Relevant bibliographies by topics / Cardiac amyloidosi

Academic literature on the topic 'Cardiac amyloidosi'

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Published: 9 March 2023
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Journal articles on the topic "Cardiac amyloidosi"

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Guan, Jian, Shikha Mishra, Rodney H. Falk, and Ronglih Liao. "Current perspectives on cardiac amyloidosis." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 3 (February 2012): H544—H552. http://dx.doi.org/10.1152/ajpheart.00815.2011.

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Amyloidosis represents a group of diseases in which proteins undergo misfolding to form insoluble fibrils with subsequent tissue deposition. While almost all deposited amyloid fibers share a common nonbranched morphology, the affected end organs, clinical presentation, treatment strategies, and prognosis vary greatly among this group of diseases and are largely dependent on the specific amyloid precursor protein. To date, at least 27 precursor proteins have been identified to result in either local tissue or systemic amyloidosis, with nine of them manifesting in cardiac deposition and resulting in a syndrome termed “cardiac amyloidosis” or “amyloid cardiomyopathy.” Although cardiac amyloidosis has been traditionally considered to be a rare disorder, as clinical appreciation and understanding continues to grow, so too has the prevalence, suggesting that this disease may be greatly underdiagnosed. The most common form of cardiac amyloidosis is associated with circulating amyloidogenic monoclonal immunoglobulin light chain proteins. Other major cardiac amyloidoses result from a misfolding of products of mutated or wild-type transthyretin protein. While the various cardiac amyloidoses share a common functional consequence, namely, an infiltrative cardiomyopathy with restrictive pathophysiology leading to progressive heart failure, the underlying pathophysiology and clinical syndrome varies with each precursor protein. Herein, we aim to provide an up-to-date overview of cardiac amyloidosis from nomenclature to molecular mechanisms and treatment options, with a particular focus on amyloidogenic immunoglobulin light chain protein cardiac amyloidosis.
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Musetti, Veronica, Francesco Greco, Vincenzo Castiglione, Alberto Aimo, Cataldo Palmieri, Dario Genovesi, Assuero Giorgetti, et al. "Tissue Characterization in Cardiac Amyloidosis." Biomedicines 10, no. 12 (November 28, 2022): 3054. http://dx.doi.org/10.3390/biomedicines10123054.

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Cardiac amyloidosis (CA) has long been considered a rare disease, but recent advancements in diagnostic tools have led to a reconsideration of the epidemiology of CA. Amyloid light-chain (AL) and transthyretin (ATTR) amyloidoses are the most common forms of cardiac amyloidosis. Due to the distinct treatments and the different prognoses, amyloid typing is crucial. Although a non-biopsy diagnosis can be obtained in ATTR amyloidosis when certain diagnostic criteria are fulfilled, tissue characterization still represents the gold standard for the diagnosis and typing of CA, particularly in AL amyloidosis. The present review focuses on the status of tissue characterization in cardiac amyloidosis, from histochemistry to immunohistochemistry and mass spectrometry, as well as on its future directions.
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Ablasser, Klemens, Nicolas Verheyen, Theresa Glantschnig, Giulio Agnetti, and Peter P. Rainer. "Unfolding Cardiac Amyloidosis –From Pathophysiology to Cure." Current Medicinal Chemistry 26, no. 16 (August 26, 2019): 2865–78. http://dx.doi.org/10.2174/0929867325666180104153338.

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Deposition of amyloidogenic proteins leading to the formation of amyloid fibrils in the myocardium causes cardiac amyloidosis. Although any form of systemic amyloidosis can affect the heart, light-chain (AL) or transthyretin amyloidosis (ATTR) account for the majority of diagnosed cardiac amyloid deposition. The extent of cardiac disease independently predicts mortality. Thus, the reversal of arrest of adverse cardiac remodeling is the target of current therapies. Here, we provide a condensed overview on the pathophysiology of AL and ATTR cardiac amyloidoses and describe treatments that are currently used or investigated in clinical or preclinical trials. We also briefly discuss acquired amyloid deposition in cardiovascular disease other than AL or ATTR.
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Yilmaz, A., J. Bauersachs, F. Bengel, R. Büchel, I. Kindermann, K. Klingel, F. Knebel, et al. "Diagnosis and treatment of cardiac amyloidosis: position statement of the German Cardiac Society (DGK)." Clinical Research in Cardiology 110, no. 4 (January 18, 2021): 479–506. http://dx.doi.org/10.1007/s00392-020-01799-3.

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AbstractSystemic forms of amyloidosis affecting the heart are mostly light-chain (AL) and transthyretin (ATTR) amyloidoses. The latter is caused by deposition of misfolded transthyretin, either in wild-type (ATTRwt) or mutant (ATTRv) conformation. For diagnostics, specific serum biomarkers and modern non-invasive imaging techniques, such as cardiovascular magnetic resonance imaging (CMR) and scintigraphic methods, are available today. These imaging techniques do not only complement conventional echocardiography, but also allow for accurate assessment of the extent of cardiac involvement, in addition to diagnosing cardiac amyloidosis. Endomyocardial biopsy still plays a major role in the histopathological diagnosis and subtyping of cardiac amyloidosis. The main objective of the diagnostic algorithm outlined in this position statement is to detect cardiac amyloidosis as reliably and early as possible, to accurately determine its extent, and to reliably identify the underlying subtype of amyloidosis, thereby enabling subsequent targeted treatment.
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Ruiz-Mori, Enrique, Leonor Ayala-Bustamante, Luis Taxa-Rojas, Cristian Pacheco-Román, Javier Alarcón-Santos, and Jorge Burgos-Bustamante. "Amiloidosis cardiaca: reporte de un caso." Horizonte Médico (Lima) 18, no. 4 (December 31, 2018): 81–89. http://dx.doi.org/10.24265/horizmed.2018.v18n4.12.

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Wisniowski, Brendan, and Ashutosh Wechalekar. "Confirming the Diagnosis of Amyloidosis." Acta Haematologica 143, no. 4 (2020): 312–21. http://dx.doi.org/10.1159/000508022.

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Amyloidosis is a general term for diseases characterised by the deposition of insoluble amyloid fibrils in organs or tissues, leading to organ dysfunction and, in many cases, death. Amyloid fibrils are derived from soluble precursor proteins, with the number of known amyloidogenic proteins increasing over time. The identity of the precursor protein often predicts the disease phenotype, although many of the amyloidoses have overlapping clinical features. Most patients with amyloidosis will require biopsy of an involved organ or tissue to confirm the diagnosis. Cardiac transthyretin amyloidosis, however, may be diagnosed without a biopsy provided stringent criteria are met. Where amyloid is confirmed histologically, the identity of the amyloidogenic protein must be determined, given several of the amyloidoses have disease-specific therapies. Laser capture microdissection and tandem mass spectrometry, LCM-MS, has revolutionised amyloid subtyping, being able to identify the amyloidogenic protein more reliably than antibody-based methods such as immunohistochemistry. Here we summarise the biopsy approach to amyloidosis, as well as the non-biopsy diagnosis of cardiac transthyretin amyloidosis. Proteomic and antibody-based methods for amyloid subtyping are reviewed. Finally, an algorithm for confirming the diagnosis of amyloidosis is presented.
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Theodorakakou, Foteini, Despina Fotiou, Meletios A. Dimopoulos, and Efstathios Kastritis. "Solid Organ Transplantation in Amyloidosis." Acta Haematologica 143, no. 4 (2020): 352–64. http://dx.doi.org/10.1159/000508262.

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Amyloidosis comprises a diverse group of diseases characterized by misfolding of precursor proteins which eventually form amyloid aggregates and preceding intermediaries, which are deposited in target tissues causing progressive organ damage. In all forms of amyloidosis, vital organs may fail; depending on the specific amyloidosis type, this may occur rapidly or progress slowly. Beyond therapies to reduce the precursor protein (chemotherapy for light chain [AL] amyloidosis, anti-inflammatory therapy in serum A amyloid­osis [AA], and antisense RNA therapy in transthyretin amyloidosis [ATTR]), organ transplantation may also be a means to reduce amyloidogenic protein, e.g., in types of amyloid­osis in which the variant precursor is produced by the liver. Heart transplantation is a life-saving approach to the treatment of patients with advanced cardiac amyloidosis; however, amyloidosis may still be considered a contraindication to the procedure despite data supporting improved outcomes, similar to patients with other indications. Kidney transplantation is associated with particularly favorable outcomes in patients with amyloidosis, especially if the precursor protein has been eliminated. Overall, outcomes of solid organ transplantation are improving, but more data are needed to refine the selection criteria and the timing for organ transplantation, which should be performed in highly experienced centers involving multidisciplinary teams with close patient follow-up to detect amyloid recurrence.
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Merlini, Giampaolo, David C. Seldin, and Morie A. Gertz. "Amyloidosis: Pathogenesis and New Therapeutic Options." Journal of Clinical Oncology 29, no. 14 (May 10, 2011): 1924–33. http://dx.doi.org/10.1200/jco.2010.32.2271.

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The systemic amyloidoses are a group of complex diseases caused by tissue deposition of misfolded proteins that results in progressive organ damage. The most common type, immunoglobulin light chain amyloidosis (AL), is caused by clonal plasma cells that produce misfolded light chains. The purpose of this review is to provide up-to-date information on diagnosis and treatment options for AL amyloidosis. Early, accurate diagnosis is the key to effective therapy, and unequivocal identification of the amyloidogenic protein may require advanced technologies and expertise. Prognosis is dominated by the extent of cardiac involvement, and cardiac staging directs the choice of therapy. Treatment for AL amyloidosis is highly individualized, determined on the basis of age, organ dysfunction, and regimen toxicities, and should be guided by biomarkers of hematologic and cardiac response. Alkylator-based chemotherapy is effective in almost two thirds of patients. Novel agents are also active, and trials are ongoing to establish their optimal use. Treatment algorithms will continue to be refined through controlled trials. Advances in basic research have led to the identification of new drug targets and therapeutic approaches, which will be integrated with chemotherapy in the future.
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Czyżewska, Emilia, Agnieszka Wiśniewska, Anna Waszczuk-Gajda, and Olga Ciepiela. "The Role of Light Kappa and Lambda Chains in Heart Function Assessment in Patients with AL Amyloidosis." Journal of Clinical Medicine 10, no. 6 (March 18, 2021): 1274. http://dx.doi.org/10.3390/jcm10061274.

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There are reports indicating that myocardial dysfunction in systemic immunoglobulin light chain amyloidosis (AL amyloidosis) stems not only from the amyloid deposit in the organ but also the cardiotoxicity of the amyloid precursor free light chains (FLCs) circulating in the blood. The aim of the study is to analyze the role of sFLC κ and λ in the assessment of heart involvement and the degree of myocardial damage in AL amyloidosis. The study involved 71 patients diagnosed with primary AL amyloidosis. The relationship between sFLC concentrations and cardiac biochemical and echocardiographic parameters was assessed. The median concentrations of N-terminal pro b-type natriuretic peptide(NT-proBNP) and troponin I (TnI) were significantly higher in patients with amyloids formed from monoclonal λ chains compared to patients with monoclonal κ proliferation. In patients with heart involvement by amyloids formed from monoclonal FLC, the study demonstrated a statistically significant positive correlation between the concentration of monoclonal antibody λ chain and TnI (R = 0.688; p < 0.05), NT-proBNP (R = 0.449; p < 0.05), and the value of diastolic dimension of the interventricular septum (IVS; R = 0.496, p < 0.05). The above data indicate that the presence of monoclonal λ chains in patients with AL amyloidosis may be associated with more severe damage to cardiomyocytes and dysfunction of the myocardium.
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Rameeva, A. S., V. V. Rameev, I. N. Bobkova, A. F. Safarova, Zh D. Kobalava, and S. V. Moiseev. "Leading Factors of Progression in Patients with Cardiac Amyloidosis." Rational Pharmacotherapy in Cardiology 18, no. 2 (May 5, 2022): 143–52. http://dx.doi.org/10.20996/1819-6446-2022-04-02.

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Aim. To describe prognostic meaning of cardiac and other principal clinical manifestations of systemic AL-amyloidosis in their interrelations.Material and methods. It has been made long-time survival analysis of 147 patients with systemic AL-amyloidosis. In the special investigation group (n=58) of AL (n=55) and ATTR (n=3) amyloidotic cardiopathy patients there were evaluated prognostically important structural and functional changes in myocardium with standard and impulse-wave tissue dopplerometric echocardiography in comparison with NTproBNP serum levels.Results. Even though significantly increased nowadays surviving of AL-amylodotic patients (Me=90 months) it has been found that as at previously time orthostatic hypotension and amyloid cardiopathy are being most severe initial syndromes (median 25 months), but after 1 year from diagnosis influence of these syndromes on surviving had decreased and most low surviving was more common in patients with CKD 3-5 (median 28 months). Influence of CKD 3-5 on surviving was associated predominantly with intracardial hemodynamics deterioration. Together with decreased systolic shortening strain rate (48,5%) decreased filtration rate (47,9%) was second of main factors contributing into NTproBNP increasing in effective multiple regression model (R=0,702, F(4,21)=5,095, p=0,005). NTproBNP level in less degree depended on renal clearance.Conclusion. Heart damage is one of the most prognostically unfavorable manifestations of systemic amyloidosis due to a sharp deterioration in the elastic properties of the myocardium, in the process of further development of amyloidosis, the leading factor in progression is the deterioration of the profile of cardiorenal interactions, the marker of which is the level of NTproBNP.
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Dissertations / Theses on the topic "Cardiac amyloidosi"

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RELLA, VALERIA. "AMILOIDOSI CARDIACA ANALISI DI PREVALENZA IN DUE STUDI MULTICENTRICI ITALIANI." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2022. http://hdl.handle.net/10281/366496.

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Tra i pazienti con diagnosi iniziale di cardiomiopatia ipertrofica afferiti a Centri di Riferimento per le Cardiomiopatie, l’AC è la malattia non riconosciuta più comune con una prevalenza complessiva del 9%, e che aumenta con l'età (dall'1% nella fascia di età tra i 40-49 anni al 26% sopra gli 80 anni). Nella popolazione generale ≥55 anni più del 7% ha almeno un reperto ecocardiografico suggestivo di AC e l’ispessimento del setto interatriale è quello più frequente. I pazienti con elevato sospetto di AC (≥3 reperti) rappresentano l’1% della popolazione generale e il 4,9% di quelli con cuore non dilatato, ipertrofico e con FE normale.
Among patients with initial diagnosis of HCM, cardiac amiloidosis has a prevalence of 9% and it increases with age. In the general population > 55 yo more than 7% has echocardiographic suspicion of the disease and echocardiography has an important role in the early diagnosis of the disease
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Lachira-Yparraguirre, Lizbeth, Ali Al-kassab-Córdova, Edgar Quispe-Silvestre, and Daniel Enriquez-Vera. "Cardiac amyloidosis secondary to waldenström macroglobulinemia." Editorial Ciencias Medicas, 2020. http://hdl.handle.net/10757/655705.

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Introduction: Waldenström's macroglobulinemia is a hematological neoplasm belonging to the group of monoclonal gammopathies, which includes systemic symptoms and those related to an increase in M paraprotein. Objective: To describe a case of cardiac amyloidosis associated with macroglobulinemia. Clinical case: Male patient who was admitted for asthenia, dysphonia, and who, during his evolution, developed progressive dyspnea, heart failure and pleural effusion. Additionally, echocardiography showed myocardial granular pattern, while pleural biopsy was positive for Congo red staining. Subsequently, he received treatment with bortezomib, dexamethasone and rituximab, with favorable evolution. Conclusions: In this disease, early diagnosis is an important advantage for survival. Therefore, its management is palliative of cardiac manifestations. The present case shows a diagnostic challenge, in which the less frequent etiologies of heart failure must be taken into account.
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Arvidsson, Sandra. "Cardiac function in hereditary transthyretin amyloidosis : an echocardiographic study." Doctoral thesis, Umeå universitet, Institutionen för folkhälsa och klinisk medicin, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-113891.

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Background: Hereditary transthyretin amyloidosis (ATTR) is a lethal disease in which misfolded transthyretin (TTR) proteins accumulate as insoluble aggregates in tissues throughout the body. A common mutation is the exchange of valine to methionine at place 30 (TTR V30M), a form endemically found in the northern parts of Sweden. The main treatment option for ATTR amyloidosis is liver transplantation as the procedure halts production of mutated transthyretin. The disease is associated with marked phenotypic diversity ranging from predominant cardiac complications to pure neuropathy. Two different types of fibril composition – one in which both fragmented and full-length TTR are present (type A) and one consisting of only full-length TTR (type B) have been suggested to account for some phenotypic differences. Cardiac amyloidosis is associated with increased myocardial thickness and the disease could easily be mistaken for other entities characterised by myocardial thickening, such as sarcomeric hypertrophic cardiomyopathy (HCM). The aims in this thesis were to investigate echocardiographic characteristics in Swedish ATTR amyloidosis patients, and to identify markers aiding in differentiating ATTR heart disease from HCM. Another objective was to examine the impact of fibril composition and sex on the phenotypic variation in amyloid heart disease. Methods: A total of 122 ATTR amyloidosis patients that had undergone thorough echocardiographic examinations were included in the studies. Analyses of ventricular geometry as well as assessment of systolic and diastolic function were performed, using both conventional echocardiographic methods and speckle tracking technique. ECG analysis was conducted in study I, allowing measurement of QRS voltage. In study I and study II ATTR patients were compared to patients with HCM. In addition, 30 healthy controls were added to study II. Results: When parameters from ECG and echocardiography were investigated, the results revealed that the combination of QRS voltage <30 mm (<3 mV) and an interventricular/posterior wall thickness quotient <1.6 could differentiate cardiac ATTR amyloidosis from HCM. Differences in degree of right ventricular involvement were also demonstrated between HCM and ATTR amyloidosis, where ATTR patients displayed a right ventricular apical sparing pattern whereas the inverse pattern was found in HCM. Analysis of fibril composition revealed increased LV wall thickness in type A patients compared to type B, but in addition type A women displayed both lower myocardial thickness and more preserved systolic function as compared to type A males. When cardiac geometry and function were evaluated pre and post liver transplantation in type A and B patients, significant deterioration was detected in type A but not in type B patients after liver transplantation. Conclusions: Increasing awareness of typical cardiac amyloidotic signs by echocardiography is important to reduce the risk of delayed diagnosis. Our classification model based on ECG and echocardiography could aid in differentiating ATTR amyloidosis from HCM. Furthermore, the apical sparing pattern found in the right ventricle may pose another clue for amyloid heart disease, although it requires to be studied further. Furthermore, we disclosed that type A fibrils, male sex and increasing age were important determinants of increased myocardial thickness. As type A fibril patients displayed rapid cardiac deterioration after liver transplantation other treatment options should probably be sought for this group of patients.
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Dungu, Jason N. "Cardiac transthyretin amyloidosis in the British African and Caribbean population." Thesis, St George's, University of London, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.676103.

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Cardiac amyloidosis is a condition characterised by infiltration of the myocardium with fibrillar proteins. Transthyretin (TTR) is a plasma protein that may form amyloid fibrils and the V122I mutant form of TTR is associated with isolated cardiac amyloidosis. Previous studies have estimated a 4% V122I allele frequency in African Americans. The prevalence of cardiac transthyretin amyloidosis (ATTR) V122I in the British population is not known. I was awarded a British Heart Foundation Clinical Research Fellowship to investigate the diagnosis and prevalence of ATTR V122I in the UK population. More than one million people of Afro-Caribbean ethnicity live in the Greater London area, and in the local ward of Wandsworth make up more than 10% of the population (2011 census data). The prevalence of ATTR V122I at St George's Hospital was high, affecting 12% of all Afro-Caribbean heart failure patients aged ~60 years. The estimated incidence of ATTR V122I in Afro-Caribbean subjects in the St George's Hospital catchment area was over twice the reported incidence of amyloidosis of all types in the general, predominantly Caucasian, UK population. The clinical phenotype is characterised by resistant heart failure, increased wall thickness and diastolic dysfunction on echocardiography and poor outcomes (median survival 29 months). The ECG had poor sensitivity to detect ATTR V122I because 25% of patients present with left ventricular hypertrophy criteria, contrary to the reported low voltage complexes widely reported in AL amyloidosis. Cardiovascular magnetic resonance (CMR) imaging demonstrated extensive late gadolinium enhancement (LGE) and I developed a novel LGE scoring system to differentiate ATTR from AL amyloidosis with high accuracy. A simple diagnostic algorithm to detect new cases of ATTR amyloidosis was retrospectively employed at a separate tertiary heart failure clinic and demonstrated that 5.2% of elderly black patients had ATTR amyloidosis, having previously been given a diagnosis of hypertensive heart failure. Improved detection of ATTR amyloidosis is increasingly important as novel treatments are now undergoing phase 3 clinical trial assessment and newly diagnosed patients now have the potential for disease modifying therapies. This will have implications for counselling and family screening of this inherited autosomal dominant condition in the future.
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Rausch, Karen. "Application of left atrial strain assessment by 2D echocardiography in cardiac conditions involving the left atrium including cardiac amyloidosis." Thesis, Griffith University, 2020. http://hdl.handle.net/10072/400573.

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The left atrium (LA) plays an important role in the modulation of LV filling and contributes to LV stroke volume with atrial contraction. Despite this important role, much research to date has been focused on the ventricles in disease, rather than the atria. In recent years there has been increasing interest and excitement in the function of the LA in normal and disease states – no longer is the LA secondary to the left ventricle (LV). The LA has three major functions: reservoir, conduit and contractile. The LA acts as a reservoir during ventricular systole as it fills with blood via the pulmonary veins and expands in size, subsequently, the mitral valve opens and the conduit phase is this passing of blood from the LA to the LV due to a small pressure gradient. Lastly, atrial systole, or the ‘atrial kick’, provides further augmentation of the LV stroke volume at the end of ventricular diastole. Methods for non-invasive assessment of these LA functions have been limited due to echocardiographic technology and the cumbersome nature data collection for these parameters. Prior techniques included assessment of LA size, phasic changes in LA size or volume as well as a variety of Doppler parameters which provided a cruder assessment of the LA functions. Strain is a unitless measurement of myocardial deformation and can be applied to assess the three LA functions in more detail. Contemporary strain research uses 2D-speckle tracking echocardiography (STE), where strain represents a fraction change in myocardial length relative to baseline and is expressed as a percentage. As strain technology surges forward with now dedicated LA strain software packages, the importance of the left atrium has become increasingly recognised. Improved strain technology has allowed easier and more widely available assessment of the three LA functions. Several studies have now documented normal LA strain values in large populations, and specifically, variations due to age and gender. Multiple literature reviews and guideline documents from cardiac imaging bodies have provided a standardised basis for acquisition of LA strain and the language used to describe LA functions and strain values. Previously, different gating techniques, software and terminology made comparison of literature more challenging. Interest and guidance from these peak bodies such as the European society of cardiovascular imaging confirms the importance of LA strain moving forward. There are many disease states which impact upon LA function and further study of LA strain in these areas may allow identification of subclinical atrial disease and impact on diagnostic or treatment pathways. In reviewing the literature, this thesis examines the current knowledge for clinical applications of LA strain in various pathologies/disease states. To contribute to current LA strain research, this thesis goes on to investigate the reproducibility of the LA strain technique, comparing strain readers of different expertise. This is an important step for uptake of LA strain into widespread use. The study showed LA strain was highly reproducible by a novice strain reader using multi-vendor analysis software and secondly, that there was good interobserver reproducibility between novice and experts. The thesis goes on to investigate the use of LA strain in a specific clinical scenario - cardiac amyloidosis (CA). Cardiac amyloidosis is a condition leading to amyloid protein deposition in cardiac tissue and subsequent organ dysfunction. Recent studies have shown that CA leads to LA dysfunction and abnormal LA strain and strain rate values. Given many different conditions can lead to reduction in LA strain, further investigation into changes and degree of LA dysfunction with CA compared to mimicking pathologies is of importance. Ventricular hypertrophy due hypertension can make differentiation of cardiac amyloidosis difficult using echocardiography alone – particularly when clinical history of hypertension is not previously known. The second original research study confirms a severe reduction in LA function in patients with cardiac amyloidosis, concordant with that seen in other studies. Additionally, LA function in CA was significantly worse compared to the hypertensive group, despite similar increases in LV wall thickness. Therefore, LA strain may provide incremental value in differentiating cardiac amyloidosis from increased LV wall thickness secondary to hypertension. Further investigation with larger cohorts and comparison between strain values in CA and other infiltrative pathologies should be considered to improve observe how specific this severe reduction in LA strain values is for CA compared to other infiltrative pathologies causing increased LV wall thickness. LA strain is a promising emerging tool, the applications of which will be further explored in this thesis.
Thesis (Masters)
Master of Philosophy (MPhil)
School of Medicine
Griffith Health
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Pilebro, Björn. "The heart in hereditary transthyretin amyloidosis : clinical studies on the impact of amyloid fibril composition." Doctoral thesis, Umeå universitet, Medicin, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-139495.

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Background Hereditary transthyretin amyloid (ATTRm) amyloidosis is a systemic disease mainly affecting the peripheral nervous system and the heart. The disease is inherited in an autosomal dominant manner with a varying penetrance. It is caused by mutations in the transthyretin (TTR) gene. Today more than 100 disease causing mutations are known. The V30M mutation that is endemic in northern Sweden is the best studied and comprises the majority of the reported disease cases in the world. In ATTRm amyloidosis caused by the V30M mutation two distinct sub populations are seen, one with disease onset early in life and a mainly neuropathic disease and the other with late onset disease and both neuropathic disease and a progressive cardiomyopathy. These phenotypical findings have in Swedish patients been tied to differences in amyloid fibril composition. Generally, patients with early onset disease have amyloid fibrils containing only full length transthyretin (type B) whereas patients with late onset disease have amyloid containing both full length and fragmented transthyretin (type A). Until recently, the only available treatment for the disease has been liver transplantation. Patients with type A fibrils, especially males, have significantly worse survival after liver transplant due to progressive amyloid cardiomyopathy. Furthermore, it appears that type A fibrils may be the most common finding in other mutations. This thesis work aims to in depth investigate the impact amyloid fibril composition has on cardiac manifestations of the disease and on the outcome of available and novel modalities for cardiac amyloid imaging. Methods The four studies included in the thesis were done as part of the on going clinical research at the Swedish centre for transthyretin amyloidosis in Umeå.  Patients in whom amyloid fibril composition had been determined were included. Available echocardiographic data were analysed to find predictors for left ventricular hypertrophy and systolic function as measured by strain analysis in a large cohort of 105 patients (paper I). Serial 12-lead electrocardiograms from 98 patients were gathered and retrospectively interpreted and analysed to investigate the impact of amyloid fibril composition and disease progression on frequency and development of ECG abnormalities (paper IV).  DPD scintigraphy, cardiac biomarkers, clinical data and echocardiograms were analysed in a cohort of 53 consecutive patients. to assess the impact of amyloid fibril composition on the outcome of DPD scintigraphy and its relationship with cardiac hypertrophy. (paper II). To evaluate the usefulness of positron emission tomography (PET) using the amyloid specific tracer PIB, 10 patients, five with each fibril type, were selected and examined. The patients selected had a similar age of onset and similar echocardiographic findings (paper III). Results Paper I: Type A fibrils, male gender and age were independent factors associated with increased LV thickness. The distribution of amyloid fibril composition did not differ between the sexes, but in patients with type A fibrils, females had lower median cardiac wall thickness (p<0.01and better left ventricular septal strain (p=0.04).The gender differences were not apparent in patients with type B fibrils. Paper II: Ninety-seven per cent of patients with type A fibrils had pathological cardiac DPD uptake compared to none of the patients with type B fibrils. Among patients with normal septal thickness, none of 15 patients with type B fibrils had positive scintigraphy compared with 2 out of 2 with type A fibrils (P<0.01) Cardiac biomarkers, demographic data and cardiac biomarkers were significantly different, but could not differentiate between type A and type B fibrils in individual patients. Paper III: All patients had pathological cardiac PIB retention. In patients with type B fibrils the retention was significantly higher (p<0.01) than in patients with type A fibrils. Based on the selection criteria, no significant differences were seen in various echocardiographic measurements. Paper IV: All patients had a high prevalence of AV-blocks, LAH and anterior infarction pattern. Patients with type A fibrils had significantly more electrocardiographic abnormalities compared to those with type B fibrils, both at an early stage of diseases and at later follow up. Conclusion Type A fibrils are associated with more pronounced cardiac involvement, which appear to be more severe in males than in females. In study II we showed that DPD scintigraphy appears to be a very good tool for non-invasive determination of amyloid fibril composition. Papers III and IV show that patients with type B amyloid have cardiac involvement even without echocardiographic or DPD-scintigraphic evidence of amyloid cardiomyopathy and that ECG abnormalities are common irrespectively of amyloid fibril composition, and increase with time for both groups.
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Hörnsten, Rolf. "Cardiac arrhythmias and heart rate variability in familial amyloidotic polyneuropathy : a clinical study before and after liver transplantation /." Umeå : Univ, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1407.

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Hörnsten, Rolf. "Cardiac arrhythmias and heart rate variability in familial amyloidotic polyneuropathy : A clinical study before and after liver transplantation." Doctoral thesis, Umeå universitet, Kirurgisk och perioperativ vetenskap, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1407.

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Familial amyloidotic polyneuropathy (FAP), found in the northernmost counties in Sweden, is a rare, lethal and inherited amyloidosis. The disease is caused by mutated transthyretin (TTR). The mutation is characterized by an exchange of valine for methionine at position 30 (ATTRVal30Met). FAP is characterised by progressive polyneuropathy affecting both the peripheral and autonomic nervous system (ANS). Cardiac arrhythmia and autonomic disturbances are common as well as gastrointestinal symptoms: such as constipation and diarrhoea. Today, orthotopic liver transplantation (LTx) is the only treatment to stop the progression of FAP. The rationale for this is because 95% of TTR is synthesized by the liver, a liver transplantation should abolish the production of new mutated amyloidogenic TTR. The first liver transplantation for FAP was performed in Sweden 1990. Heart complications and autonomic disturbances are common in FAP patients both before and after liver transplantation. The aim of the present study was three-fold: to determine whether liver transplantation affects the natural course of cardiac arrhythmias and cardiac autonomic function; to predict the risk of ventricular arrhythmias; and to elucidate heart rate variability (HRV) patterns by power spectrum analysis and Poincaré plots. In total, ninety-seven Swedish FAP patients were included in the studies. The patients underwent 24-hours electrocardiography (Holter) recordings, and/or signal averaged electrocardiography (SAECG) and heart rate variability. The study showed that many patients developed cardiac arrhythmias and conduction disturbances after LTx. Approximately 25 percent of patients were pacemaker treated after LTx. The SAECG recordings disclosed that many FAP patients had ventricular late potentials (LP) compared with healthy subjects, and that LP were associated with nonsustained ventricular arrhythmia. Analyses of heart rate variability (HRV) showed reduced autonomic function in the majority of patients. Some patients had high HRV with broadband power spectra and Poincaré graphs with a fan or complex pattern. These novel findings could be an indicator of ECG abnormalities (subtle atrial arrhythmia) in FAP patients instead of reflecting normal cardiac autonomic modulation. The HRV studies also showed that LTx preserves cardiac autonomic function in FAP. In conclusion, cardiac arrhythmias, late potentials and reduced heart rate variability were common in Swedish patients with FAP, whether they underwent liver transplantation or not. The absence of LP may indicate a low risk for ventricular tachycardia in FAP patients.
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Damerjian, Vera. "La caractérisation du speckle sur des images échocardiographiques afin de définir des indices diagnostiques de l'amylose cardiaque et personnaliser un modèle numérique du coeur." Thesis, Paris Est, 2016. http://www.theses.fr/2016PESC1035.

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L’Hypertrophie Ventriculaire Gauche (HVG) est actuellement mise en évidence par échographie. Cet examen fournit des informations anatomo-fonctionnelles mais ne permet pas de déterminer l’étiologie des HVG, ce qui engendre de graves erreurs de diagnostic et de prise en charge thérapeutique. Les HVG sont classiquement séparées en 2 catégories :1. pathologies hypertrophiques induites par la modification structurelle et fonctionnelle des cardiomyocites qui tend à compenser des insuffisances cardiaques liées par exemple à des problèmes d’hypertension artérielle, de rétrécissement aortique ou de CardioMyopathies Hypertrophiques sarcomériques ;2. pathologies infiltratives correspondant au dépôt de protéines dans la matriceextracellulaire principalement dues à différentes formes d’amyloses cardiaquesNotre hypothèse est que les différents mécanismes physiopathologiques (hypertrophique ou infiltratif) pourraient se traduire dans l’image par des propriétés spécifiques du speckle échographique. Nous avons donc développé un travail d’analyse de la texture de ces images afin de discriminer les différentes HVG.Dans cette étude, la base de données de 4795 images est divisée en une base d’apprentissage de 3770 images et une base de test de 1025 images. L’analyse de texture des images est faite par les ondelettes de Gabor avec 8 orientations, 7 tailles et 5 niveaux de décomposition. Ensuite, les caractéristiques statistiques de premier et deuxième ordre sont extraites des images. Le nombre des caractéristiques est réduit pour la base d’apprentissage en appliquant l’Analyse en Composantes Principales (ACP) suivie par l’analyse discriminante linéaire (ADL) pour une séparation supervisée des classes. Les caractéristiques extraites pour la base de test sont projetées sur les vecteurs propres sélectionnés au cours de l’apprentissage. L’ADL est appliquée à ce niveau pour la classification des données du test et la qualité de cette classification est évaluée. Les résultats obtenus sont bons (qualité totale de classification de 95,51%) et sont suivis d’une étape de cross-validation afin de vérifier la robustesse de notre méthode. A cette étape, les bases de données de l’apprentissage et du test sont mélangées et 50 combinaisons différentes sont évaluées. La même méthode décrite précédemment est appliquée. La cross-validation montre une variation de la qualité de classification (entre 30% et 99.96%) probablement due à l’hétérogénéité des caractéristiques texturelles pour les patients d’une même classe que l’on peut expliquer par des degrés différents d’avancement dans la pathologie.Ces travaux montrent qu’une analyse de texture des images échocardiographiques peut permettre de déterminer des bio-marqueurs aptes à discriminer différentes cardiopathies qui s’expriment par une HVG. Ce résultat peut avoir des retombées très importantes dans la détection précoce des amyloses cardiaques, maladies engendrant un fort taux de mortalité souvent dû à un retard de diagnostic et prise en charge des patients par un centre expert
Left-Ventricular Hypertrophy (LVH) is currently detected through echocardiography. The latter imaging modality provides anatomical and functional information. However, it does not allow the determination of the HVG etiology. This can, in turn, lead to dangerous errors in the diagnosis and treatment planning of the disease. LVH pathologies are separated into two categories:- Hypertrophic pathology caused by the structural and functional modification of cardiomyocytes that lead to cardiac failure related, for example, to arterial hypertension problems, aortic narrowing or sarcomeric hypertrophic cardiomyopathies.- Infiltrative pathologies corresponding to protein deposits on the extracellular matrix, mainly due to different forms of cardiac amyloidosisOur hypothesis is that different physiopathological mechanisms (hypertrophic or infiltrative) can be translated in the image through properties specific to echographic speckle. We have therefore developed the work of texture analysis of such images in order to discriminate the different types of LVH.In this study, the database of 4795 images is divided into a learning database of 3770 images and another testing database of 1025 images. The textural analysis of these images is done using Gabor wavelets with 8 orientations, 7 sizes and 5 decomposition levels. Next, the statistical characteristics of first and second orders are extracted from the filtered images. The number of characteristics is reduced for the learning database by applying Principal Component Analysis (PCA) followed by Linear Discriminant Analysis (LDA) for a supervised separation of the classes. The extracted characteristics for the test database are projected on the eigenvectors selected in the learning step. LDA is applied at this level for the test data classification, and the quality of this classification is evaluated. The obtained results are good (total classification quality of 95.51%). A step of cross-validation follows in order to verify the robustness of our method. At this stage, the learning and testing databases are mixed, and 50 different combinations are evaluated. The same method described previously is then applied. The cross-validation shows a variation in the classification quality (between 30% and 99.96%) probably due to the heterogeneity of the texture characteristics for the patients of the same class explained by different disease advancement stages.This work shows that the textural analysis of echocardiographic images can permit the determination of bio-markers suitable to discriminate different LVH cardiopathies. Our results can have a very important impact on the early detection of cardiac amyloidosis, a pathology causing a considerable rate of mortality often due to a belated diagnosis and support by the centers of expertise
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Nokwe, Nkumbe Cardine [Verfasser], Johannes [Akademischer Betreuer] [Gutachter] Buchner, and Bernd [Gutachter] Reif. "Molecular determinants and mechanisms of antibody light chain (AL) amyloidosis / Cardine Nokwe Nkumbe ; Gutachter: Bernd Reif, Johannes Buchner ; Betreuer: Johannes Buchner." München : Universitätsbibliothek der TU München, 2014. http://d-nb.info/1122738293/34.

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Books on the topic "Cardiac amyloidosi"

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Zacek, Pavel. Amyloidosis and Cardiac Surgery. INTECH Open Access Publisher, 2012.

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Sabharwal, Nikant, Parthiban Arumugam, and Andrew Kelion. Other nuclear cardiological investigations. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759942.003.0011.

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This chapter explains the imaging protocol physiological properties and clinical value of other nuclear cardiological investigations. It covers iodine-123-labelled radiopharmaceuticals, iodine-123-meta-iodo-benzyl-guanidine (123I-MIBG), β‎-methyl-p-[123I]iodo-phenyl-pentadecanoic acid (123I-BMIPP), and Tc-phosphate scintigraphy for cardiac amyloidosis, exploring both practical and clinical aspects. Specific prognoses and diagnoses are also detailed for the relevant investigation, including systolic heart failure, coronary artery disease, and cardiac amyloidosis.
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Lombardi, Massimo, and Antonia Camporeale. Cardiovascular magnetic resonance in less common pathologies. Edited by Dudley Pennell. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0111.

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Contrast-enhanced cardiovascular magnetic resonance plays a pivotal role in diagnostic and prognostic definition of less common pathologies such as Anderson–Fabry disease, cardiac amyloidosis, left ventricular non-compaction, sarcoidosis, and cardiac iron loading.
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Płońska-Gościniak, Edyta, Michal Ciurzynski, Marcin Fijalkowski, Piotr Gosciniak, Piotr Szymanski, Tomasz Pasierski, Daniel Rodriguez Muñoz, and José Luis Zamorano. Cardiac involvement in systemic diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0057.

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Cardiovascular features in systemic diseases are common. Transthoracic echocardiography represents a first-line diagnostic tool among these patients. Pericarditis is the most frequent cardiac complication of rheumatoid arthritis. In systemic lupus erythematosus, echocardiography shows usually small or moderate pericardial effusion in up to 55% of patients. In this group, Libman-Sacks vegetations develop mainly on the mitral valve but also can be seen on other valves. Pulmonary hypertension is one of the most important complications adversely influencing survival of systemic sclerosis patients. In antiphospholipid syndrome, the most common echocardiographic abnormality is diffuse or focal leaflet thickening, seen in 40-60% of subjects. Among Marfan syndrome patients, aortic root aneurysm is the most dangerous complication. In this chapter the authors also report the echocardiographic abnormalities occurring in rare systemic diseases including carcinoid, haemochromatosis, sarcoidosis, and amyloidosis. Moreover, echocardiographic changes in neoplastic disease and in patients undergoing chemotherapy and/or radiotherapy are also described.
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Klarich, Kyle W. The Heart and Systemic Disease, Pregnancy and Heart Disease, and Miscellaneous Cardiac Disorders. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0047.

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Many systemic diseases may have manifestations in the heart. This section describes those that are most likely to be included on the examination: hyperthyroidism, hypothyroidism, diabetes mellitus, amyloidosis, hemochromatosis, carcinoid disease, systemic lupus erythematosus, hypereosinophilic syndrome, scleroderma, and rheumatoid arthritis, among others, are included. Sections on pericardial disease, tumors of the heart, and valve diseases are covered. Physiologic changes of the heart in pregnancy and their effect on existing heart disease are also reviewed.
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Lancellotti, Patrizio, and Bernard Cosyns. Systemic Disease and Other Conditions. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713623.003.0017.

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This chapter describes the effect of various activities on the heart and associated disorders. It details the echocardiographic findings of athlete’s heart and differential diagnosis. It considers pregnancy which induces several haemodynamic changes: increase in heart rate, stroke volume, cardiac output, and decrease in systemic vascular resistance. Several echocardiographic changes may also present in normal pregnancy and these must be recognized. Echocardiography should be performed in each pregnant woman with cardiac signs or symptoms to search for new cardiac disease occurring during pregnancy and especially peripartum cardiomyopathy. Pregnancy is well tolerated by most woman with cardiac disease. Pregnancy in contraindicated in woman with pulmonary hypertension. Although the heart is not the principal affected organ in systemic disease there is some involvement. This chapter also details the echo findings of a range of systemic diseases including amyloidosis, connective tissue disease, endocrine disease, and HIV.
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Dorbala, Sharmila, and Katarina H. Nelson. Inflammatory and Infiltrative Diseases and Tumors. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199392094.003.0026.

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This chapter highlights some of the novel clinical radionuclide imaging strategies beyond perfusion imaging including inflammatory diseases, infiltrative diseases and tumors. Targeted molecular imaging techniques to evaluate cardiac amyloidosis as well as myocardial and vascular inflammation are addressed. Clinical 18F-FDG imaging of cardiac sarcoidosis, cardiovascular prosthetic valve and device infections, systemic vasculitis, and tumors are discussed in detail. For each of these pathologies, a concise overview of the disease pathophysiology and management pertinent to understanding of imaging techniques is provided followed by details of imaging including radiotracers, imaging techniques and image interpretation with a reference to societal guidelines. The published data on the utility of radionuclide imaging tests to assess diagnosis, prognosis and to monitor response to therapy are discussed. Clinical scenarios and available societal recommendations on the use of imaging are illustrated. The strengths and limitations of radionuclide techniques are discussed in the context of a comparison to echocardiography, cardiac magnetic resonance imaging, cardiac CT and endomyocardial biopsy. Future directions in imaging and ongoing clinical trials in these areas are listed at the end of each section.
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Kelion, Andrew, Parthiban Arumugam, and Nikant Sabharwal. Nuclear Cardiology (Oxford Specialist Handbooks in Cardiology). Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759942.001.0001.

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Readable, practical, and concise, the Oxford Specialist Handbook in Nuclear Cardiology is a self-contained guide to this cardiac imaging subspecialty. Including both technical and clinical aspects, it provides a foundation of essential knowledge common to practitioners from any background.This title covers radiation physics, biology and protection, and addresses all areas of imaging including the design and operation of the gamma camera (including solid-state cameras), single photon emission computed tomography (SPECT) acquisition and processing, and image interpretation and writing of reports. Stress testing and radiopharmaceuticals are explained in detail, as is the evidence base underpinning myocardial perfusion scintigraphy. Newer radionuclide imaging techniques are well covered (e.g. phosphate scintigraphy in cardiac amyloidosis), as is the expanding field of cardiac positron emission tomography (PET). Fully updated with coverage of new indications for gamma camera imaging, increased focus on attenuation correction and SPECT-CT, and detail on the design use and clinical implications of solid-state gamma cameras throughout, this second edition of the essential text for nuclear cardiology trainees and practitioners is fully illustrated with colour plates to aid clinical practice. Presented in the bestselling Oxford Handbook format, Nuclear Cardiology provides core knowledge for those training in the subspecialty, whether at a basic or advanced level or from a medical or technical background, and is a key resource for those seeking to accredit in the subspecialty.
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Book chapters on the topic "Cardiac amyloidosi"

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Tan, Carmela D., and E. Rene Rodriguez. "Cardiac Amyloidosis." In Current Clinical Pathology, 391–411. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19294-9_29.

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Alpert, Martin A. "Cardiac Amyloidosis." In Cancer and the Heart, 162–74. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4612-4898-9_14.

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Barbarossa, Alessandro, and Erika Baiocco. "Cardiac Amyloidosis." In Clinical Cases in Cardiology, 129–39. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19926-9_12.

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Tan, Carmela D., and E. Rene Rodriguez. "Cardiac Amyloidosis." In Amyloid and Related Disorders, 319–37. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-60761-389-3_26.

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Wong, Liza S. M., and Daniel P. Judge. "Cardiac Amyloidosis." In Clinical Cardiogenetics, 167–77. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-45457-9_10.

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Sun, Jing Ping, Xing Sheng Yang, Bryan P. Yan, and Ka-Tak Wong. "Cardiac Amyloidosis." In Comparative Cardiac Imaging, 267–79. Chichester, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119453192.ch49.

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Sun, Jing Ping, and Dan Sorescu. "Cardiac Amyloidosis." In Practical Handbook of Echocardiography, 275–78. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444320367.ch84.

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Lee Chuy, Katherine, Saurabh Malhotra, and Jennifer E. Liu. "Cardiac Amyloidosis." In Atlas of Imaging in Cardio-Oncology, 153–71. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-70998-3_18.

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Haaf, Philip, Irene A. Burger, Michael J. Zellweger, Pankaj Garg, and Cristina E. Popescu. "Cardiac Amyloidosis." In Imaging of Inflammation and Infection in Cardiovascular Diseases, 37–69. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-81131-0_3.

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Drozdz, J., and R. Erbel. "Cardiac Amyloidosis." In Atlas of Tissue Doppler Echocardiography — TDE, 101–13. Heidelberg: Steinkopff, 1995. http://dx.doi.org/10.1007/978-3-642-47067-7_11.

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Conference papers on the topic "Cardiac amyloidosi"

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Connolly, M., A. Fallon, D. Waterhouse, and R. O’Hanlon. "45 Progression of cardiac amyloid fibril infiltration in cardiac amyloidosis using cardiac magnetic resonance." In Irish Cardiac Society Annual Scientific Meeting & AGM, Thursday October 4th – Saturday October 6th 2018, Galway Bay Hotel, Galway, Ireland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-ics.45.

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Tran, T., K. Tsarova, H. Desai, and W. G. Carlos. "An Atypical and Acute Presentation of Cardiac Amyloidosis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3491.

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Kotecha, Tushar, Esther Gonzalez-Lopez, Andrej Corovic, Sarah Anderson, Liza Chacko, James Brown, Dan S Knight, et al. "21 Intracardiac thrombi in cardiac amyloidosis, a common finding." In British Society of Cardiovascular Magnetic Resonance 2019 annual meeting, March 26 – 27th, Oxford UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bscmr.21.

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Khalique, Z., PF Ferreira, AD Scott, S. Nielles-Vallespin, R. Wage, A. Martinez-Naharro, M. Fontana, PN Hawkins, DN Firmin, and DJ Pennell. "7 Diffusion tensor cardiovascular magnetic resonance in cardiac amyloidosis." In British Society of Cardiovascular Magnetic Resonance 2019 annual meeting, March 26 – 27th, Oxford UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bscmr.7.

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Ouzir, Nora, Olivier Lairez, Adrian Basarab, and Jean-Yves Tourneret. "Tissue motion estimation using dictionary learning: Application to cardiac amyloidosis." In 2017 IEEE International Ultrasonics Symposium (IUS). IEEE, 2017. http://dx.doi.org/10.1109/ultsym.2017.8092152.

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Ouzir, Nora, Olivier Lairez, Adrian Basarab, and Jean-Yves Tourneret. "Tissue motion estimation using dictionary learning: Application to cardiac amyloidosis." In 2017 IEEE International Ultrasonics Symposium (IUS). IEEE, 2017. http://dx.doi.org/10.1109/ultsym.2017.8092317.

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Scully, Paul R., Thomas A. Treibel, Marianna Fontana, Neil Hartman, Guy Lloyd, Francesca Pugliese, Nikant Sabharwal, et al. "1 A multi-centre study of cardiac amyloidosis in tavi patients." In British Cardiovascular Imaging Meeting 2018, 2–4th May 2018, Edinburgh. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcvi.42.

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Scully, Paul R., Thomas A. Treibel, Ernst Klotz, Emily Castle, Joanna Yap-Sanderson, Bunny Saberwal, Shahram Ahmadvazir, et al. "3 The detection of cardiac amyloidosis using extracellular volume quantification by computed tomography." In British Cardiovascular Imaging Meeting 2018, 2–4th May 2018, Edinburgh. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcvi.3.

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Giblin, G., A. Gray, L. Murphy, E. Kavanagh, C. Tracey, C. Howley, and N. Murphy. "35 Observational study to determine the prevalence of transthyretin amyloidosis in an undifferentiated heart failure with preserved ejection fraction population." In Irish Cardiac Society Annual Scientific Meeting & AGM (Virtual), October 1st – 3rd 2020. BMJ Publishing Group Ltd and British Cardiovascular Society, 2020. http://dx.doi.org/10.1136/heartjnl-2020-ics.35.

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Kotecha, Tushar, Ana Martinez-Naharro, James Brown, Callum Little, Daniel Knight, Alexandros Steriotis, Niket Patel, et al. "19 Myocardial perfusion mapping in cardiac amyloidosis- unearthing the spectrum from infiltration to ischaemia." In British Society of Cardiovascular Magnetic Resonance 2019 annual meeting, March 26 – 27th, Oxford UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bscmr.19.

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