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Circulation. 2007;115:2459
doi: 10.1161/CIRCULATIONAHA.107.183257
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(Circulation. 2007;115:2459.)
© 2007 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.
 


*    ANNUAL RATE OF TRANSVENOUS DEFIBRILLATION LEAD DEFECTS IN IMPLANTABLE CARDIOVERTER-DEFIBRILLATORS OVER A PERIOD OF >10 YEARS, by Kleemann et al.
 
Implantable cardioverter-defibrillator systems consist of a pulse generator and transvenous leads for sensing arrhythmias and applying pacing and high-voltage shocks for treatment. Pulse generator malfunctions, although rare, have received recent attention. Like pacemaker leads, implantable cardioverter-defibrillator leads are subject to continuous cardiac motion and susceptible to failure from fracture of the conducting wires and insulation breaks. In a single-center registry, Kleemann and colleagues analyzed the frequency of lead malfunction in 990 patients who received their transvenous implantable cardioverter-defibrillators between 1992 and 2005. They observed that 15% of leads failed over time, with 40% estimated to fail by 8 years of follow-up. That only 4 subjects died suddenly suggests that lead failures are often detected during follow-up before a potentially lethal arrhythmia occurs. The findings show that transvenous leads are a weak mechanical link in this life-saving therapy and support the importance of close patient follow-up for the prompt detection of these failures. See p 2474 (editorial p 2461).


*    HERITABILITY OF PLATELET RESPONSIVENESS TO ASPIRIN IN ACTIVATION PATHWAYS DIRECTLY AND INDIRECTLY RELATED TO CYCLOOXYGENASE-1, by Faraday et al.
 
A significant number of people have acute coronary syndrome events despite being on aspirin or a platelet inhibitor. Little is known, however, about what causes individual variability in platelet function and thrombosis. In the current issue of Circulation, Faraday and colleagues ask if measurable or inherited conditions contribute to interindividual variability in platelet function in the presence or absence of aspirin treatment. They examined platelet function in 1908 subjects from 309 white and 208 black families and report an inherited basis for both platelet function and aspirin response using select . . . [Full Text of this Article]


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