Susumu Tao1, Michael A Guttman2, Sarah Fink2, Hassan Elahi3, Kaustubha D Patil2, Hiroshi Ashikaga4, Aravindan D Kolandaivelu2, Ronald D Berger2, Marc K Halushka5, Ehud J Schmidt2, Daniel A Herzka3, Henry R Halperin6. 1. Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland. Electronic address: stao5.1978@gmail.com. 2. Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland. 3. Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland. 4. Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland; Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland. 5. Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland. 6. Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland; Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland; Department of Radiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Abstract
OBJECTIVES: This study examined radiofrequency catheter ablation (RFCA) lesions within and around scar by cardiac magnetic resonance (CMR) imaging and histology. BACKGROUND: Substrate modification by RFCA is the cornerstone therapy for ventricular arrhythmias. RFCA in scarred myocardium, however, is not well understood. METHODS: We performed electroanatomic mapping and RFCA in the left ventricles of 8 swine with myocardial infarction. Non-contrast-enhanced T1-weighted (T1w) and contrast-enhanced CMR after RFCA were compared with gross pathology and histology. RESULTS: Of 59 lesions, 17 were in normal myocardium (voltage >1.5 mV), 21 in border zone (0.5 to 1.5 mV), and 21 in scar (<0.5 mV). All RFCA lesions were enhanced in T1w CMR, whereas scar was hypointense, allowing discrimination among normal myocardium, scar, and RFCA lesions. With contrast-enhancement, lesions and scar were similarly enhanced and not distinguishable. Lesion width and depth in T1w CMR correlated with necrosis in pathology (both; r2 = 0.94, p < 0.001). CMR lesion volume was significantly different in normal myocardium, border zone, and scar (median: 397 [interquartile range (IQR): 301 to 474] mm3, 121 [IQR: 87 to 201] mm3, 66 [IQR: 33 to 123] mm3, respectively). RFCA force-time integral, impedance, and voltage changes did not correlate with lesion volume in border zone or scar. Histology showed that ablation necrosis extended into fibrotic tissue in 26 lesions and beyond in 14 lesions. In 7 lesions, necrosis expansion was blocked and redirected by fat. CONCLUSIONS: T1w CMR can selectively enhance necrotic tissue in and around scar and may allow determination of the completeness of ablation intra- and post-procedure. Lesion formation in scar is affected by tissue characteristics, with fibrosis and fat acting as thermal insulators.
OBJECTIVES: This study examined radiofrequency catheter ablation (RFCA) lesions within and around scar by cardiac magnetic resonance (CMR) imaging and histology. BACKGROUND: Substrate modification by RFCA is the cornerstone therapy for ventricular arrhythmias. RFCA in scarred myocardium, however, is not well understood. METHODS: We performed electroanatomic mapping and RFCA in the left ventricles of 8 swine with myocardial infarction. Non-contrast-enhanced T1-weighted (T1w) and contrast-enhanced CMR after RFCA were compared with gross pathology and histology. RESULTS: Of 59 lesions, 17 were in normal myocardium (voltage >1.5 mV), 21 in border zone (0.5 to 1.5 mV), and 21 in scar (<0.5 mV). All RFCA lesions were enhanced in T1w CMR, whereas scar was hypointense, allowing discrimination among normal myocardium, scar, and RFCA lesions. With contrast-enhancement, lesions and scar were similarly enhanced and not distinguishable. Lesion width and depth in T1w CMR correlated with necrosis in pathology (both; r2 = 0.94, p < 0.001). CMR lesion volume was significantly different in normal myocardium, border zone, and scar (median: 397 [interquartile range (IQR): 301 to 474] mm3, 121 [IQR: 87 to 201] mm3, 66 [IQR: 33 to 123] mm3, respectively). RFCA force-time integral, impedance, and voltage changes did not correlate with lesion volume in border zone or scar. Histology showed that ablation necrosis extended into fibrotic tissue in 26 lesions and beyond in 14 lesions. In 7 lesions, necrosis expansion was blocked and redirected by fat. CONCLUSIONS: T1w CMR can selectively enhance necrotic tissue in and around scar and may allow determination of the completeness of ablation intra- and post-procedure. Lesion formation in scar is affected by tissue characteristics, with fibrosis and fat acting as thermal insulators.
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