BACKGROUND: Ischemic cardiomyopathy (ICM) can provide the substrate for ventricular tachycardia (VT). OBJECTIVE: To map noninvasively with high resolution the electrophysiologic (EP) scar substrate, identify its relationship to reentry circuits during VT, and stratify VT risk in ICM patients. METHODS: Noninvasive high-resolution epicardial mapping with electrocardiographic imaging (ECGI) was performed in 32 ICM patients (17 with clinical VT, 15 without VT). Abnormal scar EP substrate was determined based on electrogram (EGM) amplitude (as percentage of maximal peak-to-peak voltage over the entire ventricular epicardium; total scar [TS] < 30%; dense scar [DS] < 15%), fractionation, and presence of late potentials (LPs). Scar burden was defined as the ratio of the scar size to the total epicardial surface area. The VT activation pattern was mapped and correlated with the EP substrate to identify components of the reentry circuit. RESULTS: Patients with VT had higher scar burden (TS: 51.0 ± 9.3% vs 36.5 ± 5.4%, P < 0.05; DS: 29.5 ± 7.3% vs 16.8 ± 6.8%, P < 0.05) with lower normalized unipolar EGM voltage (TS: 0.107 ± 0.027 vs 0.153 ± 0.031, P < 0.05; DS: 0.073 ± 0.023 vs 0.098 ± 0.026, P < 0.05), greater prevalence of fractionated EGMs (TS: 44.1 ± 10.6% vs 26.8 ± 6.3%, P < 0.05; DS: 50.8 ± 10.8% vs 30.9 ± 7.0%, P < 0.05), and LPs (TS: 26.8 ± 10.7% vs 15.8 ± 5.3, P < 0.05). VTs were mapped in eight patients; the reentry circuits were closely related to the EP substrate. CONCLUSIONS: ECGI noninvasively identified scar EP substrate that underlies abnormal conduction in ICM patients. It identified regions within the scar that aligned with critical elements of the reentry circuit during VT. ECGI can potentially be used for VT risk stratification in ICM patients.
BACKGROUND:Ischemic cardiomyopathy (ICM) can provide the substrate for ventricular tachycardia (VT). OBJECTIVE: To map noninvasively with high resolution the electrophysiologic (EP) scar substrate, identify its relationship to reentry circuits during VT, and stratify VT risk in ICM patients. METHODS: Noninvasive high-resolution epicardial mapping with electrocardiographic imaging (ECGI) was performed in 32 ICM patients (17 with clinical VT, 15 without VT). Abnormal scar EP substrate was determined based on electrogram (EGM) amplitude (as percentage of maximal peak-to-peak voltage over the entire ventricular epicardium; total scar [TS] < 30%; dense scar [DS] < 15%), fractionation, and presence of late potentials (LPs). Scar burden was defined as the ratio of the scar size to the total epicardial surface area. The VT activation pattern was mapped and correlated with the EP substrate to identify components of the reentry circuit. RESULTS:Patients with VT had higher scar burden (TS: 51.0 ± 9.3% vs 36.5 ± 5.4%, P < 0.05; DS: 29.5 ± 7.3% vs 16.8 ± 6.8%, P < 0.05) with lower normalized unipolar EGM voltage (TS: 0.107 ± 0.027 vs 0.153 ± 0.031, P < 0.05; DS: 0.073 ± 0.023 vs 0.098 ± 0.026, P < 0.05), greater prevalence of fractionated EGMs (TS: 44.1 ± 10.6% vs 26.8 ± 6.3%, P < 0.05; DS: 50.8 ± 10.8% vs 30.9 ± 7.0%, P < 0.05), and LPs (TS: 26.8 ± 10.7% vs 15.8 ± 5.3, P < 0.05). VTs were mapped in eight patients; the reentry circuits were closely related to the EP substrate. CONCLUSIONS: ECGI noninvasively identified scar EP substrate that underlies abnormal conduction in ICM patients. It identified regions within the scar that aligned with critical elements of the reentry circuit during VT. ECGI can potentially be used for VT risk stratification in ICM patients.
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