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(Circulation. 2007;115:2369.)
© 2007 American Heart Association, Inc.

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An extract of the first 250 words of the full text is provided, because this article has no abstract.

	INDUCTIONLESS OR LIMITED SHOCK TESTING IS POSSIBLE IN MOST PATIENTS WITH IMPLANTABLE CARDIOVERTER-DEFIBRILLATORS/CARDIAC RESYNCHRONIZATION THERAPY DEFIBRILLATORS: RESULTS OF THE MULTICENTER ASSURE STUDY (ARRHYTHMIA SINGLE SHOCK DEFIBRILLATION THRESHOLD TESTING VERSUS UPPER LIMIT OF VULNERABILITY: RISK REDUCTION EVALUATION WITH IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR IMPLANTATIONS), by Day et al.

 
Ensuring that an implantable defibrillator is configured to provide a shock of sufficient energy for a high probability of defibrillation has traditionally required induction of ventricular fibrillation, usually at the time of implantation. Although the risks of this defibrillation testing are low, adverse hemodynamic consequences occasionally occur. In a multicenter trial, Day et al exploited the known relationship between the shock strength required to induce ventricular fibrillation and the energy required to defibrillate in their evaluation of a testing scheme that seeks to establish that adequate defibrillation energy is programmed, based on the effect of serial shocks during the T wave that infrequently induced ventricular fibrillation. Although the procedure still requires sufficient analgesia and sophisticated methods for timing the test shocks and is not appropriate for all patients, the results suggest that a substantial number of patients receiving implantable cardioverter-defibrillators could potentially be spared induction of ventricular fibrillation. See p 2382 (editorial p 2370).

	EVIDENCE FOR MICROVASCULAR DYSFUNCTION IN HYPERTROPHIC CARDIOMYOPATHY: NEW INSIGHTS FROM MULTIPARAMETRIC MAGNETIC RESONANCE IMAGING, by Petersen et al.

 
Seminal studies almost 30 years ago documented the presence of inducible ischemia, often clinically silent, in patients with hypertrophic cardiomyopathy (HCM). Ischemia may contribute to many of the pathophysiological features of HCM, including diastolic dysfunction, and potentially creates a milieu for lethal arrhythmias. In this issue of Circulation, Petersen and colleagues report on a comprehensive analysis of HCM patients using cardiovascular magnetic resonance imaging of rest and hyperemic myocardial blood flow and fibrosis and their relation to wall thickness. Hyperemic blood flow was blunted compared to referent controls. The frequency of endocardial blood flow . . . [Full Text of this Article]