Characteristic cardiac phenotypes are detected by cardiovascular magnetic resonance in patients with different clinical phenotypes and genotypes of mitochondrial myopathy
Mitochondrial myopathies (MM) are a heterogeneous group of inherited conditions resulting from a primary defect in the mitochondrial respiratory chain with consecutively impaired cellular energy metabolism. Small sized studies using mainly electrocardiography (ECG) and echocardiography have revealed...
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Published in | Journal of cardiovascular magnetic resonance Vol. 17; no. 1; p. 40 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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22.05.2015
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Abstract | Mitochondrial myopathies (MM) are a heterogeneous group of inherited conditions resulting from a primary defect in the mitochondrial respiratory chain with consecutively impaired cellular energy metabolism. Small sized studies using mainly electrocardiography (ECG) and echocardiography have revealed cardiac abnormalities ranging from conduction abnormalities and arrhythmias to hypertrophic or dilated cardiomyopathy in these patients. Recently, characteristic patterns of cardiac involvement were documented by cardiovascular magnetic resonance (CMR) in patients with chronic progressive external ophthalmoplegia (CPEO)/Kearns-Sayre syndrome (KSS) and with mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS). The present study aimed to characterize the prevalence and pattern of cardiac abnormalities and to test the additional diagnostic value of CMR in this patient population. The hypothesis that different neuromuscular MM syndromes present with different cardiac disease phenotypes was evaluated.
Sixty-four MM patients (50 ± 15 years, 44% male) and 25 matched controls (52 ± 14 years, 36% male) prospectively underwent cardiac evaluations including CMR (comprising cine- and late-gadolinium-enhancement (LGE) imaging). Based on the neuromuscular phenotype and genotype, the patients were grouped: (a) CPEO/KSS (N = 33); (b) MELAS/-like (N = 11); c) myoclonic epilepsy with ragged-red fibers (MERRF) (N = 3) and d) other non-specific MM forms (N = 17).
Among the 64 MM patients, 34 (53%) had at least one abnormal CMR finding: 18 (28%) demonstrated an impaired left ventricular ejection-fraction (LV-EF <60%), 14 (22%) had unexplained LV hypertrophy and 21 (33%) were LGE-positive. Compared to controls, MM patients showed significantly higher maximal wall thickness (10 ± 3 vs. 8 ± 2 mm, p = 0.005) and concentricity (LV mass to end-diastolic volume: 0.84 ± 0.27 vs. 0.67 ± 0.11, p < 0.0001) with frequent presence of non-ischemic LGE (30% vs. 0%, p = 0.001). CPEO/KSS showed a predominantly intramural pattern of LGE mostly confined to the basal LV inferolateral wall (8/10; 80%) in addition to a tendency toward concentric remodelling. MELAS/-like patients showed the highest frequency of cardiac disease (in 10/11 (91%)), a mostly concentric LV hypertrophy (6/9; 67%) with or without LV systolic dysfunction and a predominantly focal, patchy LGE equally distributed among LV segments (8/11; 73%). Patients with MERRF and non-specific MM had no particular findings. Pathological CMR findings indicating cardiac involvement were detected significantly more often than pathological ECG results or elevated cardiac serum biomarkers (34 (53%) vs. 18 (28%) vs. 21 (33%); p = 0.008).
Cardiac involvement is a frequent finding in MM patients - and particularly present in KSS/CPEO as well as MELAS/-like patients. Despite a high variability in clinical presentation, CPEO/KSS patients typically show an intramural pattern of LGE in the basal inferolateral wall whereas MELAS patients are characterized by overt concentric hypertrophy and a rather unique, focally accentuated and diffusely distributed LGE. |
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AbstractList | BACKGROUNDMitochondrial myopathies (MM) are a heterogeneous group of inherited conditions resulting from a primary defect in the mitochondrial respiratory chain with consecutively impaired cellular energy metabolism. Small sized studies using mainly electrocardiography (ECG) and echocardiography have revealed cardiac abnormalities ranging from conduction abnormalities and arrhythmias to hypertrophic or dilated cardiomyopathy in these patients. Recently, characteristic patterns of cardiac involvement were documented by cardiovascular magnetic resonance (CMR) in patients with chronic progressive external ophthalmoplegia (CPEO)/Kearns-Sayre syndrome (KSS) and with mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS). The present study aimed to characterize the prevalence and pattern of cardiac abnormalities and to test the additional diagnostic value of CMR in this patient population. The hypothesis that different neuromuscular MM syndromes present with different cardiac disease phenotypes was evaluated.METHODSSixty-four MM patients (50 ± 15 years, 44% male) and 25 matched controls (52 ± 14 years, 36% male) prospectively underwent cardiac evaluations including CMR (comprising cine- and late-gadolinium-enhancement (LGE) imaging). Based on the neuromuscular phenotype and genotype, the patients were grouped: (a) CPEO/KSS (N = 33); (b) MELAS/-like (N = 11); c) myoclonic epilepsy with ragged-red fibers (MERRF) (N = 3) and d) other non-specific MM forms (N = 17).RESULTSAmong the 64 MM patients, 34 (53%) had at least one abnormal CMR finding: 18 (28%) demonstrated an impaired left ventricular ejection-fraction (LV-EF <60%), 14 (22%) had unexplained LV hypertrophy and 21 (33%) were LGE-positive. Compared to controls, MM patients showed significantly higher maximal wall thickness (10 ± 3 vs. 8 ± 2 mm, p = 0.005) and concentricity (LV mass to end-diastolic volume: 0.84 ± 0.27 vs. 0.67 ± 0.11, p < 0.0001) with frequent presence of non-ischemic LGE (30% vs. 0%, p = 0.001). CPEO/KSS showed a predominantly intramural pattern of LGE mostly confined to the basal LV inferolateral wall (8/10; 80%) in addition to a tendency toward concentric remodelling. MELAS/-like patients showed the highest frequency of cardiac disease (in 10/11 (91%)), a mostly concentric LV hypertrophy (6/9; 67%) with or without LV systolic dysfunction and a predominantly focal, patchy LGE equally distributed among LV segments (8/11; 73%). Patients with MERRF and non-specific MM had no particular findings. Pathological CMR findings indicating cardiac involvement were detected significantly more often than pathological ECG results or elevated cardiac serum biomarkers (34 (53%) vs. 18 (28%) vs. 21 (33%); p = 0.008).CONCLUSIONCardiac involvement is a frequent finding in MM patients - and particularly present in KSS/CPEO as well as MELAS/-like patients. Despite a high variability in clinical presentation, CPEO/KSS patients typically show an intramural pattern of LGE in the basal inferolateral wall whereas MELAS patients are characterized by overt concentric hypertrophy and a rather unique, focally accentuated and diffusely distributed LGE. Mitochondrial myopathies (MM) are a heterogeneous group of inherited conditions resulting from a primary defect in the mitochondrial respiratory chain with consecutively impaired cellular energy metabolism. Small sized studies using mainly electrocardiography (ECG) and echocardiography have revealed cardiac abnormalities ranging from conduction abnormalities and arrhythmias to hypertrophic or dilated cardiomyopathy in these patients. Recently, characteristic patterns of cardiac involvement were documented by cardiovascular magnetic resonance (CMR) in patients with chronic progressive external ophthalmoplegia (CPEO)/Kearns-Sayre syndrome (KSS) and with mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS). The present study aimed to characterize the prevalence and pattern of cardiac abnormalities and to test the additional diagnostic value of CMR in this patient population. The hypothesis that different neuromuscular MM syndromes present with different cardiac disease phenotypes was evaluated. Sixty-four MM patients (50 [+ or -] 15 years, 44 % male) and 25 matched controls (52 [+ or -] 14 years, 36 % male) prospectively underwent cardiac evaluations including CMR (comprising cine- and late-gadolinium-enhancement (LGE) imaging). Based on the neuromuscular phenotype and genotype, the patients were grouped: a) CPEO/KSS (N = 33); b) MELAS/-like (N = 11); c) myoclonic epilepsy with ragged-red fibers (MERRF) (N = 3) and d) other non-specific MM forms (N = 17). Among the 64 MM patients, 34 (53 %) had at least one abnormal CMR finding: 18 (28 %) demonstrated an impaired left ventricular ejection-fraction (LV-EF <60 %), 14 (22 %) had unexplained LV hypertrophy and 21 (33 %) were LGE-positive. Compared to controls, MM patients showed significantly higher maximal wall thickness (10 [+ or -] 3 vs. 8 [+ or -] 2 mm, p = 0.005) and concentricity (LV mass to end-diastolic volume: 0.84 [+ or -] 0.27 vs. 0.67 [+ or -] 0.11, p < 0.0001) with frequent presence of non-ischemic LGE (30 % vs. 0 %, p = 0.001). CPEO/KSS showed a predominantly intramural pattern of LGE mostly confined to the basal LV inferolateral wall (8/10; 80 %) in addition to a tendency toward concentric remodelling. MELAS/-like patients showed the highest frequency of cardiac disease (in 10/11 (91 %)), a mostly concentric LV hypertrophy (6/9; 67 %) with or without LV systolic dysfunction and a predominantly focal, patchy LGE equally distributed among LV segments (8/11; 73 %). Patients with MERRF and non-specific MM had no particular findings. Pathological CMR findings indicating cardiac involvement were detected significantly more often than pathological ECG results or elevated cardiac serum biomarkers (34 (53 %) vs. 18 (28 %) vs. 21 (33 %); p = 0.008). Cardiac involvement is a frequent finding in MM patients - and particularly present in KSS/CPEO as well as MELAS/-like patients. Despite a high variability in clinical presentation, CPEO/KSS patients typically show an intramural pattern of LGE in the basal inferolateral wall whereas MELAS patients are characterized by overt concentric hypertrophy and a rather unique, focally accentuated and diffusely distributed LGE. Background Mitochondrial myopathies (MM) are a heterogeneous group of inherited conditions resulting from a primary defect in the mitochondrial respiratory chain with consecutively impaired cellular energy metabolism. Small sized studies using mainly electrocardiography (ECG) and echocardiography have revealed cardiac abnormalities ranging from conduction abnormalities and arrhythmias to hypertrophic or dilated cardiomyopathy in these patients. Recently, characteristic patterns of cardiac involvement were documented by cardiovascular magnetic resonance (CMR) in patients with chronic progressive external ophthalmoplegia (CPEO)/Kearns-Sayre syndrome (KSS) and with mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS). The present study aimed to characterize the prevalence and pattern of cardiac abnormalities and to test the additional diagnostic value of CMR in this patient population. The hypothesis that different neuromuscular MM syndromes present with different cardiac disease phenotypes was evaluated. Methods Sixty-four MM patients (50 [+ or -] 15 years, 44 % male) and 25 matched controls (52 [+ or -] 14 years, 36 % male) prospectively underwent cardiac evaluations including CMR (comprising cine- and late-gadolinium-enhancement (LGE) imaging). Based on the neuromuscular phenotype and genotype, the patients were grouped: a) CPEO/KSS (N = 33); b) MELAS/-like (N = 11); c) myoclonic epilepsy with ragged-red fibers (MERRF) (N = 3) and d) other non-specific MM forms (N = 17). Results Among the 64 MM patients, 34 (53 %) had at least one abnormal CMR finding: 18 (28 %) demonstrated an impaired left ventricular ejection-fraction (LV-EF <60 %), 14 (22 %) had unexplained LV hypertrophy and 21 (33 %) were LGE-positive. Compared to controls, MM patients showed significantly higher maximal wall thickness (10 [+ or -] 3 vs. 8 [+ or -] 2 mm, p = 0.005) and concentricity (LV mass to end-diastolic volume: 0.84 [+ or -] 0.27 vs. 0.67 [+ or -] 0.11, p < 0.0001) with frequent presence of non-ischemic LGE (30 % vs. 0 %, p = 0.001). CPEO/KSS showed a predominantly intramural pattern of LGE mostly confined to the basal LV inferolateral wall (8/10; 80 %) in addition to a tendency toward concentric remodelling. MELAS/-like patients showed the highest frequency of cardiac disease (in 10/11 (91 %)), a mostly concentric LV hypertrophy (6/9; 67 %) with or without LV systolic dysfunction and a predominantly focal, patchy LGE equally distributed among LV segments (8/11; 73 %). Patients with MERRF and non-specific MM had no particular findings. Pathological CMR findings indicating cardiac involvement were detected significantly more often than pathological ECG results or elevated cardiac serum biomarkers (34 (53 %) vs. 18 (28 %) vs. 21 (33 %); p = 0.008). Conclusion Cardiac involvement is a frequent finding in MM patients - and particularly present in KSS/CPEO as well as MELAS/-like patients. Despite a high variability in clinical presentation, CPEO/KSS patients typically show an intramural pattern of LGE in the basal inferolateral wall whereas MELAS patients are characterized by overt concentric hypertrophy and a rather unique, focally accentuated and diffusely distributed LGE. Keywords: Mitochondrial myopathy, Cardiomyopathy, Cardiovascular magnetic resonance, MELAS, CPEO Mitochondrial myopathies (MM) are a heterogeneous group of inherited conditions resulting from a primary defect in the mitochondrial respiratory chain with consecutively impaired cellular energy metabolism. Small sized studies using mainly electrocardiography (ECG) and echocardiography have revealed cardiac abnormalities ranging from conduction abnormalities and arrhythmias to hypertrophic or dilated cardiomyopathy in these patients. Recently, characteristic patterns of cardiac involvement were documented by cardiovascular magnetic resonance (CMR) in patients with chronic progressive external ophthalmoplegia (CPEO)/Kearns-Sayre syndrome (KSS) and with mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS). The present study aimed to characterize the prevalence and pattern of cardiac abnormalities and to test the additional diagnostic value of CMR in this patient population. The hypothesis that different neuromuscular MM syndromes present with different cardiac disease phenotypes was evaluated. Sixty-four MM patients (50 ± 15 years, 44% male) and 25 matched controls (52 ± 14 years, 36% male) prospectively underwent cardiac evaluations including CMR (comprising cine- and late-gadolinium-enhancement (LGE) imaging). Based on the neuromuscular phenotype and genotype, the patients were grouped: (a) CPEO/KSS (N = 33); (b) MELAS/-like (N = 11); c) myoclonic epilepsy with ragged-red fibers (MERRF) (N = 3) and d) other non-specific MM forms (N = 17). Among the 64 MM patients, 34 (53%) had at least one abnormal CMR finding: 18 (28%) demonstrated an impaired left ventricular ejection-fraction (LV-EF <60%), 14 (22%) had unexplained LV hypertrophy and 21 (33%) were LGE-positive. Compared to controls, MM patients showed significantly higher maximal wall thickness (10 ± 3 vs. 8 ± 2 mm, p = 0.005) and concentricity (LV mass to end-diastolic volume: 0.84 ± 0.27 vs. 0.67 ± 0.11, p < 0.0001) with frequent presence of non-ischemic LGE (30% vs. 0%, p = 0.001). CPEO/KSS showed a predominantly intramural pattern of LGE mostly confined to the basal LV inferolateral wall (8/10; 80%) in addition to a tendency toward concentric remodelling. MELAS/-like patients showed the highest frequency of cardiac disease (in 10/11 (91%)), a mostly concentric LV hypertrophy (6/9; 67%) with or without LV systolic dysfunction and a predominantly focal, patchy LGE equally distributed among LV segments (8/11; 73%). Patients with MERRF and non-specific MM had no particular findings. Pathological CMR findings indicating cardiac involvement were detected significantly more often than pathological ECG results or elevated cardiac serum biomarkers (34 (53%) vs. 18 (28%) vs. 21 (33%); p = 0.008). Cardiac involvement is a frequent finding in MM patients - and particularly present in KSS/CPEO as well as MELAS/-like patients. Despite a high variability in clinical presentation, CPEO/KSS patients typically show an intramural pattern of LGE in the basal inferolateral wall whereas MELAS patients are characterized by overt concentric hypertrophy and a rather unique, focally accentuated and diffusely distributed LGE. |
ArticleNumber | 40 |
Audience | Academic |
Author | Young, Peter Florian, Anca Sechtem, Udo Yilmaz, Ali Ludwig, Anna Waltenberger, Johannes Stubbe-Dräger, Bianca Boentert, Matthias Rösch, Sabine |
Author_xml | – sequence: 1 givenname: Anca surname: Florian fullname: Florian, Anca email: ancarezeda.florian@ukmuenster.de organization: Department of Cardiology and Angiology, University Hospital Münster, Albert-Schweitzer-Campus 1, building A1, 48149, Münster, Germany. ancarezeda.florian@ukmuenster.de – sequence: 2 givenname: Anna surname: Ludwig fullname: Ludwig, Anna email: anna.ludwig@rbk.de organization: Division of Cardiology, Robert-Bosch-Krankenhaus, Stuttgart, Germany. anna.ludwig@rbk.de – sequence: 3 givenname: Bianca surname: Stubbe-Dräger fullname: Stubbe-Dräger, Bianca email: bianca.draeger@ukmuenster.de organization: Department of Sleep Medicine and Neuromuscular Disorders, University Hospital Münster, Münster, Germany. bianca.draeger@ukmuenster.de – sequence: 4 givenname: Matthias surname: Boentert fullname: Boentert, Matthias email: matthias.boentert@ukmuenster.de organization: Department of Sleep Medicine and Neuromuscular Disorders, University Hospital Münster, Münster, Germany. matthias.boentert@ukmuenster.de – sequence: 5 givenname: Peter surname: Young fullname: Young, Peter email: peter.young@ukmuenster.de organization: Department of Sleep Medicine and Neuromuscular Disorders, University Hospital Münster, Münster, Germany. peter.young@ukmuenster.de – sequence: 6 givenname: Johannes surname: Waltenberger fullname: Waltenberger, Johannes email: johannes.waltenberger@ukmuenster.de organization: Department of Cardiology and Angiology, University Hospital Münster, Albert-Schweitzer-Campus 1, building A1, 48149, Münster, Germany. johannes.waltenberger@ukmuenster.de – sequence: 7 givenname: Sabine surname: Rösch fullname: Rösch, Sabine email: sabine.roesch@rbk.de organization: Division of Cardiology, Robert-Bosch-Krankenhaus, Stuttgart, Germany. sabine.roesch@rbk.de – sequence: 8 givenname: Udo surname: Sechtem fullname: Sechtem, Udo email: udo.sechtem@rbk.de organization: Division of Cardiology, Robert-Bosch-Krankenhaus, Stuttgart, Germany. udo.sechtem@rbk.de – sequence: 9 givenname: Ali surname: Yilmaz fullname: Yilmaz, Ali email: ali.yilmaz@ukmuenster.de organization: Department of Cardiology and Angiology, University Hospital Münster, Albert-Schweitzer-Campus 1, building A1, 48149, Münster, Germany. ali.yilmaz@ukmuenster.de |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26001801$$D View this record in MEDLINE/PubMed |
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References | Raman (10.1186/s12968-015-0145-x_bib23) 2011; 32 Bates (10.1186/s12968-015-0145-x_bib17) 2013; 14 Bruder (10.1186/s12968-015-0145-x_bib33) 2010; 56 Baik (10.1186/s12968-015-0145-x_bib8) 2010; 53 Yilmaz (10.1186/s12968-015-0145-x_bib18) 2012; 101 Cheng (10.1186/s12968-015-0145-x_bib21) 2009; 2 DiMauro (10.1186/s12968-015-0145-x_bib25) 2003; 348 Cooper (10.1186/s12968-015-0145-x_bib36) 2007; 50 Limongelli (10.1186/s12968-015-0145-x_bib4) 2010; 12 Pfeffer (10.1186/s12968-015-0145-x_bib1) 2013; 45 Finsterer (10.1186/s12968-015-0145-x_bib30) 2007; 119 O'Hanlon (10.1186/s12968-015-0145-x_bib35) 2010; 56 Myerson (10.1186/s12968-015-0145-x_bib31) 2001; 103 Wahbi (10.1186/s12968-015-0145-x_bib12) 2010; 74 Holmgren (10.1186/s12968-015-0145-x_bib2) 2003; 24 Partington (10.1186/s12968-015-0145-x_bib16) 2011; 123 Dutta (10.1186/s12968-015-0145-x_bib22) 2012; 110 Stalder (10.1186/s12968-015-0145-x_bib27) 2012; 5 Bates (10.1186/s12968-015-0145-x_bib6) 2012; 33 McMurray (10.1186/s12968-015-0145-x_bib19) 2012; 14 Elliott (10.1186/s12968-015-0145-x_bib32) 2014; 35 Nakanishi (10.1186/s12968-015-0145-x_bib14) 2007; 116 Weidemann (10.1186/s12968-015-0145-x_bib24) 2013; 126 Sato (10.1186/s12968-015-0145-x_bib11) 1994; 128 Dominic (10.1186/s12968-015-0145-x_bib26) 2014; 100 Pfeffer (10.1186/s12968-015-0145-x_bib10) 2012; 46 Majamaa-Voltti (10.1186/s12968-015-0145-x_bib9) 2002; 2 Klopstock (10.1186/s12968-015-0145-x_bib3) 1999; 53 Hannah-Shmouni (10.1186/s12968-015-0145-x_bib29) 2014; 12 Palecek (10.1186/s12968-015-0145-x_bib15) 2012; 53 Khouri (10.1186/s12968-015-0145-x_bib20) 2010; 3 Jose (10.1186/s12968-015-0145-x_bib13) 2011; 149 Scaglia (10.1186/s12968-015-0145-x_bib5) 2004; 114 Meyers (10.1186/s12968-015-0145-x_bib7) 2013; 40 Ismail (10.1186/s12968-015-0145-x_bib34) 2014; 100 Finsterer (10.1186/s12968-015-0145-x_bib28) 2009; 137 |
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Snippet | Mitochondrial myopathies (MM) are a heterogeneous group of inherited conditions resulting from a primary defect in the mitochondrial respiratory chain with... Background Mitochondrial myopathies (MM) are a heterogeneous group of inherited conditions resulting from a primary defect in the mitochondrial respiratory... BACKGROUNDMitochondrial myopathies (MM) are a heterogeneous group of inherited conditions resulting from a primary defect in the mitochondrial respiratory... |
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SubjectTerms | Adult Aged Analysis Arrhythmia Cardiac patients Cardiomyopathies - epidemiology Cardiomyopathies - genetics Cardiomyopathies - pathology Cardiomyopathies - physiopathology Care and treatment Case-Control Studies Diagnosis Electrocardiogram Electrocardiography Epilepsy Female Genetic aspects Genetic Predisposition to Disease Germany - epidemiology Humans Hypertrophy, Left Ventricular - genetics Hypertrophy, Left Ventricular - pathology Hypertrophy, Left Ventricular - physiopathology Kearns-Sayre Syndrome - genetics Kearns-Sayre Syndrome - pathology Magnetic Resonance Imaging Male MELAS Syndrome - genetics MELAS Syndrome - pathology MERRF Syndrome - genetics MERRF Syndrome - pathology Middle Aged Mitochondrial Myopathies - epidemiology Mitochondrial Myopathies - genetics Mitochondrial Myopathies - pathology Mitochondrial Myopathies - physiopathology Myocardium - pathology Ophthalmoplegia, Chronic Progressive External - genetics Ophthalmoplegia, Chronic Progressive External - pathology Phenotype Physiological aspects Predictive Value of Tests Prevalence Prospective Studies Stroke Volume Ventricular Function, Left Ventricular Remodeling |
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Title | Characteristic cardiac phenotypes are detected by cardiovascular magnetic resonance in patients with different clinical phenotypes and genotypes of mitochondrial myopathy |
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