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Circulation. 2008;117:1909
doi: 10.1161/CIRCULATIONAHA.107.189186
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(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.
 


*    Death Without Prior Appropriate Implantable Cardioverter-Defibrillator Therapy: A Competing Risk Study
 
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.


*    Cardiac Sodium Channel (SCN5A) Variants Associated with Atrial Fibrillation
 
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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