Cardiovascular Magnetic Resonance in Cardiac Amyloidosis
2005; Lippincott Williams & Wilkins; Volume: 111; Issue: 2 Linguagem: Italiano
10.1161/01.cir.0000153623.02240.20
ISSN1524-4539
AutoresRaymond Y. Kwong, Rodney H. Falk,
Tópico(s)Sarcoidosis and Beryllium Toxicity Research
ResumoHomeCirculationVol. 111, No. 2Cardiovascular Magnetic Resonance in Cardiac Amyloidosis Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBCardiovascular Magnetic Resonance in Cardiac Amyloidosis Raymond Y. Kwong and Rodney H. Falk Raymond Y. KwongRaymond Y. Kwong From the Department of Medicine, Cardiovascular Division, Brigham and Women's Hospital (R.Y.K., R.H.F.), and Harvard Vanguard Medical Associates (R.H.F.), Boston, Mass. and Rodney H. FalkRodney H. Falk From the Department of Medicine, Cardiovascular Division, Brigham and Women's Hospital (R.Y.K., R.H.F.), and Harvard Vanguard Medical Associates (R.H.F.), Boston, Mass. Originally published18 Jan 2005https://doi.org/10.1161/01.CIR.0000153623.02240.20Circulation. 2005;111:122–124Amyloidosis represents a diverse group of diseases characterized by the common factor of deposition of twisted β-pleated sheet fibrils (amyloid) formed as a result of the misfolding of various proteins produced in several different pathological states. The different forms of amyloidosis are classified by the composition of the amyloid fibril. AL amyloidosis (previously designated as primary amyloidosis) is derived from light-chain immunoglobulin produced by monoclonal plasma cells.1 It is the most severe and probably, at least in the United States, the most common form of amyloidosis. The accumulation of amyloid disrupts the tissue architecture and, possibly in conjunction with a toxic effect from the light chains,2 leads to severe organ damage that may involve the kidneys, heart, liver, or peripheral nerves. Familial amyloidosis is an uncommon, autosomal dominant disease with a high degree of penetrance. Most cases result from the production of an unstable variant of the serum protein transthyretin (ATTR amyloidosis). More than 80 point mutations have been identified for ATTR amyloidosis, which predominantly results in neurological or cardiac dysfunction or both.1,3 A particularly common mutant transthyretin resulting from the substitution of isoleucine for valine at position 122 is found in ≈4% of the African American population, with an unknown penetrance. This mutation results in a cardiomyopathy that has been suggested to be one of the most common types of cardiomyopathy in older adult African American patients.4Senile systemic amyloidosis is the result of the deposition of wild-type transthyretin and is almost exclusively limited to the heart. This disease may be becoming more prevalent because of the increasing age of the general population. Reactive systemic amyloidosis is the result of an overproduction of a nonimmunoglobulin protein AA and is rarely associated with any cardiac involvement.See p 186In AL amyloidosis, cardiac involvement is common and is the cause of death in most of these patients.5 Effective treatments for AL amyloidosis exist, but treatment options are limited once cardiac disease becomes clinically apparent. Recently, the use of high-dose melphalan with rescue autologous peripheral blood stem cell transplantation has resulted in reversal of the clinical manifestations of AL amyloidosis in a significant proportion of patients who survived the procedure.6–10 Cardiac involvement not only indicates a poor prognosis in most forms of amyloidosis11 but also predicts poor tolerance to high-dose chemotherapy and stem cell transplantation. Although cardiac biopsy can reliably diagnose cardiac amyloidosis, its procedural risks and uncertainty about sampling error limit its applications in monitoring the clinical course of the disease. Therefore, noninvasive diagnostic techniques that can stage cardiac amyloidosis should have important prognostic and treatment implications.Echocardiography is considered the noninvasive test of choice to diagnose cardiac amyloidosis. Typical abnormalities seen on echocardiography include a small left ventricular size, biventricular and atrial septal thickening, atrial enlargement, and, in the late stages, a restrictive left ventricular filling pattern.12 Imaging of the structural and morphological changes, however, is often insufficient in addressing the spectrum of disease in cardiac amyloidosis. Whereas a combination of ECG and echocardiographic features may raise the suspicion of cardiac amyloidosis with a high accuracy in selected subsets of patients presenting with heart failure,12 advanced patient age and common comorbidities such as hypertension render ventricular hypertrophy nonspecific to the underlying disease process. Substantial echocardiographic evidence of cardiac amyloid such as hypertrophied ventricles and restrictive filling pattern is a late finding that is associated with a median survival of only 6 months.13 Therefore, it has limited impact in guiding treatment decisions, and a noninvasive technique to detect earlier changes in the disease would be of great value. Furthermore, after effective treatments such as intravenous melphalan and autologous stem cell transplantation, echocardiographic monitoring is problematic because regression of abnormalities often is not observed despite a favorable clinical or hematologic response to the treatment.14,15 This may be a result of the difficulty of obtaining precisely reproducible echocardiographic measurements in individual patients. Recent advances in longitudinal myocardial strain and peak systolic strain rate hold promise for early diagnosis and treatment monitoring of cardiac amyloidosis.14 These advanced echocardiographic modalities are minimally affected by passive motion and may detect the effects of cardiac amyloidosis at an early stage of the disease, when ejection fraction is normal. They do not function as diagnostic tools but, rather, they reflect the early functional abnormalities produced by amyloid infiltration. Nuclear scintigraphy with 99Tc pyrophosphate or indium-labeled antimyosin antibody has been reported to detect extensive cardiac involvement of cardiac amyloidosis.16–18 Detection of the less extensive or early disease in the heart appears to be less reliable, however, and needs to be studied further.19In this issue of Circulation, Maceira et al20 studied 29 patients with systemic amyloidosis and 16 hypertensive controls using gadolinium-enhanced cardiac MRI. The study aimed to explore the pattern of abnormal myocardial characteristics in patients with biopsy-proven amyloidosis and echocardiographic evidence of cardiac amyloidosis. Although echocardiography was used to select patients with probable cardiac amyloidosis, this was not a comparative study of echocardiography versus cardiac MRI for distinguishing amyloidosis from true hypertrophy, because the data Maceira et al provide in their table imply that control patients did not undergo echocardiography. Thus, no conclusions about the superiority of cardiac MRI over echocardiography should be drawn. The MRI data did, however, show some interesting features in cardiac amyloid patients. With the high spatial resolution (≈2 mm) and tissue contrast differentiation of cardiac MRI, amyloidosis patients were noted to have qualitative global and subendocardial gadolinium enhancement of the myocardium. Myocardial enhancement was associated with increased ventricular mass and impaired left ventricular systolic function. Shortly after intravenous administration of gadolinium contrast, amyloidosis patients had faster gadolinium clearance from the blood pool marked by a blood T1 value over time that was higher than that in controls. This resulted in a diminished T1 difference between the myocardium and blood in amyloid patients as compared with that observed in control patients.Although the descriptive findings of this study represent structural myocardial changes from amyloid infiltration, several limitations must be considered in the noninvasive diagnosis of cardiac amyloidosis via the MRI techniques presented in this study. The patient sample consisted of a group of 29 amyloidosis patients and 16 "matched" hypertensive controls. All 29 amyloid patients had biopsy-proven amyloidosis and were considered to have cardiac amyloidosis on the basis of the presence of morphological and diastolic filling changes on echocardiography. Only 2 of the 29 patients had endomyocardial biopsy confirmation of cardiac amyloid infiltration. Because amyloidosis patients without clearly abnormal changes on echocardiography were not part of the study sample, it is unlikely that the amyloidosis patients included in this study sample adequately represented the spectrum of early cardiac involvement. The authors conclude that the combined assessment of myocardial T1 with demonstration of global subendocardial late gadolinium enhancement yielded an 87% accuracy for the detection of cardiac amyloidosis and that this improved to 97% with the more complicated parameter of the difference in T1 between subendocardium and blood. There are several problems with this seemingly highly accurate method for distinguishing amyloid infiltration from true cardiac hypertrophy. The 2 groups are said to have statistically insignificant difference in left ventricular mass, but the amyloid patients did have greater mean mass, which reaches statistical significance (P=0.03) if calculated by 1-tailed analysis. Furthermore, although the mean ejection fraction did not differ between the groups, 40% of the amyloid patients with late enhancement are described as having "impaired systolic function," and late enhancement was associated with more severe cardiac amyloid, characterized by greater left and right ventricular mass.As the prevalence of cardiac amyloidosis in the general population is a minute fraction of the population with true left ventricular hypertrophy, it is important to recognize that this will dramatically decrease the predictive accuracy of any individual noninvasive test that does not have a virtually 100% sensitivity and specificity for cardiac amyloidosis. We therefore cannot draw any conclusions about the clinical utility of gadolinium enhancement and kinetics for the diagnosis of cardiac amyloidosis in patients with increased left ventricular mass on cardiac MRI, nor can the staging of the extent of cardiac involvement in patients with systemic amyloidosis be fully addressed with the present results. These practical issues, as well as the prognostic value of the contrast-enhanced MRI technique, need to be investigated by a prospective study. As yet, the mechanism of the altered gadolinium kinetics in amyloidosis remains unclear. Although the authors speculated that a faster gadolinium washout from blood and myocardium among amyloid patients represented gadolinium distribution into the total body amyloid load, there was no correlation between the blood and myocardial gadolinium clearance and measures of total body amyloid load. This may represent a limitation of serum amyloid P component scintigraphy for accurately assessing total body amyloid load or it may suggest another as yet unknown mechanism.How, then, does the present study help us? Gadolinium-enhanced MRI techniques have proven clinical value in characterizing myocardial infarction and fibrosis in other cardiac disorders21,22,24–26; however, the histological basis of gadolinium delayed enhancement remains incompletely understood. Current evidence suggests that it is related to a combination of delayed washout kinetics and an increased volume of distribution of gadolinium in the interstitial space of abnormal myocardium. The pathological result presented by Maceira et al20 from the sole cardiac amyloidosis patient who died shortly after MRI extends our current understanding of the histological basis of delayed enhancement.27–30 Regions of delayed enhancement have been reported to correlate with the increased collagen content of myocardial fibrosis in hypertrophic cardiomyopathy.31 In contrast, and similar to previous pathological reports of cardiac amyloidosis,32,33 histological assessment of this patient indicated little local tissue reaction invoked by amyloid infiltration with minimal myocardial fibrosis, yet extensive delayed enhancement was demonstrated in matched regions where >40% of the subendocardial volume was infiltrated by amyloid. This finding suggested that interstitial expansion from amyloid infiltration without interstitial fibrosis could also cause delayed enhancement detectable by MRI. Therefore, the present study may provide insights into the histological basis of MRI gadolinium-related abnormalities in patients with amyloidosis and other infiltrative processes.Despite the described limitations, abnormal myocardial characteristics and gadolinium washout kinetics, as presented by Maceira et al,20 may be valuable in advancing our knowledge of cardiac amyloidosis. If further studies show that this noninvasive method can allow serial quantification of the extent of myocardial infiltration, then we may gain further insight into the natural history of cardiac amyloidosis. Noninvasive imaging with highly reproducible and quantifiable results such as can be obtained by cardiac MRI also may help to estimate the prevalence of cardiac involvement in systemic amyloidosis when cardiac morphological changes are not apparent by echocardiography. Screening of subclinical early cardiac involvement may become possible should delayed enhancement prove to have adequate sensitivity in detecting amyloid infiltration. Better knowledge of the disease process and improved noninvasive surveillance may, as the authors suggest, also aid in the evaluation of current and novel chemotherapeutic agents. With advances in imaging technology, the future direction in the diagnosis or surveillance (or both) of this disease may be further improved by the development of specific contrast agents that target sites of the amyloid proteins. Hand in hand with improvements in treatment, advances in imaging may offer the patients who battle amyloidosis an improved outlook in the future.The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.FootnotesCorrespondence to Dr Raymond Y. Kwong, Dept of Medicine, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. E-mail [email protected] References 1 Lachmann HJ, Booth DR, Booth SE, Bybee A, Gilbertson JA, Gillmore JD, Pepys MB, Hawkins PN. Misdiagnosis of hereditary amyloidosis as AL (primary) amyloidosis. N Engl J Med. 2002; 346: 1786–1791.CrossrefMedlineGoogle Scholar2 Brenner DA, Jain M, Pimentel DR, Wang B, Connors LH, Skinner M, Apstein CS, Liao R. Human amyloidogenic light chains directly impair cardiomyocyte function through an increase in cellular oxidant stress. Circ Res. 2004; 94: 1008–1010.LinkGoogle Scholar3 Puille M, Altland K, Linke RP, Steen-Muller MK, Kiett R, Steiner D, Bauer R. 99mTc-DPD scintigraphy in transthyretin-related familial amyloidotic polyneuropathy. Eur J Nucl Med Mol Imaging. 2002; 29: 376–379.CrossrefMedlineGoogle Scholar4 Jacobson DR, Pastore RD, Yaghoubian R, Kane I, Gallo G, Buck FS, Buxbaum JN. Variant-sequence transthyretin (isoleucine 122) in late-onset cardiac amyloidosis in black Americans. N Engl J Med. 1997; 336: 466–473.CrossrefMedlineGoogle Scholar5 Gertz MA, Rajkumar SV. Primary systemic amyloidosis. Curr Treat Options Oncol. 2002; 3: 261–271.CrossrefMedlineGoogle Scholar6 Comenzo RL, Vosburgh E, Falk RH, Sanchorawala V, Reisinger J, Dubrey S, Dember LM, Berk JL, Akpek G, LaValley M, O'hara C, Arkin CF, Wright DG, Skinner M. Dose-intensive melphalan with blood stem-cell support for the treatment of AL (amyloid light-chain) amyloidosis: survival and responses in 25 patients. Blood. 1998; 91: 3662–3670.CrossrefMedlineGoogle Scholar7 Comenzo RL, Gertz MA. Autologous stem cell transplantation for primary systemic amyloidosis. Blood. 2002; 99: 4276–4282.CrossrefMedlineGoogle Scholar8 Gertz MA, Lacy MQ, Gastineau DA, Inwards DJ, Chen MG, Tefferi A, Kyle RA, Litzow MR. Blood stem cell transplantation as therapy for primary systemic amyloidosis (AL). Bone Marrow Transplant. 2000; 26: 963–969.CrossrefMedlineGoogle Scholar9 Gillmore JD, Davies J, Iqbal A, Madhoo S, Russell NH, Hawkins PN. Allogeneic bone marrow transplantation for systemic AL amyloidosis. Br J Haematol. 1998; 100: 226–228.CrossrefMedlineGoogle Scholar10 Moreau P, Leblond V, Bourquelot P, Facon T, Huynh A, Caillot D, Hermine O, Attal M, Hamidou M, Nedellec G, Ferrant A, Audhuy B, Bataille R, Milpied N, Harousseau JL. Prognostic factors for survival and response after high-dose therapy and autologous stem cell transplantation in systemic AL amyloidosis: a report on 21 patients. Br J Haematol. 1998; 101: 766–769.CrossrefMedlineGoogle Scholar11 Dubrey SW, Cha K, Skinner M, LaValley M, Falk RH. Familial and primary (AL) cardiac amyloidosis: echocardiographically similar diseases with distinctly different clinical outcomes. Heart. 1997; 78: 74–82.CrossrefMedlineGoogle Scholar12 Rahman JE, Helou EF, Gelzer-Bell R, Thompson RE, Kuo C, Rodriguez ER, Hare JM, Baughman KL, Kasper EK. Noninvasive diagnosis of biopsy-proven cardiac amyloidosis. J Am Coll Cardiol. 2004; 43: 410–415.CrossrefMedlineGoogle Scholar13 Kyle RA, Greipp PR, O'Fallon WM. Primary systemic amyloidosis: multivariate analysis for prognostic factors in 168 cases. Blood. 1986; 68: 220–224.CrossrefMedlineGoogle Scholar14 Koyama J, Ray-Sequin PA, Falk RH. Longitudinal myocardial function assessed by tissue velocity, strain, and strain rate tissue Doppler echocardiography in patients with AL (primary) cardiac amyloidosis. Circulation. 2003; 107: 2446–2452.LinkGoogle Scholar15 Sanchorawala V, Wright DG, Seldin DC, Dember LM, Finn K, Falk RH, Berk J, Quillen K, Skinner M. An overview of the use of high-dose melphalan with autologous stem cell transplantation for the treatment of AL amyloidosis. Bone Marrow Transplant. 2001; 28: 637–642.CrossrefMedlineGoogle Scholar16 Hawkins PN, Pepys MB. Imaging amyloidosis with radiolabelled SAP. Eur J Nucl Med. 1995; 22: 595–599.CrossrefMedlineGoogle Scholar17 Wald DS, Gray HH. Restrictive cardiomyopathy in systemic amyloidosis. QJM. 2003; 96: 380–382.CrossrefMedlineGoogle Scholar18 Singer R, Schnabel A, Strasser RH. Images in cardiovascular medicine. Restrictive cardiomyopathy in familial amyloidosis TTR-Arg-50. Circulation. 2003; 107: 643–644.LinkGoogle Scholar19 Tanaka M, Hongo M, Kinoshita O, Takabayashi Y, Fujii T, Yazaki Y, Isobe M, Sekiguchi M. Iodine-123 metaiodobenzylguanidine scintigraphic assessment of myocardial sympathetic innervation in patients with familial amyloid polyneuropathy. J Am Coll Cardiol. 1997; 29: 168–174.CrossrefMedlineGoogle Scholar20 Maceira AM, Joshi J, Prasad SK, Moon JC, Perugini E, Harding I, Sheppard MN, Poole-Wilson PA, Hawkins PN, Pennell DJ. Cardiovascular magnetic resonance in cardiac amyloidosis. Circulation. 2005; 111: 186–193.LinkGoogle Scholar21 Kim RJ, Fieno DS, Parrish TB, Harris K, Chen EL, Simonetti O, Bundy J, Finn JP, Klocke FJ, Judd RM. Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation. 1999; 100: 1992–2002.CrossrefMedlineGoogle Scholar22 Kim RJ, Wu E, Rafael A, Chen EL, Parker MA, Simonetti O, Klocke FJ, Bonow RO, Judd RM. The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med. 2000; 343: 1445–1453.CrossrefMedlineGoogle Scholar23 Deleted in proof.Google Scholar24 Ricciardi MJ, Wu E, Davidson CJ, Choi KM, Klocke FJ, Bonow RO, Judd RM, Kim RJ. Visualization of discrete microinfarction after percutaneous coronary intervention associated with mild creatine kinase-MB elevation. Circulation. 2001; 103: 2780–2783.CrossrefMedlineGoogle Scholar25 Nemeth MA, Muthupillai R, Wilson JM, Awasthi M, Flamm SD. Cardiac sarcoidosis detected by delayed-hyperenhancement magnetic resonance imaging. Tex Heart Inst J. 2004; 31: 99–102.MedlineGoogle Scholar26 Chandra M, Silverman ME, Oshinski J, Pettigrew R. Diagnosis of cardiac sarcoidosis aided by MRI. Chest. 1996; 110: 562–565.CrossrefMedlineGoogle Scholar27 Shan K, Constantine G, Sivananthan M, Flamm SD. Role of cardiac magnetic resonance imaging in the assessment of myocardial viability. Circulation. 2004; 109: 1328–1334.LinkGoogle Scholar28 Lima JA, Judd RM, Bazille A, Schulman SP, Atalar E, Zerhouni EA. Regional heterogeneity of human myocardial infarcts demonstrated by contrast-enhanced MRI. Potential mechanisms. Circulation. 1995; 92: 1117–1125.CrossrefMedlineGoogle Scholar29 Kim RJ, Chen EL, Lima JA, Judd RM. Myocardial Gd-DTPA kinetics determine MRI contrast enhancement and reflect the extent and severity of myocardial injury after acute reperfused infarction. Circulation. 1996; 94: 3318–3326.CrossrefMedlineGoogle Scholar30 Arheden H, Saeed M, Higgins CB, Gao DW, Ursell PC, Bremerich J, Wyttenbach R, Dae MW, Wendland MF. Reperfused rat myocardium subjected to various durations of ischemia: estimation of the distribution volume of contrast material with echo-planar MR imaging. Radiology. 2000; 215: 520–528.CrossrefMedlineGoogle Scholar31 Moon JC, Reed E, Sheppard MN, Elkington AG, Ho SY, Burke M, Petrou M, Pennell DJ. The histologic basis of late gadolinium enhancement cardiovascular magnetic resonance in hypertrophic cardiomyopathy. J Am Coll Cardiol. 2004; 43: 2260–2264.CrossrefMedlineGoogle Scholar32 Guidelines Working Group of UK Myeloma Forum; British Committee for Standards in Haematology, British Society for Haematology. Guidelines on the diagnosis and management of AL amyloidosis. Br J Haematol. 2004; 125: 681–700.CrossrefMedlineGoogle Scholar33 Lie JT. Pathology of amyloidosis and amyloid heart disease. Appl Pathol. 1984; 2: 341–356.MedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Fu Z, Lv J, Gao X, Zhang B, Li Y, Xu X, Zheng H, Wu H and Song Q (2023) Research trends and hotspots evolution of cardiac amyloidosis: a bibliometric analysis from 2000 to 2022, European Journal of Medical Research, 10.1186/s40001-023-01026-5, 28:1 Huang S, Shi K, Zhang Y, Yan W, Guo Y, Li Y and Yang Z (2022) Texture analysis of T2-weighted cardiovascular magnetic resonance imaging to discriminate between cardiac amyloidosis and hypertrophic cardiomyopathy, BMC Cardiovascular Disorders, 10.1186/s12872-022-02671-0, 22:1, Online publication date: 1-Dec-2022. Clifton M, Merritt R and Adrian Howansky (2022) Cardiac magnetic resonance imaging: the role of an essential imaging modality in cardiac assessment before surgical debulking Debulking in Cardiovascular Interventions and Revascularization Strategies, 10.1016/B978-0-12-821451-0.00041-0, (567-575), . Simões M, Fernandes F, Marcondes-Braga F, Scheinberg P, Correia E, Rohde L, Bacal F, Alves S, Mangini S, Biolo A, Beck-da-Silva L, Szor R, Marques W, Oliveira A, Cruz M, Bueno B, Hajjar L, Issa A, Ramires F, Coelho O, Schmidt A, Pinto I, Rochitte C, Vieira M, Mesquita C, Ramos C, Soares-Junior J, Romano M, Mathias W, Garcia M, Montera M, Melo M, Silva S, Garibaldi P, Alencar A, Lopes R, Ávila D, Viana D, Saraiva J, Canesin M, Oliveira G and Mesquita E (2021) Posicionamento sobre Diagnóstico e Tratamento da Amiloidose Cardíaca – 2021, Arquivos Brasileiros de Cardiologia, 10.36660/abc.20210718, 117:3, (561-598), Online publication date: 1-Sep-2021. Schöppenthau D, Schatka I, Berger A, Pieske B, Hahn K, Knebel F, Kleefeld F, Alexander T, Gerds‐Li J and Messroghli D (2020) Isolated atrial amyloidosis suspected by electrophysiological voltage mapping and diagnosed by 99m Tc‐DPD scintigraphy , ESC Heart Failure, 10.1002/ehf2.12964, 7:6, (4305-4310), Online publication date: 1-Dec-2020. Martinez-Naharro A, Baksi A, Hawkins P and Fontana M (2020) Diagnostic imaging of cardiac amyloidosis, Nature Reviews Cardiology, 10.1038/s41569-020-0334-7, 17:7, (413-426), Online publication date: 1-Jul-2020. Biersmith M, Tong M, Guha A, Simonetti O and Addison D (2020) Multimodality Cardiac Imaging in the Era of Emerging Cancer Therapies, Journal of the American Heart Association, 9:2, Online publication date: 21-Jan-2020. Massalha S and Ruddy T (2017) Emerging role of echocardiography, cardiac magnetic resonance imaging and 99mTc-labeled bone tracer scintigraphy for the diagnosis of cardiac amyloidosis, Journal of Nuclear Cardiology, 10.1007/s12350-017-0943-7, 25:6, (2080-2083), Online publication date: 1-Dec-2018. Nam B, Kim S, Jung H, Kim Y and Choe Y (2018) Comparison of quantitative imaging parameters using cardiovascular magnetic resonance between cardiac amyloidosis and hypertrophic cardiomyopathy: inversion time scout versus T1 mapping, The International Journal of Cardiovascular Imaging, 10.1007/s10554-018-1385-2, 34:11, (1769-1777), Online publication date: 1-Nov-2018. Bozkurt B, Colvin M, Cook J, Cooper L, Deswal A, Fonarow G, Francis G, Lenihan D, Lewis E, McNamara D, Pahl E, Vasan R, Ramasubbu K, Rasmusson K, Towbin J and Yancy C (2016) Current Diagnostic and Treatment Strategies for Specific Dilated Cardiomyopathies: A Scientific Statement From the American Heart Association, Circulation, 134:23, (e579-e646), Online publication date: 6-Dec-2016. Kováčik F, Táborský M, Hutyra M, Moravec O and Přeček J (2016) Cardiac amyloidosis: a case report, Intervenční a akutní kardiologie, 10.36290/kar.2016.029, 15:3, (145-147), Online publication date: 1-Oct-2016. Morgan R and Kwong R (2015) Role of Cardiac MRI in the Assessment of Cardiomyopathy, Current Treatment Options in Cardiovascular Medicine, 10.1007/s11936-015-0410-1, 17:11, Online publication date: 1-Nov-2015. Fontana M, Chung R, Hawkins P and Moon J (2014) Cardiovascular magnetic resonance for amyloidosis, Heart Failure Reviews, 10.1007/s10741-014-9470-7, 20:2, (133-144), Online publication date: 1-Mar-2015. Bokhari S, Shahzad R and Maurer M (2015) Radionuclide Imaging in Cardiac Amyloidosis: Are Nuclear Bone Tracers a Foreseeable Future?, Current Cardiovascular Imaging Reports, 10.1007/s12410-014-9317-6, 8:2, Online publication date: 1-Feb-2015. (2014) References Cardiac CT Made Easy, 10.1201/b16792-17, (323-356), Online publication date: 19-May-2014. White J, Kim H, Shah D, Fine N, Kim K, Wendell D, Al-Jaroudi W, Parker M, Patel M, Gwadry-Sridhar F, Judd R and Kim R (2014) CMR Imaging With Rapid Visual T1 Assessment Predicts Mortality in Patients Suspected of Cardiac Amyloidosis, JACC: Cardiovascular Imaging, 10.1016/j.jcmg.2013.09.019, 7:2, (143-156), Online publication date: 1-Feb-2014. Lala A, Joyce E, Groarke J and Mehra M (2014) Challenges in Long-Term Mechanical Circulatory Support and Biological Replacement of the Failing Heart, Circulation Journal, 10.1253/circj.CJ-13-1498, 78:2, (288-299), . Palladini G and Merlini G (2013) Systemic amyloidoses: What an internist should know, European Journal of Internal Medicine, 10.1016/j.ejim.2013.10.007, 24:8, (729-739), Online publication date: 1-Dec-2013. Campbell-Washburn A, Price A, Ellmerich S, Simons J, Al-Shawi R, Kalber T, Ghatrora R, Hawkins P, Moon J, Ordidge R, Pepys M and Lythgoe M (2013) Monitoring systemic amyloidosis using MRI measurements of the extracellular volume fraction, Amyloid, 10.3109/13506129.2013.787984, 20:2, (93-98), Online publication date: 1-Jun-2013. Gertz M and Kyle R (2013) Diagnosis and Therapy of Immunoglobulin Light Chain Amyloidosis (AL Amyloidosis) Neoplastic Diseases of the Blood, 10.1007/978-1-4614-3764-2_37, (729-750), . O'Donnell D, Abbara S, Chaithiraphan V, Yared K, Killeen R, Martos R, Keane D, Cury R and Dodd J (2012) Cardiac MR Imaging of Nonischemic Cardiomyopathies: Imaging Protocols and Spectra of Appearances, Radiology, 10.1148/radiol.11100284, 262:2, (403-422), Online publication date: 1-Feb-2012. Palladini G and Comenzo R (2012) The Challenge of Systemic Immunoglobulin Light-Chain Amyloidosis (AL) Protein Aggregation and Fibrillogenesis in Cerebral and Systemic Amyloid Disease, 10.1007/978-94-007-5416-4_22, (609-642), . Roditi G (2011) MR in hypertension, Journal of Magnetic Resonance Imaging, 10.1002/jmri.22675, 34:5, (989-1006), Online publication date: 1-Nov-2011. Myerson S, Holloway C, Francis J and Neubauer S (2011) Cardiovascular magnetic resonance (CMR) – An update and review, Progress in Nuclear Magnetic Resonance Spectroscopy, 10.1016/j.pnmrs.2010.12.001, 59:3, (213-222), Online publication date: 1-Oct-2011. Tsai S, Seldin D, Wu H, O'Hara C, Ruberg F and Sanchorawala V (2011) Myocardial infarction with "clean coronaries" caused by amyloid light-chain AL amyloidosis: a case report and literature review, Amyloid, 10.3109/13506129.2011.571319, 18:3, (160-164), Online publication date: 1-Sep-2011. Al-Mallah M and Shareef M (2010) The role of cardiac magnetic resonance imaging in the assessment of non-ischemic cardiomyopathy, Heart Failure Reviews, 10.1007/s10741-010-9221-3, 16:4, (369-380), Online publication date: 1-Jul-2011. Schwitter J and Arai A (2011) Assessment of cardiac ischaemia and viability: role of cardiovascular magnetic resonance, European Heart Journal, 10.1093/eurheartj/ehq481, 32:7, (799-809), Online publication date: 1-Apr-2011. El-Feky M and Radswiki T (2010) Cardiac amyloidosis Radiopaedia.org, 10.53347/rID-12599 Wang J, Kong X, Xu H, Zhou G, Chang D, Liu D, Zhang L and Xie M (2010) Noninvasive diagnosis of cardiac amyloidosis by MRI and echochardiography, Journal of Huazhong University of Science and Technology [Medical Sciences], 10.1007/s11596-010-0464-y, 30:4, (536-540), Online publication date: 1-Aug-2010. Gertz M (2010) Diagnosis of Systemic Amyloid Diseases Protein Misfolding Diseases, 10.1002/9780470572702.ch31, (673-688) Syed I, Glockner J, Feng D, Araoz P, Martinez M, Edwards W, Gertz M, Dispenzieri A, Oh J, Bellavia D, Tajik A and Grogan M (2010) Role of Cardiac Magnetic Resonance Imaging in the Detection of Cardiac Amyloidosis, JACC: Cardiovascular Imaging, 10.1016/j.jcmg.2009.09.023, 3:2, (155-164), Online publication date: 1-Feb-2010. Desai H, Aronow W, Peterson S and Frishman W (2010) Cardiac Amyloidosis, Cardiology in Review, 10.1097/CRD.0b013e3181bdba8f, 18:1, (1-11), Online publication date: 1-Jan-2010. Falk R and Dubrey S (2010) Amyloid Heart Disease, Progress in Cardiovascular Diseases, 10.1016/j.pcad.2009.11.007, 52:4, (347-361), Online publication date: 1-Jan-2010. Palladini G, Perlini S and Merlini G (2010) Imaging of Systemic Amyloidosis Amyloidosis, 10.1007/978-1-60761-631-3_2, (15-32), . Zannad N, Cosnay P, Guyetant S, May M, Mohty D and Casset-Senon D (2009) Diagnostic de l'amylose cardiaque sénile par la scintigraphie au 99mTc-DPD, La Presse Médicale, 10.1016/j.lpm.2008.03.021, 38:4, (672-675), Online publication date: 1-Apr-2009. Casares Santiago M, Pastrana M and Cavero M (2009) Caso 8. Amiloidosis cardíaca en resonancia magnética, Radiología, 10.1016/j.rx.2008.09.002, 51:2, (221-222), Online publication date: 1-Mar-2009. Morbach C, Breunig M, Weidemann F, Topp M, Ritter C, Schneider P, Einsele H, Störk S and Angermann C (2009) 52-jähriger Patient mit schwerer Herzinsuffizienz bei multiplem Myelom52 year-old patient with severe heart failure due to multiple myeloma, Der Internist, 10.1007/s00108-008-2241-6, 50:2, (225-229), Online publication date: 1-Feb-2009. Sideras K and Gertz M (2009) Chapter 1 Amyloidosis Advances in Clinical Chemistry Volume 47, 10.1016/S0065-2423(09)47001-X, (1-44), . Feliu E, Ribes R and Mejia S (2009) Imaging cardiovascolare Imaging diagnostico, 10.1007/978-88-470-1510-4_2, (27-51), . Belloni E, De Cobelli F, Esposito A, Mellone R, Perseghin G, Canu T and Del Maschio A (2008) MRI of Cardiomyopathy, American Journal of Roentgenology, 10.2214/AJR.07.3997, 191:6, (1702-1710), Online publication date: 1-Dec-2008. BRAHMBHATT T, HARI P, CINQUEGRANI M, KUMAR N, KOMOROWSKI R and MIGRINO R (2008) Delayed enhancement on cardiac MRI in a patient with multiple myeloma without amyloidosis, The British Journal of Radiology, 10.1259/bjr/58586915, 81:971, (e272-e275), Online publication date: 1-Nov-2008. Steel K and Kwong R (2008) Application of cardiac magnetic resonance imaging in cardiomyopathy, Current Heart Failure Reports, 10.1007/s11897-008-0021-1, 5:3, (128-135), Online publication date: 1-Sep-2008. Abdelmoneim S, Bernier M, Bellavia D, Syed I, Mankad S, Chandrasekaran K, Pellikka P and Mulvagh S (2008) Myocardial contrast echocardiography in biopsy-proven primary cardiac amyloidosis, European Heart Journal - Cardiovascular Imaging, 10.1093/ejechocard/jen017, 9:2, (338-341), Online publication date: 1-Mar-2008., Online publication date: 1-Mar-2008. Vogelsberg H, Mahrholdt H, Deluigi C, Yilmaz A, Kispert E, Greulich S, Klingel K, Kandolf R and Sechtem U (2008) Cardiovascular Magnetic Resonance in Clinically Suspected Cardiac Amyloidosis, Journal of the American College of Cardiology, 10.1016/j.jacc.2007.10.049, 51:10, (1022-1030), Online publication date: 1-Mar-2008. Feliu E, Ribes R and Mejia S Cardiovascular Imaging Learning Diagnostic Imaging, 10.1007/978-3-540-71207-7_2, (27-51) Ischemic Heart Disease and Non-Ischemic Cardiomyopathies Cardiovascular MRI in Practice, 10.1007/978-1-84800-090-2_3, (25-40) (2008) Diseases of the Myocardium and Pericardium Cardiovascular MRI, 10.1007/978-1-59745-511-4_4, (57-101), . Tzelepis G, Kelekis N, Plastiras S, Mitseas P, Economopoulos N, Kampolis C, Gialafos E, Moyssakis I and Moutsopoulos H (2007) Pattern and distribution of myocardial fibrosis in systemic sclerosis: A delayed enhanced magnetic resonance imaging study, Arthritis & Rheumatism, 10.1002/art.22971, 56:11, (3827-3836), Online publication date: 1-Nov-2007. Mikami Y, Funabashi N, Kijima T, Uehara M, Shiina Y, Lee K, Nakayama T, Daimon M, Kuroda N, Kobayashi Y, Takano H and Komuro I (2007) Focal fibrosis in the left ventricle of subjects with cardiac amyloidosis evaluated by multislice computed tomography, International Journal of Cardiology, 10.1016/j.ijcard.2006.11.036, 122:1, (72-75), Online publication date: 1-Oct-2007. Garibaldi B and Zaas D (2007) AUTHOR REPLY—An Unusual Case of Cardiac Amyloidosis, Journal of General Internal Medicine, 10.1007/s11606-007-0287-0, 22:9, (1383-1383), Online publication date: 10-Aug-2007. Narumi H, Funabashi N, Takano H, Sekine T, Ueda M, Hori Y, Fukawa T, Minamino T, Kobayashi Y and Komuro I (2007) Remarkable thickening of right atrial wall in subjects with cardiac amyloidosis complicated with sick sinus syndrome, International Journal of Cardiology, 10.1016/j.ijcard.2006.07.103, 119:2, (222-224), Online publication date: 1-Jul-2007. NAQVI T (2007) Restrictive Cardiomyopathy: Diagnosis and Prognostic Implications The Practice of Clinical Echocardiography, 10.1016/B978-1-4160-3640-1.50033-2, (679-709), . Van Geluwe F, Dymarkowski S, Crevits I, De Wever W and Bogaert J (2006) Amyloidosis of the heart and respiratory system, European Radiology, 10.1007/s00330-006-0249-7, 16:10, (2358-2365), Online publication date: 1-Oct-2006. Plastiras S, Kelekis N and Tzelepis G (2006) Magnetic Resonance Imaging for the Detection of Myocardial Fibrosis in Scleroderma, New England Journal of Medicine, 10.1056/NEJMc053128, 354:20, (2194-2196), Online publication date: 18-May-2006. Parikh S and Lemos J (2005) Current therapeutic strategies in cardiac amyloidosis, Current Treatment Options in Cardiovascular Medicine, 10.1007/s11936-005-0029-8, 7:6, (443-448), Online publication date: 1-Nov-2005. January 18, 2005Vol 111, Issue 2 Advertisement Article InformationMetrics https://doi.org/10.1161/01.CIR.0000153623.02240.20PMID: 15657385 Originally publishedJanuary 18, 2005 Keywordsmagnetic resonance imagingEditorialsamyloidosisechocardiographyPDF download Advertisement SubjectsComputerized Tomography (CT)Heart FailureImagingMyocardial Biology
Referência(s)