Abstract

The extent of peri-infarct zone (PIZ) by contrast-enhanced cardiac magnetic resonance (ce-CMR) has been related to inducibility of ventricular arrhythmia in patients with ischemic cardiomyopathy. However, this relationship has not been established in postmyocardial infarction (post-MI) patients with relatively reserved left ventricular (LV) systolic function yet. In this study, we investigated myocardial scar size and characteristics and its relationship with ventricular arrhythmia inducibility in patients with relatively preserved LV systolic function. This study enrolled 28 post-MI patients with a left ventricular ejection fraction between 40% and 50% and nonsustained ventricular tachycardia who underwent programmed ventricular stimulation (PVS) for risk stratification. Cine and gadolinium-enhanced cardiac magnetic resonance imaging was performed before PVS. A computer-assisted algorithm quantified the total scar (TS) size and divided it into the dense scar (DS) and the PIZ based on signal intensity thresholds (>6 standard deviations [SDs] and 2 to 6 SDs above remote normal myocardium, respectively). Scar measurements were determined and compared among noninducible (n = 19) and inducible patients (n = 9). The groups had similar baseline clinical characteristics. The LV masses, volumes, and ejection fractions did not differ significantly between the groups. For the inducible versus noninducible patients, DS percent was similar (3.11 ± 1.02% vs 3.44 ± 0.79%, P = NS). PIZ percent (28.02 ± 7.49% vs 19.86 ± 7.82%, P = 0.01) and TS percent (31.14 ± 7.96% vs 23.31 ± 8.21%, P = 0.02) were associated with inducibility of monomorphic VT. Multivariate analysis demonstrated that PIZ percent (P = 0.021, OR [odds ratio] 1.18, 95% CI [confidence interval] 1.03-1.35), and TS percent (P = 0.03, OR 1.15, 95% CI 1.01-1.30) were independent predictors of inducibility. Higher PIZ percent and TS percent were correlated with increased ventricular inducibility. These data support the hypothesis that ce-CMR may be used to identify the substrate for ventricular arrhythmia in this cohort.

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