FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2004764583> ?p ?o ?g. }

• W2004764583 endingPage "264" @default.
• W2004764583 startingPage "258" @default.
• W2004764583 abstract "We evaluated the clinical utility of cardiac magnetic resonance imaging (CMR) combined with a novel high-sensitivity troponin T assay (hs-cTnT) in the diagnosis of inflammatory cardiomyopathy. CMR, measurement of hs-cTnT, and endomyocardial biopsy were performed in 42 patients with dilated cardiomyopathy and a short-term history of heart failure (median 2 months, interquartile range 1 to 3.5). The patients were followed up for 25 ± 9 months for events. Endomyocardial biopsy revealed myocarditis in 15 subjects (36%). The sensitivity, specificity, and diagnostic accuracy of the individual CMR tissue parameters for myocardial inflammation was 40%, 96%, and 76% for early gadolinium enhancement, 87%, 44%, and 60% for late gadolinium enhancement, 47%, 89%, and 74% for pericardial effusion, and 67%, 85%, and 79% for any 2 of the criteria simultaneously, respectively. An assessment of myocardial edema on T2-weighted imaging and/or hs-cTnT assay were inadequate for the diagnosis. The extent of late gadolinium enhancement and increased hs-cTnT concentration were significant predictors of a composite end point of cardiac death, urgent heart transplantation, and hospitalization for worsening heart failure (hazard ratio 1.1, 95% confidence interval 1.0 to 1.2, per percentage of left ventricular mass; and hazard ratio 2.2, 95% confidence interval 1.4 to 3.5, per ln ng/L; p = 0.008 and p = 0.001, respectively). In conclusion, the results of the present study have demonstrated a modest performance for CMR and a limited use of the hs-cTnT assay in the diagnosis of inflammatory cardiomyopathy. Nonetheless, in these patients, CMR and/or hs-cTnT assessment seems to be useful for the prediction of the clinical outcome. We evaluated the clinical utility of cardiac magnetic resonance imaging (CMR) combined with a novel high-sensitivity troponin T assay (hs-cTnT) in the diagnosis of inflammatory cardiomyopathy. CMR, measurement of hs-cTnT, and endomyocardial biopsy were performed in 42 patients with dilated cardiomyopathy and a short-term history of heart failure (median 2 months, interquartile range 1 to 3.5). The patients were followed up for 25 ± 9 months for events. Endomyocardial biopsy revealed myocarditis in 15 subjects (36%). The sensitivity, specificity, and diagnostic accuracy of the individual CMR tissue parameters for myocardial inflammation was 40%, 96%, and 76% for early gadolinium enhancement, 87%, 44%, and 60% for late gadolinium enhancement, 47%, 89%, and 74% for pericardial effusion, and 67%, 85%, and 79% for any 2 of the criteria simultaneously, respectively. An assessment of myocardial edema on T2-weighted imaging and/or hs-cTnT assay were inadequate for the diagnosis. The extent of late gadolinium enhancement and increased hs-cTnT concentration were significant predictors of a composite end point of cardiac death, urgent heart transplantation, and hospitalization for worsening heart failure (hazard ratio 1.1, 95% confidence interval 1.0 to 1.2, per percentage of left ventricular mass; and hazard ratio 2.2, 95% confidence interval 1.4 to 3.5, per ln ng/L; p = 0.008 and p = 0.001, respectively). In conclusion, the results of the present study have demonstrated a modest performance for CMR and a limited use of the hs-cTnT assay in the diagnosis of inflammatory cardiomyopathy. Nonetheless, in these patients, CMR and/or hs-cTnT assessment seems to be useful for the prediction of the clinical outcome. Clinical experience with the use of cardiac magnetic resonance imaging (CMR) for noninvasive detection of myocardial inflammation in those presenting with unexplained recent-onset dilated cardiomyopathy (DC) is currently lacking. Some of the CMR features typically found in acute myocarditis are less likely to be expected at a later stage of myocardial inflammation, such as in the case of inflammatory DC.1Friedrich M.G. Sechtem U. Schulz-Menger J. Holmvang G. Alakija P. Cooper L.T. White J.A. Abdel-Aty H. Gutberlet M. Prasad S. Aletras A. Laissy J.P. Paterson I. Filipchuk N.G. Kumar A. Pauschinger M. Liu P. Cardiovascular magnetic resonance in myocarditis: a JACC White Paper.J Am Coll Cardiol. 2009; 53: 1475-1487Abstract Full Text Full Text PDF PubMed Scopus (1671) Google Scholar, 2Friedrich M.G. Strohm O. Schulz-Menger J. Marciniak H. Luft F.C. Dietz R. Contrast media-enhanced magnetic resonance imaging visualizes myocardial changes in the course of viral myocarditis.Circulation. 1998; 97: 1802-1809Crossref PubMed Scopus (484) Google Scholar, 3Zagrosek A. Abdel-Aty H. Boye P. Wassmuth R. Messroghli D. Utz W. Rudolph A. Bohl S. Dietz R. Schulz-Menger J. Cardiac magnetic resonance monitors reversible and irreversible myocardial injury in myocarditis.JACC Cardiovasc Imaging. 2009; 2: 131-138Abstract Full Text Full Text PDF PubMed Scopus (134) Google Scholar Moreover, some CMR findings in inflammatory DC might be attributable, not only to myocardial inflammation, but also to pathologic processes related to the heart failure itself.4Alter P. Rupp H. Adams P. Stoll F. Figiel J.H. Klose K.J. Rominger M.B. Maisch B. Occurrence of late gadolinium enhancement is associated with increased left ventricular wall stress and mass in patients with non-ischaemic dilated cardiomyopathy.Eur J Heart Fail. 2011; 13: 937-944Crossref PubMed Scopus (47) Google Scholar, 5Assomull R.G. Prasad S.K. Lyne J. Smith G. Burman E.D. Khan M. Sheppard M.N. Poole-Wilson P.A. Pennell D.J. Cardiovascular magnetic resonance, fibrosis, and prognosis in dilated cardiomyopathy.J Am Coll Cardiol. 2006; 48: 1977-1985Abstract Full Text Full Text PDF PubMed Scopus (882) Google Scholar The high-sensitivity cardiac troponin T (hs-cTnT) assay permits detection of ongoing myocyte necrosis in quantities much lower than the resolution capability of CMR for myocardial damage. We hypothesized that the combined strategy of CMR and hs-cTnT assessment could provide a sensitive and clinically applicable noninvasive diagnosis of inflammatory DC. In addition, we sought to investigate whether the hs-cTnT and CMR findings could be useful in the estimation of prognosis in patients with recent-onset DC.MethodsFrom November 2008 to September 2010, 42 consecutive patients with DC and a history of heart failure symptoms for <6 months were enrolled in the present study. DC was defined by the presence of left ventricular dilation (left ventricular end-diastolic diameter >33 mm/m in men and >32 mm/m in women) and left ventricular systolic dysfunction (left ventricular ejection fraction <45%) in the absence of coronary artery disease (ruled out by cardiac catheterization), severe systemic arterial hypertension, and primary valve disease.6Elliott P. Andersson B. Arbustini E. Bilinska Z. Cecchi F. Charron P. Dubourg O. Kuhl U. Maisch B. McKenna W.J. Monserrat L. Pankuweit S. Rapezzi C. Seferovic P. Tavazzi L. Keren A. Classification of the cardiomyopathies: a position statement from the European Society Of Cardiology Working Group on Myocardial and Pericardial Diseases.Eur Heart J. 2008; 29: 270-276Crossref PubMed Scopus (1898) Google Scholar, 7Lang R.M. Bierig M. Devereux R.B. Flachskampf F.A. Foster E. Pellikka P.A. Picard M.H. Roman M.J. Seward J. Shanewise J. Solomon S. Spencer K.T. St John Sutton M. Stewart W. Recommendations for chamber quantification.Eur J Echocardiogr. 2006; 7: 79-108Crossref PubMed Scopus (2853) Google Scholar Subjects with a history of drug abuse or excessive alcohol consumption and/or presenting with sustained supraventricular tachyarrhythmias were excluded. At baseline, all patients underwent a thorough cardiologic examination, assessment of hs-cTnT and B-type natriuretic peptide, CMR, and endomyocardial biopsy (EMB). The institutional review board approved the present study, and all patients provided written informed consent. All patients were treated according to the current guidelines for the management of heart failure, and they were followed up in a dedicated heart failure clinic. The heart failure medication was usually initiated at a referring community hospital before recruitment to the study.All biopsies were performed within 2 days after the CMR examination. The procedure and analyses of the EMB specimens were performed using methods previously described in detail.8Kubanek M. Sramko M. Berenova D. Hulinska D. Hrbackova H. Maluskova J. Lodererova A. Malek I. Kautzner J. Detection of Borrelia burgdorferi sensu lato in endomyocardial biopsy specimens in individuals with recent-onset dilated cardiomyopathy.Eur J Heart Fail. 2012; 14: 588-596Crossref PubMed Scopus (39) Google Scholar In brief, EMB was performed by way of the internal jugular vein using a flexible bioptome (7F diameter, Cordis Europe, Waterloo, Belgium) under fluoroscopic guidance. Eight to ten samples were obtained from the right ventricular side of the interventricular septum. Histopathologic analysis was based on the Dallas criteria.9Aretz H.T. Billingham M.E. Edwards W.D. Factor S.M. Fallon J.T. Fenoglio Jr., J.J. Olsen E.G. Schoen F.J. Myocarditis: a histopathologic definition and classification.Am J Cardiovasc Pathol. 1987; 1: 3-14PubMed Google Scholar Immunohistochemistry for the characterization of inflammatory cell infiltrates was performed on paraffin sections treated with monoclonal antibodies (anti-CD3 and anti-CD68, Dako, Glostrup, Denmark). The immunohistochemical criteria for myocardial inflammation were determined by the detection of ≥14 infiltrative leukocytes/mm2 (CD3+ T lymphocytes and CD68+ macrophages) and/or ≥7 CD3+ T lymphocytes/mm2.10Kuhl U. Noutsias M. Seeberg B. Schultheiss H.P. Immunohistological evidence for a chronic intramyocardial inflammatory process in dilated cardiomyopathy.Heart. 1996; 75: 295-300Crossref PubMed Scopus (193) Google Scholar Quantitative polymerase chain reaction was performed for the detection of common cardiotropic viruses in the EMB specimens, as previously described.8Kubanek M. Sramko M. Berenova D. Hulinska D. Hrbackova H. Maluskova J. Lodererova A. Malek I. Kautzner J. Detection of Borrelia burgdorferi sensu lato in endomyocardial biopsy specimens in individuals with recent-onset dilated cardiomyopathy.Eur J Heart Fail. 2012; 14: 588-596Crossref PubMed Scopus (39) Google Scholar The extent of interstitial and replacement fibrosis was assessed visually by morphometric study according to Loud and Anversa.11Loud A.V. Anversa P. Morphometric analysis of biologic processes.Lab Invest. 1984; 50: 250-261PubMed Google ScholarPeripheral venous blood samples were drawn in the morning before EMB. Detection of hs-cTnT was performed using an electrochemiluminescent immunoassay (T hs STAT, Cobas e411, Roche Diagnostics GmbH, Mannheim, Germany) according to the manufacturer’s recommendations. The parameters of the assay were as follows: the lower limit of detection at 5 ng/L, measuring range 3 to 10,000 ng/L, 10% intra-assay coefficient of variation at 13 ng/L, intra-assay coefficient of variation <3.2% and interassay coefficient of variation <6.2% at a concentration of 12.6 ng/L. The upper reference limit was set at 13.5 ng/L. The B-type natriuretic peptide plasma levels were measured using chemiluminescent immunoanalysis (Architect B-type natriuretic peptide, Abbott Diagnostics, Abbott Park, Illinois). The parameters of the assay were as follows: lower limit of detection 10 ng/L, intra-assay coefficient of variation <3.8%, and interassay coefficient of variation <5.3%.The CMR studies were performed using a clinical 1.5 Tesla MR scanner (Avanto, Siemens Medical Solutions, Erlangen, Germany). Cine images were obtained by a TrueFISP sequence (repetition time/echo time 65/1.2 ms, flip angle 70°, slice thickness 8 mm, without gaps) in short-axis and orthogonal long-axis planes. A breath-hold T2-weighted dark blood sequence (repetition time/echo time 2 RR/58 ms, inversion time 140 ms, slice thickness 8 mm, gap 2 mm) was acquired in short-axis slices. Images for assessment of early enhancement were acquired in basal, mid-papillary, and apical short-axis slices using a T1-weighted turboFLASH sequence (repetition time/echo time 170/1.05 ms, flip angle 12°, inversion time 100 ms, slice thickness 10 mm) before and at 40 to 70 seconds after intravenous bolus injection of 0.2 mmol/kg of gadobutrol (Gadovist, Bayer Schering, Berlin, Germany). Images for late gadolinium enhancement (LGE) were acquired 10 to 15 minutes after the administration of contrast in the short-axis and orthogonal long-axis planes using phase-sensitive inversion-recovery sequences (repetition time/echo time 690 to 850/3.2 ms, inversion time adjusted to null normal myocardium, slice thickness 8 mm, gap 0.8 mm, in-plane resolution 1.7 × 1.7 mm).The quality of the CMR images was good to acceptable in all patients. No sequence was excluded from the present analysis. Ventricular volumes, mass, and ejection fractions were determined from cine images using Segment, version 1.8 (available at: http://segment.heiberg.se).12Heiberg E. Wigstrom L. Carlsson M. Bolger A.F. Karlsson M. Time resolved three-dimensional automated segmentation of the left ventricle. Proceedings of IEEE: Computers in Cardiology. IEEE Conference Publications, Lyon, France2005Google Scholar The presence and distribution of LGE was independently determined by 2 expert radiologists (D.K. and J.W.) in a blinded fashion. The agreement between the 2 radiologists was a kappa of 0.75 (95% confidence interval 0.53 to 0.97, p = 0.001). To quantify the extent of LGE on the short-axis stacks, a semiautomated thresholding technique implemented in Matlab (Mathworks, Natick, Massachusetts) was performed by applying 2 SD above the mean signal intensity of a selected region in the normal myocardium.13Kim R.J. Fieno D.S. Parrish T.B. Harris K. Chen E.L. Simonetti O. Bundy J. Finn J.P. Klocke F.J. Judd R.M. Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function.Circulation. 1999; 100: 1992-2002Crossref PubMed Scopus (2080) Google Scholar A quantitative assessment of myocardial edema and early enhancement followed previously described methods.1Friedrich M.G. Sechtem U. Schulz-Menger J. Holmvang G. Alakija P. Cooper L.T. White J.A. Abdel-Aty H. Gutberlet M. Prasad S. Aletras A. Laissy J.P. Paterson I. Filipchuk N.G. Kumar A. Pauschinger M. Liu P. Cardiovascular magnetic resonance in myocarditis: a JACC White Paper.J Am Coll Cardiol. 2009; 53: 1475-1487Abstract Full Text Full Text PDF PubMed Scopus (1671) Google Scholar An edema ratio of ≥1.9 and early enhancement of ≥45% were regarded as abnormal findings.1Friedrich M.G. Sechtem U. Schulz-Menger J. Holmvang G. Alakija P. Cooper L.T. White J.A. Abdel-Aty H. Gutberlet M. Prasad S. Aletras A. Laissy J.P. Paterson I. Filipchuk N.G. Kumar A. Pauschinger M. Liu P. Cardiovascular magnetic resonance in myocarditis: a JACC White Paper.J Am Coll Cardiol. 2009; 53: 1475-1487Abstract Full Text Full Text PDF PubMed Scopus (1671) Google Scholar, 14Laissy J.P. Messin B. Varenne O. Iung B. Karila-Cohen D. Schouman-Claeys E. Steg P.G. MRI of acute myocarditis: a comprehensive approach based on various imaging sequences.Chest. 2002; 122: 1638-1648Crossref PubMed Scopus (193) Google Scholar The myocardial edema ratio, early enhancement, and quantity of LGE were analyzed by a single observer (M.S.), who was unaware of the results of EMB. The corresponding intraobserver relative variability was 7 ± 7%, 10 ± 7%, and 5 ± 3%, respectively. The amount of pericardial effusion was quantified by summation of the disks on the short-axis cine images. A total effusion volume of >50 ml was regarded as a pathologic finding.15Bogaert J. Francone M. Cardiovascular magnetic resonance in pericardial diseases.J Cardiovasc Magn Reson. 2009; 11: 14Crossref PubMed Scopus (146) Google Scholar Representative images of the CMR techniques used are displayed in Figure 1.Continuous variables were compared using the t tests and are expressed as the mean ± SD or median and interquartile range. Owing to the right-skewed distribution, the biomarker concentrations were transformed to natural logarithm before analysis. Categorical variables are expressed as frequencies and were compared using the chi-square or Fisher’s exact test. The EMB results were used as a reference standard to calculate the sensitivity and specificity of CMR and hs-cTnT for detection of myocardial inflammation. A stepwise logistic regression analysis was performed to identify the variables predictive of inflammatory DC and the variables associated with LGE. The log-rank test and Cox’s proportional hazard models were performed to analyze the associations with the composite end point, using the time to the first event. All statistical analyses were conducted with SPSS, version 16.0 (SPSS, Chicago, Illinois). p Values <0.05 were considered statistically significant.ResultsThe baseline clinical, biochemical, and EMB findings are summarized in Table 1. All 42 patients presented with recent-onset congestive heart failure. At recruitment, none of the patients showed a clinical picture suggestive of acute myocarditis. Inflammatory DC was found by immuhistochemical analysis of the EMB specimens in 15 patients (36%). In these patients, the mean count of CD3+ T lymphocytes was 12 ± 5/mm2. The classic Dallas (histologic) criteria were met in only 3 patients presenting with borderline myocarditis. The remaining 27 patients (64%) were diagnosed with idiopathic DC. The most common genome found in the EMB specimens was parvovirus B19 (n = 25), followed by human cytomegalovirus (n = 4) and enterovirus (n = 1).Table 1Baseline clinical, biochemical, and biopsy findingsVariableIdiopathic DC (n = 27)Inflammatory DC (n = 15)p ValueAge (yrs)45 ± 1242 ± 80.29Men19 (70%)11 (73%)0.81Duration of heart failure (mo)2 (1–3)2 (1–3)0.58Prodromes of viral disease5 (19%)6 (40%)0.13New York Heart Association class2.4 ± 0.72.8 ± 0.90.23Diabetes mellitus1 (4%)1 (7%)0.66Systemic hypertension2 (7%)1 (7%)0.93Glomerular filtration rate (ml/min/1.73 m2)81 ± 2379 ± 150.69Angiotensin-converting enzyme inhibitors24 (89%)14 (93%)0.64Angiotensin receptor blockers4 (15%)1 (7%)0.63β Blockers5 (19%)4 (27%)0.54Loop diuretics24 (89%)14 (93%)0.66Spironolactone20 (74%)13 (87%)0.34Normal sinus rhythm26 (96%)15 (100%)0.45Left bundle branch block3 (11%)2 (13%)0.83High-sensitivity troponin T level (ng/L)11 (5–32)17 (5–30)0.55High-sensitivity troponin T >13.5 ng/L12 (44%)10 (67%)0.20Conventional troponin I >0.03 μg/L7 (26%)6 (40%)0.34Maximum conventional troponin I (μg/L)1.273.61—C-reactive protein (mg/L)2 (1–7)3 (2–9)0.36B-type natriuretic peptide (ng/L)963 (240–1,508)647 (279–1,180)0.27Viral genome in biopsy specimen16 (59%)11 (73%)0.36Extent of fibrosis in biopsy specimen (%)14 ± 715 ± 90.61 Open table in a new tab The comparison of CMR findings in inflammatory and idiopathic DC are summarized in Table 2. LGE was present in 67% of the study group and was significantly more common in inflammatory than in idiopathic DC. LGE had a pattern of a single, thin, mid-wall stripe located in the interventricular septum (n = 12) or within the inferolateral or lateral wall (n = 4), multiple mid-wall stripes located in different areas (n = 7), or a patchy transmural lesion found predominantly in the lateral wall (n = 5; Figure 1). The prevalence of myocardial inflammation found by right ventricular EMB did not differ significantly with respect to localization of LGE in the left ventricular (interventricular septum vs nonseptal regions 16 of 28 [50%] vs 12 of 28 [42%], p = 0.66). No characteristic localizations or patterns of LGE were observed with regard to a particular viral genome found in the EMB specimen. A positive correlation was found between the extent of LGE in the left ventricle and the hs-cTnT and B-type natriuretic peptide levels (r = 0.68 and r = 0.53, respectively; p <0.001). The variables associated with the occurrence of LGE are listed in Table 3. On multivariate logistic analysis, the finding of myocardial inflammation in the EMB specimens and increased B-type natriuretic peptide plasma levels (per ln ng/L) were independently associated with LGE (odds ratio 11.0, 95% confidence interval 1.3 to 96 and odds ratio 3.5, 95% confidence interval 1.3 to 9.8; p = 0.03 and p = 0.017, respectively). Myocardial early enhancement proved to have moderate reliability for the detection of inflammation (area under receiver operating characteristic curve 0.68, 95% confidence interval 0.5 to 0.89, p = 0.049). The assessment of the myocardial edema ratio was not useful for the identification of inflammation (area under receiver operating characteristic curve 0.49). Abnormal pericardial effusion with a mean volume of 76 ml (range 52 to 185) was more common in inflammatory than in idiopathic DC. Considering all the possible combinations of the 4 CMR techniques, the best diagnostic accuracy for the detection of inflammation was achieved when the criterion for the diagnosis was defined as the simultaneous presence of any 2 of the CMR features (Table 4).Table 2Cardiovascular magnetic resonance imaging (CMR) findingsCharacteristicIdiopathic DC (n = 27)Inflammatory DC (n = 15)p ValueLeft ventricular ejection fraction (%)22 ± 1121 ± 90.74Left ventricular end-diastolic volume (ml/m2)137 ± 39148 ± 460.43Left ventricular end-diastolic diameter (mm)67 ± 871 ± 70.14Left ventricular mass (g/m2)106 ± 26106 ± 270.96Right ventricular ejection fraction (%)24 ± 923 ± 80.64Right ventricular end-diastolic volume (ml/m2)80 ± 3576 ± 230.71Interventricular septum (mm)9 ± 29 ± 20.45Edema ratio1.5 ± 0.31.5 ± 0.40.67Edema ratio >1.92 (7%)2 (13%)0.63Early gadolinium enhancement (%)22 ± 1338 ± 320.030†Statistically significant.Early gadolinium enhancement >45%1 (4%)6 (40%)0.005†Statistically significant.Late gadolinium enhancement present15 (56%)13 (87%)0.049†Statistically significant.Late gadolinium enhancement extent in left ventricle∗Only in patients with LGE. (%)6 ± 45 ± 30.625Late enhancement mid-wall stripe pattern11 (41%)9 (60%)0.23Pericardial effusion >50 ml3 (11%)7 (47%)0.020†Statistically significant.∗ Only in patients with LGE.† Statistically significant. Open table in a new tab Table 3Association of late gadolinium enhancement (LGE) with clinical, biochemical, and biopsy findingsVariableLGEp ValueAbsent (n = 14)Present (n = 28)New York Heart Association class2.2 ± 0.73.0 ± 0.80.006∗Statistically significant.Left ventricular ejection fraction (%)23 ± 1121 ± 90.44Left ventricular end diastolic volume (ml/m2)128 ± 38147 ± 420.19Left ventricular end diastolic diameter (mm)67 ± 969 ± 70.47Left ventricular mass (g/m2)108 ± 28123 ± 230.59B-type natriuretic peptide (ng/L)283 (113–812)1,031 (592–1,469)0.003∗Statistically significant.High-sensitivity troponin T (ng/L)6 (4–16)18 (9–54)0.021∗Statistically significant.High-sensitivity troponin T >13.5 pg/L4 (28%)19 (68%)0.023∗Statistically significant.Conventional troponin I >0.03 μg/L3 (21%)10 (36%)0.35Maximum conventional troponin I (μg/L)0.33.6—Glomerular filtration rate (ml/min/1.73 m2)74 ± 2482 ± 180.40Myocardial inflammation in biopsy2 (14%)13 (46%)0.04∗Statistically significant.Fibrosis extent in biopsy (%)12 ± 516 ± 90.18∗ Statistically significant. Open table in a new tab Table 4Performance of cardiovascular magnetic resonance imaging (CMR) and high-sensitivity cardiac troponin T (hs-cTnT) for detection of inflammatory cardiomyopathyVariableSensitivity (%)Specificity (%)Accuracy (%)OR (95% CI)Tissue edema∗Edema ratio >1.9.139364NSIncreased early gadolinium enhancement†Early enhancement >45%.40967617 (2–164)Late gadolinium enhancement present8744605 (1–28)Pericardial effusion‡Pericardial effusion >50 ml.4789747 (1.5–34)Any criteria simultaneously67857912 (3–52)Late and early gadolinium enhancement86747617 (2–164)Late gadolinium enhancement plus pericardial effusion7075747 (1.5–37)High-sensitivity troponin T elevated§hs-cTnT concentration >13.5 ng/L.675660NSCardiovascular magnetic resonance feature plus elevated high-sensitivity troponin T Tissue edema710066NS Increased early gadolinium enhancement2710074NS Pericardial effusion47937611 (2–64) Late gadolinium enhancement present6767674 (1–15) Any 2 criteria simultaneously53937814 (2–28) Late gadolinium enhancement plus pericardial effusion78767611 (2–64)Cardiovascular magnetic resonance feature or elevated high-sensitivity troponin T Tissue edema734857NS Increased early gadolinium enhancement125257NS Pericardial effusion675257NS Late gadolinium enhancement present873352NSCI = confidence interval; NS = not statistically significant by logistic regression analysis; OR = odds ratio.∗ Edema ratio >1.9.† Early enhancement >45%.‡ Pericardial effusion >50 ml.§ hs-cTnT concentration >13.5 ng/L. Open table in a new tab The assessment of hs-cTnT was unable to differentiate between inflammatory and idiopathic DC because the serum concentrations did not differ in the 2 groups. Elevated hs-cTnT in the patients with abnormal CMR findings (or vice versa) increased the specificity for the diagnosis, but at the cost of decreased sensitivity (Table 4).Of the 42 patients, 12 (29%) reached a composite clinical end point of cardiac death (n = 4), urgent heart transplantation (n = 4), or hospitalization for decompensation of heart failure (n = 4) during a mean follow-up of 25 ± 9 months. A ventricular assist device was implanted in 4 of these patients. In addition, 12 patients (29%) received an implantable cardioverter-defibrillator. Four of the implantable cardioverter-defibrillators were with biventricular pacing. An appropriate implantable cardioverter-defibrillator shock was observed in 1 patient. A significant functional improvement was observed in most of the surviving nontransplanted 34 patients (New York Heart Association at baseline vs follow-up 2.6 ± 0.8 vs 1.5 ± 0.6, p <0.001). The adverse clinical events were associated with greater New York Heart Association class, a greater extent of LGE in the left ventricle, and increased B-type natriuretic peptide and hs-cTnT levels (Table 5). In the Cox proportional hazard models including either B-type natriuretic peptide or New York Heart Association class (because of a strong mutual correlation) plus LGE and hs-cTnT as continuous or binary variables only the increased the hs-cTnT–retained independent prognostic significance (hazard ratio 1.9 to 5.3, 95% confidence interval 1.2 to 21, p <0.05, per ln ng/L).Table 5Univariate analysis of predictors of composite end Point of cardiac death, urgent heart transplantation, or hospitalization for worsening of heart failureVariableHR (95% CI)p ValueMale gender1.3 (0.4–4.3)0.72Age (per year)0.96 (0.9–1.0)0.14Serum creatinine (per mg/dl)0.99 (0.9–1.0)0.49New York Heart Association class2.2 (1.1–4.8)0.028∗Statistically significant.B-type natriuretic peptide (per ln ng/L)2.7 (1.2–6.2)0.022∗Statistically significant.High-sensitivity troponin T (per ln ng/L)2.2 (1.4–3.5)0.001∗Statistically significant.High-sensitivity troponin T >13.5 pg/L5.1 (1.1–23)0.035∗Statistically significant.Late gadolinium enhancement (per % of left ventricle)1.1 (1.0–1.2)0.008∗Statistically significant.Late gadolinium enhancement present6.3 (0.8–49)0.044∗Statistically significant.Edema ratio (per unit)0.5 (0.1–3.6)0.46Early gadolinium enhancement (per %)1.0 (1.0–1.0)0.33Pericardial effusion (per ml)2.5 (0.8–8.2)0.13Myocardial inflammation in biopsy specimen1.3 (0.4–4.2)0.64Viral genome in biopsy1.6 (0.5–5.0)0.44Extent of fibrosis in biopsy (per %)1.0 (0.9–1.1)0.27HR = hazard ratio.∗ Statistically significant. Open table in a new tab DiscussionThis is the first study to systematically evaluate the clinical utility of a comprehensive CMR protocol combined with a novel hs-cTnT assay in the noninvasive diagnosis of inflammatory DC using the EMB results as the reference standard. In summary, we found rather a modest overall performance of CMR for the diagnosis. Although the occurrence of LGE on CMR was a sensitive sign for myocardial inflammation, it was also a hallmark of more advanced heart failure. The addition of hs-cTnT assessment to CMR did not improve the diagnosis. Nonetheless, both the hs-cTnT levels and the extent of LGE were strong predictors of the mid-term clinical outcomes. Finally, yet importantly, the concurrent use of CMR, EMB, and novel cardiac biomarkers provided new insights into the pathophysiology of LGE in DC.Although there is good evidence of the performance of CMR in the diagnosis of clinically suspected acute myocarditis,1Friedrich M.G. Sechtem U. Schulz-Menger J. Holmvang G. Alakija P. Cooper L.T. White J.A. Abdel-Aty H. Gutberlet M. Prasad S. Aletras A. Laissy J.P. Paterson I. Filipchuk N.G. Kumar A. Pauschinger M. Liu P. Cardiovascular magnetic resonance in myocarditis: a JACC White Paper.J Am Coll Cardiol. 2009; 53: 1475-1487Abstract Full Text Full Text PDF PubMed Scopus (1671) Google Scholar, 2Friedrich M.G. Strohm O. Schulz-Menger J. Marciniak H. Luft F.C. Dietz R. Contrast media-enhanced magnetic resonance imaging visualizes myocardial changes in the course of viral myocarditis.Circulation. 1998; 97: 1802-1809Crossref PubMed Scopus (484) Google Scholar, 3Zagrosek A. Abdel-Aty H. Boye P. Wassmuth R. Messroghli D. Utz W. Rudolph A. Bohl S. Dietz R. Schulz-Menger J. Cardiac magnetic resonance monitors reversible and irreversible myocardial injury in myocarditis.JACC Cardiovasc Imaging. 2009; 2: 131-138Abstract Full Text Full Text PDF PubMed Scopus (134) Google Scholar, 4Alter P. Rupp H. Adams P. Stoll F. Figiel J.H. Klose K.J. Rominger M.B. Maisch B. Occurrence of late gadolinium enhancement is associated with increased left ventricular wall stress and mass in patients with non-ischaemic di" @default.
• W2004764583 created "2016-06-24" @default.
• W2004764583 creator A5005443694 @default.
• W2004764583 creator A5014297802 @default.
• W2004764583 creator A5014877072 @default.
• W2004764583 creator A5016937291 @default.
• W2004764583 creator A5017744229 @default.
• W2004764583 creator A5021398156 @default.
• W2004764583 creator A5052148639 @default.
• W2004764583 creator A5073033425 @default.
• W2004764583 date "2013-01-01" @default.
• W2004764583 modified "2023-10-17" @default.
• W2004764583 title "Utility of Combination of Cardiac Magnetic Resonance Imaging and High-Sensitivity Cardiac Troponin T Assay in Diagnosis of Inflammatory Cardiomyopathy" @default.
• W2004764583 cites W1977647599 @default.
• W2004764583 cites W1986446977 @default.
• W2004764583 cites W1986823781 @default.
• W2004764583 cites W1990612198 @default.
• W2004764583 cites W2004659005 @default.
• W2004764583 cites W2014182808 @default.
• W2004764583 cites W2032182532 @default.
• W2004764583 cites W2052299447 @default.
• W2004764583 cites W2065509096 @default.
• W2004764583 cites W2080094758 @default.
• W2004764583 cites W2090975399 @default.
• W2004764583 cites W2100411489 @default.
• W2004764583 cites W2105523526 @default.
• W2004764583 cites W2116707537 @default.
• W2004764583 cites W2131719250 @default.
• W2004764583 cites W2135302420 @default.
• W2004764583 cites W2136847876 @default.
• W2004764583 cites W2138524724 @default.
• W2004764583 cites W2146578470 @default.
• W2004764583 cites W2161947705 @default.
• W2004764583 cites W2168659064 @default.
• W2004764583 doi "https://doi.org/10.1016/j.amjcard.2012.09.024" @default.
• W2004764583 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23102878" @default.
• W2004764583 hasPublicationYear "2013" @default.
• W2004764583 type Work @default.
• W2004764583 sameAs 2004764583 @default.
• W2004764583 citedByCount "20" @default.
• W2004764583 countsByYear W20047645832014 @default.
• W2004764583 countsByYear W20047645832015 @default.
• W2004764583 countsByYear W20047645832016 @default.
• W2004764583 countsByYear W20047645832017 @default.
• W2004764583 countsByYear W20047645832019 @default.
• W2004764583 countsByYear W20047645832020 @default.
• W2004764583 countsByYear W20047645832021 @default.
• W2004764583 countsByYear W20047645832022 @default.
• W2004764583 countsByYear W20047645832023 @default.
• W2004764583 crossrefType "journal-article" @default.
• W2004764583 hasAuthorship W2004764583A5005443694 @default.
• W2004764583 hasAuthorship W2004764583A5014297802 @default.
• W2004764583 hasAuthorship W2004764583A5014877072 @default.
• W2004764583 hasAuthorship W2004764583A5016937291 @default.
• W2004764583 hasAuthorship W2004764583A5017744229 @default.
• W2004764583 hasAuthorship W2004764583A5021398156 @default.
• W2004764583 hasAuthorship W2004764583A5052148639 @default.
• W2004764583 hasAuthorship W2004764583A5073033425 @default.
• W2004764583 hasConcept C126322002 @default.
• W2004764583 hasConcept C126838900 @default.
• W2004764583 hasConcept C143409427 @default.
• W2004764583 hasConcept C164705383 @default.
• W2004764583 hasConcept C2776008845 @default.
• W2004764583 hasConcept C2776127602 @default.
• W2004764583 hasConcept C2778198053 @default.
• W2004764583 hasConcept C2778797674 @default.
• W2004764583 hasConcept C2987145844 @default.
• W2004764583 hasConcept C36036425 @default.
• W2004764583 hasConcept C500558357 @default.
• W2004764583 hasConcept C71924100 @default.
• W2004764583 hasConceptScore W2004764583C126322002 @default.
• W2004764583 hasConceptScore W2004764583C126838900 @default.
• W2004764583 hasConceptScore W2004764583C143409427 @default.
• W2004764583 hasConceptScore W2004764583C164705383 @default.
• W2004764583 hasConceptScore W2004764583C2776008845 @default.
• W2004764583 hasConceptScore W2004764583C2776127602 @default.
• W2004764583 hasConceptScore W2004764583C2778198053 @default.
• W2004764583 hasConceptScore W2004764583C2778797674 @default.
• W2004764583 hasConceptScore W2004764583C2987145844 @default.
• W2004764583 hasConceptScore W2004764583C36036425 @default.
• W2004764583 hasConceptScore W2004764583C500558357 @default.
• W2004764583 hasConceptScore W2004764583C71924100 @default.
• W2004764583 hasIssue "2" @default.
• W2004764583 hasLocation W20047645831 @default.
• W2004764583 hasLocation W20047645832 @default.
• W2004764583 hasOpenAccess W2004764583 @default.
• W2004764583 hasPrimaryLocation W20047645831 @default.
• W2004764583 hasRelatedWork W1981430297 @default.
• W2004764583 hasRelatedWork W1983527543 @default.
• W2004764583 hasRelatedWork W2028377927 @default.
• W2004764583 hasRelatedWork W2029624016 @default.
• W2004764583 hasRelatedWork W2080790488 @default.
• W2004764583 hasRelatedWork W3022163056 @default.
• W2004764583 hasRelatedWork W3190507020 @default.
• W2004764583 hasRelatedWork W4244696355 @default.
• W2004764583 hasRelatedWork W4283219633 @default.
• W2004764583 hasRelatedWork W4296822144 @default.
• W2004764583 hasVolume "111" @default.

• next