OBJECTIVES: We performed noninvasive identification of post-infarction sustained monomorphic ventricular tachycardia (SMVT)-related slow conduction channels (CC) by contrast-enhanced magnetic resonance imaging (ceMRI). BACKGROUND: Conduction channels identified by voltage mapping are the critical isthmuses of most SMVT. We hypothesized that CC are formed by heterogeneous tissue (HT) within the scar that can be detected by ceMRI. METHODS: We studied 18 consecutive VT patients (SMVT group) and 18 patients matched for age, sex, infarct location, and left ventricular ejection fraction (control group). We used ceMRI to quantify the infarct size and differentiate it into scar core and HT based on signal-intensity (SI) thresholds (>3 SD and 2 to 3 SD greater than remote normal myocardium, respectively). Consecutive left ventricle slices were analyzed to determine the presence of continuous corridors of HT (channels) in the scar. In the SMVT group, color-coded shells displaying ceMRI subendocardial SI were generated (3-dimensional SI mapping) and compared with endocardial voltage maps. RESULTS: No differences were observed between the 2 groups in myocardial, necrotic, or heterogeneous mass. The HT channels were more frequently observed in the SMVT group (88%) than in the control group (33%, p < 0.001). In the SMVT group, voltage mapping identified 26 CC in 17 of 18 patients. All CC corresponded, in location and orientation, to a similar channel detected by 3-dimensional SI mapping; 15 CC were related to 15 VT critical isthmuses. CONCLUSIONS: SMVT substrate can be identified by ceMRI scar heterogeneity analysis. This information could help identify patients at risk of VT and facilitate VT ablation.
OBJECTIVES: We performed noninvasive identification of post-infarction sustained monomorphic ventricular tachycardia (SMVT)-related slow conduction channels (CC) by contrast-enhanced magnetic resonance imaging (ceMRI). BACKGROUND: Conduction channels identified by voltage mapping are the critical isthmuses of most SMVT. We hypothesized that CC are formed by heterogeneous tissue (HT) within the scar that can be detected by ceMRI. METHODS: We studied 18 consecutive VTpatients (SMVT group) and 18 patients matched for age, sex, infarct location, and left ventricular ejection fraction (control group). We used ceMRI to quantify the infarct size and differentiate it into scar core and HT based on signal-intensity (SI) thresholds (>3 SD and 2 to 3 SD greater than remote normal myocardium, respectively). Consecutive left ventricle slices were analyzed to determine the presence of continuous corridors of HT (channels) in the scar. In the SMVT group, color-coded shells displaying ceMRI subendocardial SI were generated (3-dimensional SI mapping) and compared with endocardial voltage maps. RESULTS: No differences were observed between the 2 groups in myocardial, necrotic, or heterogeneous mass. The HT channels were more frequently observed in the SMVT group (88%) than in the control group (33%, p < 0.001). In the SMVT group, voltage mapping identified 26 CC in 17 of 18 patients. All CC corresponded, in location and orientation, to a similar channel detected by 3-dimensional SI mapping; 15 CC were related to 15 VT critical isthmuses. CONCLUSIONS: SMVT substrate can be identified by ceMRI scar heterogeneity analysis. This information could help identify patients at risk of VT and facilitate VT ablation.
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