Julia Anna Lurz1, Christian Luecke2, David Lang3, Christian Besler3, Karl-Philipp Rommel3, Karin Klingel4, Reinhard Kandolf4, Volker Adams3, Katharina Schöne1, Gerhard Hindricks1, Gerhard Schuler3, Axel Linke3, Holger Thiele5, Matthias Gutberlet2, Philipp Lurz6. 1. Department of Electrophysiology, University of Leipzig-Heart Center, Leipzig, Germany. 2. Department of Diagnostic and Interventional Radiology, University of Leipzig-Heart Center, Leipzig, Germany. 3. Department of Internal Medicine/Cardiology, University of Leipzig-Heart Center, Leipzig, Germany. 4. Department of Molecular Pathology, University Hospital Tuebingen, Tuebingen, Germany. 5. University Heart Center Luebeck, University of Schleswig-Holstein, Medical Clinic II (Cardiology, Angiology, Intensive Care Medicine), Luebeck, Germany. 6. Department of Internal Medicine/Cardiology, University of Leipzig-Heart Center, Leipzig, Germany. Electronic address: philipp.lurz@gmx.de.
Abstract
OBJECTIVES: The aim of the present study was to evaluate whether extracellular volume fraction (ECV) can reliably inform on the extent of diffuse fibrosis in the simultaneous presence of myocardial inflammation, which has not been verified to date. BACKGROUND: Diffuse myocardial fibrosis is associated with unfavorable outcome in patients with cardiomyopathy, and is of prognostic relevance. Assessment of ECV bears promise for being a noninvasive surrogate parameter, but it may be altered by other pathologies. METHODS: In this prospective study, 107 consecutive patients with clinical suspicion of inflammatory cardiomyopathy were included. All patients underwent left ventricular (LV) endomyocardial biopsy (EMB) and cardiac magnetic resonance imaging on a 1.5-T scanner. T1 mapping was obtained with the modified Look-Locker inversion recovery sequence, and ECV was calculated. RESULTS: Myocardial inflammation was present in 66 patients. Patients with and without inflammation were of similar age and had comparable LV ejection fraction (37 ± 17% vs. 36 ± 18%; p = 0.9) and symptom duration (median 14 days [interquartile range: 5 to 36 days] vs. median 14 days [interquartile range: 7 to 30 days]; p = 0.73). Although LV collagen volume percentage was comparable between groups (inflammation 12.3 ± 17.8% vs. noninflammation 11.4 ± 7.9%; p = 0.577), ECV was significantly higher in patients with inflammation (0.37 ± 0.06%) than in those without inflammation (0.33 ± 0.08%; p = 0.02). Importantly, ECV adequately estimated the degree of LV fibrosis percentage only in patients without inflammation (r = 0.72; p < 0.0001) and not in those with inflammation (r = 0.24; p = 0.06). CONCLUSIONS: These findings prove the theoretical concept of ECV as an estimate for diffuse myocardial fibrosis, but only in the absence of significant myocardial inflammation. Assuming that various degrees of myocardial inflammation and fibrosis coexist in such a scenario, the measured ECV will reflect a sum of these different pathologies but will not inform solely on the extent of diffuse fibrosis.
OBJECTIVES: The aim of the present study was to evaluate whether extracellular volume fraction (ECV) can reliably inform on the extent of diffuse fibrosis in the simultaneous presence of myocardial inflammation, which has not been verified to date. BACKGROUND: Diffuse myocardial fibrosis is associated with unfavorable outcome in patients with cardiomyopathy, and is of prognostic relevance. Assessment of ECV bears promise for being a noninvasive surrogate parameter, but it may be altered by other pathologies. METHODS: In this prospective study, 107 consecutive patients with clinical suspicion of inflammatory cardiomyopathy were included. All patients underwent left ventricular (LV) endomyocardial biopsy (EMB) and cardiac magnetic resonance imaging on a 1.5-T scanner. T1 mapping was obtained with the modified Look-Locker inversion recovery sequence, and ECV was calculated. RESULTS:Myocardial inflammation was present in 66 patients. Patients with and without inflammation were of similar age and had comparable LV ejection fraction (37 ± 17% vs. 36 ± 18%; p = 0.9) and symptom duration (median 14 days [interquartile range: 5 to 36 days] vs. median 14 days [interquartile range: 7 to 30 days]; p = 0.73). Although LV collagen volume percentage was comparable between groups (inflammation 12.3 ± 17.8% vs. noninflammation 11.4 ± 7.9%; p = 0.577), ECV was significantly higher in patients with inflammation (0.37 ± 0.06%) than in those without inflammation (0.33 ± 0.08%; p = 0.02). Importantly, ECV adequately estimated the degree of LV fibrosis percentage only in patients without inflammation (r = 0.72; p < 0.0001) and not in those with inflammation (r = 0.24; p = 0.06). CONCLUSIONS: These findings prove the theoretical concept of ECV as an estimate for diffuse myocardial fibrosis, but only in the absence of significant myocardial inflammation. Assuming that various degrees of myocardial inflammation and fibrosis coexist in such a scenario, the measured ECV will reflect a sum of these different pathologies but will not inform solely on the extent of diffuse fibrosis.
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