Abstract

Background— Myocardial scarring from infarction or nonischemic fibrosis forms an arrhythmogenic substrate. The Selvester QRS score has been extensively validated for estimating myocardial infarction scar size in the absence of ECG confounders, but has not been tested to quantify scar in patients with hypertrophy, bundle branch/fascicular blocks, or nonischemic cardiomyopathy. We assessed the hypotheses that (1) QRS scores (modified for each ECG confounder) correctly identify and quantify scar in ischemic and nonischemic patients when compared with the reference standard of cardiac magnetic resonance using late-gadolinium enhancement, and (2) QRS-estimated scar size predicts inducible sustained monomorphic ventricular tachycardia during electrophysiological testing. Methods and Results— One hundred sixty-two patients with left ventricular ejection fraction ≤35% (95 ischemic, 67 nonischemic) received 12-lead ECG and cardiac magnetic resonance using late-gadolinium enhancement before implantable cardioverter defibrillator placement for primary prevention of sudden cardiac death. QRS scores correctly diagnosed cardiovascular magnetic resonance scar presence with receiver operating characteristics area under the curve of 0.91 and correlation for scar quantification of r =0.74 ( P <0.0001) for all patients. Performance within hypertrophy, conduction defect, and nonischemic subgroups ranged from area under the curve of 0.81 to 0.94 and r =0.60 to 0.80 ( P <0.001 for all). Among the 137 patients undergoing electrophysiological or device testing, each 3-point QRS-score increase (9% left ventricular scarring) was associated with an odds ratio for inducing monomorphic ventricular tachycardia of 2.2 (95% CI, 1.5 to 3.2; P <0.001) for all patients, 1.7 (1.0 to 2.7, P =0.04) for ischemics, and 2.2 (1.0 to 5.0, P =0.05) for nonischemics. Conclusions— QRS scores identify and quantify scar in ischemic and nonischemic cardiomyopathy patients despite ECG confounders. Higher QRS-estimated scar size is associated with increased arrhythmogenesis and warrants further study as a risk-stratifying tool.

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