacement, particularly in a routine-care population.
Here, we demonstrate how the relevant risk of prior death may
be integrated into such risk stratification tools. See p 1918.
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Cardiac Sodium Channel (SCN5A) Variants Associated with Atrial Fibrillation
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The human cardiac sodium channel is responsible for the fast
depolarization upstroke of the cardiac action potential and
is a molecular target
. . . [Full Text of this Article]
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