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Volume 42, Issue 2, Pages 138.e1-138.e8 (March 2009)


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Imaging myocardial scar and arrhythmic risk prediction—a role for the electrocardiogram?

David G. Strauss, BAabc, Katherine C. Wu, MDaCorresponding Author Informationemail address

Received 6 November 2008 published online 02 February 2009.

Abstract 

Risk stratification for sudden cardiac death (SCD) has become increasingly important to identify candidates for implantable cardioverter-defibrillators (ICDs). Existing clinical guidelines to identify patients for ICDs focus on reduced left ventricular ejection fraction (LVEF); however, the average annual rate of appropriate ICD shocks is only 5.1% in this select group (LVEF ≤35%), and these patients only represent a small fraction of the total number of patients who die of SCD. Magnetic resonance imaging (MRI) with late gadolinium enhancement has recently emerged as the in vivo gold standard for detecting and quantifying myocardial scar after infarction and in nonischemic cardiomyopathies. Myocardial scar, particularly in the scar border zone, interrupts electrical conduction providing regions that support reentrant ventricular arrhythmias. Recent studies have shown that increased MRI scar in both prior infarction and nonischemic cardiomyopathy patients is associated with arrhythmogenesis, worsening heart failure, and cardiac mortality. This review will focus on the emerging role of MRI to quantify scar and predict arrhythmogenesis in patients with prior infarction and with nonischemic cardiomyopathies—including idiopathic, hypertrophic, Fabry's disease, myocarditis, Chagas' disease, and sarcoidosis. Furthermore, this review will discuss the potential role of the 12-lead electrocardiographic Selvester QRS scoring system to quantify myocardial scar and predict arrhythmogenesis in prior infarct and nonischemic cardiomyopathy patients.

a Division of Cardiology, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, MD, USA

b Department of Clinical Physiology, Lund University Hospital, Lund, Sweden

c School of Medicine, Duke University, Durham, NC, USA

Corresponding Author InformationCorresponding author. Tel.: +1 410 502 7283; fax: +1 410 502 0231.

 Financial support: DGS is supported by the Sarnoff Cardiovascular Research Foundation, (Great Falls, VA). KCW is supported by the Donald W. Reynolds Cardiovascular Research Center at Johns Hopkins University (Baltimore, MD).

PII: S0022-0736(08)00498-6

doi:10.1016/j.jelectrocard.2008.12.010


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