Literatura académica sobre el tema "Primary dilated cardiomyopathy"
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Artículos de revistas sobre el tema "Primary dilated cardiomyopathy"
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YACOUB, A. "Pregnancy With Primary Dilated Cardiomyopathy". Obstetrics & Gynecology 99, n.º 5 (mayo de 2002): 928–30. http://dx.doi.org/10.1016/s0029-7844(01)01745-8.
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Subedi, Deepika, Diptesh Aryal y Anil Shrestha. "Anesthetic Management of an Elderly Patient with Dilated Cardiomyopathy and Hypothyroidism for Inter-Trochanteric Fracture". Journal of Chitwan Medical College 9, n.º 3 (25 de septiembre de 2019): 97–99. http://dx.doi.org/10.3126/jcmc.v9i3.25791.
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Dilated cardiomyopathy is a primary myocardial disease characterized by left ventricular or biventricular dilation and impaired contractility. The anesthetic management of a patient with dilated cardiomyopathy undergoing a non-cardiac surgery is always challenging and may be associated with high mortality. Furthermore, perioperative morbidity becomes more frequent in the elderly with steep increases after the age of 75. We are reporting the successful anaesthetic management of a 93 years old patient with severe dilated cardiomyopathy planned for surgical repair of inter-trochanteric fracture under combined spinal anesthesia.
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Shin, Gil Ja. "A Clinical Study of Primary Dilated Cardiomyopathy". Ewha Medical Journal 14, n.º 1 (1991): 61. http://dx.doi.org/10.12771/emj.1991.14.1.61.
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Pace, Charlotte. "Diet associated canine dilated cardiomyopathy". Veterinary Nurse 12, n.º 4 (2 de mayo de 2021): 170–75. http://dx.doi.org/10.12968/vetn.2021.12.4.170.
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Dilated cardiomyopathy (DCM) is a common cause of heart failure in the dog. Primary DCM is often a disease of exclusion, but inherited genetic breed dispositions have been reported. Secondary causes of DCM include toxins, nutritional deficiency, systemic and infectious disease. The number of dogs diagnosed with DCM has increased significantly in the last 20 years, and has been linked to the rise in popularity of boutique, exotic and grain-free, legume-rich diets. Veterinary cardiologists raised concerns as DCM was being reported in atypical breeds. Subsequently, the United States Food and Drug Agency released a statement in 2018 warning pet owners of the risks of grain-free and novel protein diets. It is assumed that the problem also occurs in the UK because these diets are popular here also. Contrary to primary causes of DCM, dogs have improved clinically and on echocardiograph when their diet has been changed and/or supplemented. No clear cause has yet been identified between these diets and DCM, but the potential reasons seem to be multifactorial and limited by a lack of understanding of the bioavailability, digestibility and metabolism of the novel proteins and legume-rich diets.
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Cheng, Zhenli, Shiv Kumar Yadav, Xiaoyan Liu y Qijian Yi. "A reversible hypocalcemic dilated cardiomyopathy caused by primary hypoparathyroidism". Asian Journal of Medical Sciences 10, n.º 2 (1 de marzo de 2019): 65–68. http://dx.doi.org/10.3126/ajms.v10i2.22323.
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Dilated cardiomyopathy (DCM) is characterized by dilation and impaired contraction of one or both ventricles. Affected patients have impaired systolic function and may or may not develop overt heart failure (HF). Prognosis is generally poor without heart transplantation. We experienced a case of a 10-year-old child with dilated cardiomyopathy (DCM) accompanied by undiagnosed primary hypoparathyroidism. In our case,aggressive management of hypoparathyroidism significantly improved the manifestations of DCM. The case presentation highlights the importance of considering hypoparathyroidism as a cause of reversible myocardial dysfunction.
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Kesici, Selman, Hüseyin Demirbilek, Murat Tanyıldız, Mehmet Gumustas, Benan Bayrakci y Mutlu Yazici. "Reversible Dilated Cardiomyopathy Due to Combination of Vitamin D–Deficient Rickets and Primary Hypomagnesemia in an 11-Month-Old Infant". Journal of Pediatric Intensive Care 07, n.º 01 (2 de mayo de 2017): 046–48. http://dx.doi.org/10.1055/s-0037-1602803.
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AbstractVitamin D–deficient rickets is still an important and common health problem in developing countries. Since calcium is an essential ion for cardiac muscle contraction, calcium deficiency caused by rickets can cause secondary dilated cardiomyopathy. This situation can be exacerbated by coexisting hypomagnesemia. Here, we report a case of dilated cardiomyopathy due to hypocalcemia induced by vitamin D–deficient rickets and accompanying primary hypomagnesemia in an infant whose cardiomyopathy was successfully treated by replacement of calcium, vitamin D, and magnesium. In addition to genetic causes, viral infections, and idiopathic factors, metabolic abnormalities are important etiologic factors in pathogenesis of dilated cardiomyopathy and since they are treatable, prompt diagnosis of these disorders is crucial.
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Yacoub, Ashraf y M. Jocelyne Martel. "Pregnancy in a Patient With Primary Dilated Cardiomyopathy". Obstetrics & Gynecology 99, n.º 5, Part 2 (mayo de 2002): 928–30. http://dx.doi.org/10.1097/00006250-200205001-00022.
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Kroumpouzou, E., I. P. Gomatos, A. Kataki, M. Karayannis, G. D. Dangas y P. Toutouzas. "Common Pathways for Primary Hypertrophic and Dilated Cardiomyopathy". Hybridoma and Hybridomics 22, n.º 1 (febrero de 2003): 41–45. http://dx.doi.org/10.1089/153685903321538071.
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Agnetti, Aldo, Lee Bitton, Bertrand Tchana, Akamin Raymond y Nicola Carano. "Primary carnitine deficiency dilated cardiomyopathy: 28years follow-up". International Journal of Cardiology 162, n.º 2 (enero de 2013): e34-e35. http://dx.doi.org/10.1016/j.ijcard.2012.05.038.
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ALFONSO, F., A. L. P. CAFOALO, J. DEL TORO, E. TORRECILLA, M. REY y P. DE RABAGO. "Right ventricular dilated cardiomyopathy associated with primary biliary cirrhosis". European Heart Journal 12, n.º 11 (1 de noviembre de 1991): 1240–43. http://dx.doi.org/10.1093/eurheartj/12.11.1240.
Texto completoTesis sobre el tema "Primary dilated cardiomyopathy"
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Gretteau, Paul-Antoine. "Identification d’échanges génétiques modulaires entre des populations d’ARN complets ou tronqués en région 5’non codante d’Entérovirus du groupe B dans des cardiomyocytes humains primaires : impact sur la pathogénèse des cardiomyopathies dilatées inexpliquées chez l’Homme". Thesis, Reims, 2018. http://www.theses.fr/2018REIMM203.
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Les entérovirus du groupe B (EV-B) sont une cause majeure de myocardite aiguë, précurseur de la myocardite chronique et de la cardiomyopathie dilatée (CMD) chez l’homme. Les mécanismes moléculaires viraux impliqués dans la progression de la myocardite aiguë vers la phase chronique et la CMD restent inconnus. En utilisant une approche NGS, nous avons détecté des populations persistantes majoritaires d’EV-B tronquées en extrémité 5’, associées à des formes complètes mineures dans des cas de CMD. Afin évaluer leur impact sur la fonctionnalité des cardiomyocytes, nous avons transfecté dans des cardiomyocytes primaires (HCM) des ARN viraux clonés et identiques à ceux détectés dans les cas de CMD. Les formes EV-B majoritaires tronquées en extrémité 5’, seules ou associées à des populations complètes « auxiliaires » pourraient altérer les fonctions des HCM par des activités de la P2A virale. L'existence de mécanismes de recombinaison génomique entre les populations virales persistantes tronquées et complètes a été étudiée par un test de recombinaison d’ARN EV-B défectifs transfectés dans des HCM. Cette approche in vitro a produit majoritairement des recombinants non-homologues caractérisés par des échanges génétiques dans la région 5’NC (spacer1/2). Nos résultats indiquent l’existence d’événements de recombinaison génomique en région 5’ entre les populations d’EV-B tronquées et complètes qui pourraient contribuer au développement de la CMD. Une meilleure compréhension des mécanismes de persistance virale permettra le développement de nouvelles stratégies thérapeutiques pour lutter contre les infections chroniques par les EV-BGroup-B Enteroviruses (EV-B) are a common cause of human acute myocarditis, a disease that is a precursor of chronic myocarditis and dilated cardiomyopathy (DCM). However, the viral molecular mechanisms involved in the progression of acute to chronic myocarditis and subsequently to DCM remain unknown. Using NGS approach, we detected persistent major EV-B populations characterized by 5’ terminal genomic deletions ranging from 17 to 50 nucleotides associated with minor complete viral forms in explanted hearts of DCM cases. To assess their impact on cardiomyocyte functions, we transfected viral RNA clones mimicking the viral genomes found in patients’ tissues into primary human cardiomyocytes (HCM). Our findings demonstrated that the major persistent 5’ deleted viral forms alone or associated with full-length populations of helper RNAs could impair cardiomyocyte functions by viral 2Apro activities in EV-DCM cases. To assess the existence of genomic recombination mechanisms between persistent deleted and full-length viral helper populations, we used a recombination assay based on the rescue of non-replicative EV-B RNAs transfected in HCM. This in vitro approach produced major (75%) non-homologous recombinants that nucleotides sequencing characterized modular exchanges into the spacers 1 & 2 of the 5’NC region. Our findings indicate the existence of genomic recombination events through which, 5’ deleted and complete collaborative EV-B populations could significantly contribute to the pathogenesis of unexplained DCM cases. A better understanding of these viral persistence mechanisms will stimulate new therapeutic strategies research for chronic infections caused by EV-B
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Canha, Mariana Gusmão Pinheiro Magano. "Cardiomiopatia dilatada canina – da etiologia à terapêutica, o que há de novo?" Master's thesis, 2019. http://hdl.handle.net/10400.26/29712.
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As doenças cardíacas são muito prevalentes na população canina e são responsáveis por uma
elevada morbilidade e mortalidade nesta espécie. Esta dissertação de mestrado integrado tem como
objetivo efetuar uma revisão bibliográfica no que respeita ao estado da arte sobre a cardiomiopatia
dilatada na espécie canina, desde a sua etiologia, apresentação clínica, diagnóstico e terapêutica.
A seguir à doença degenerativa da válvula mitral, a cardiomiopatia dilatada (CMD) é a patologia
cardíaca mais comum na prática clínica veterinária e caracteriza-se por uma dilatação das câmaras
cardíacas, redução da contratilidade do miocárdio e, consequentemente, uma disfunção sistólica e
diastólica. Esta doença é de evolução lenta e progressiva, levando à insuficiência cardíaca congestiva
(ICC) e a arritmias que podem culminar com a morte do animal.
A etiologia da CMD é geralmente desconhecida, no entanto existem diversos fatores
predisponentes para o seu desenvolvimento. Os fatores genéticos representam uma das principais
causas desta doença, como tem sido evidenciado nos últimos anos por múltiplos estudos que suportam
e comprovam o seu carácter hereditário, nomeadamente em linhas familiares de raça Doberman
Pinscher, tida classicamente como modelo de estudo desta patologia. O diagnóstico de CMD baseiase
essencialmente no uso da ecocardiografia, acompanhado da eletrocardiografia, da radiografia
torácica e de exames laboratoriais. Mais recentemente também a medicina nuclear tem sido aplicada
nesta área da clínica veterinária. O seu tratamento é fundamentalmente de suporte e tem como objetivo
controlar os sintomas da ICC, promover a qualidade de vida do animal e aumentar a sua sobrevivência.
Na CMD verifica-se que ocorrem alterações na dinâmica do cálcio e do ritmo da apoptose dos
cardiomiócitos, o que justifica um prognóstico reservado em animais tratados de forma paliativa. Tanto
em medicina veterinária como em medicina humana têm-se procurado formas de restabelecer a
funcionalidade cardíaca, sendo que a terapia génica, por transferência de genes está na vanguarda da
investigação translacional uma vez que há indícios de que permite alterar a distribuição do cálcio e
reduzir a apoptose dos cardiomiócitos. Neste sentido múltiplos estudos em animais e humanos estão
já em curso.Heart diseases are very prevalent in canine population and are responsible for high morbidity and mortality in this specie. This master thesis aims to carry out a bibliographical review regarding the state of the art on dilated cardiomyopathy, focusing on etiology, clinical presentation, diagnosis and therapeutics. After mitral valve degenerative disease, dilated cardiomyopathy (DCM) is the most common cardiac pathology in veterinary clinical practice and is characterized by dilation of the cardiac chambers, reduction of myocardial contractility, and consequently systolic and diastolic dysfunction. This disease is of slow and progressive evolution, leading to congestive heart failure (CHF) and arrhythmias that can culminate in the death of the animal. The etiology of DCM is generally unknown, however there are several predisposing factors to its development. Genetic factors represent one of the main causes of this disease, as it has been evidenced in recent years by multiple studies that support and prove its hereditary nature, especially in family lines of Doberman Pinscher breed, classically considered as a model of this pathology. The diagnosis of DCM is based essentially on the use of echocardiography, accompanied by electrocardiography, thoracic radiography and laboratory tests. More recently also nuclear medicine has been applied in this area of veterinary clinics. Its treatment is essentially palliative and aims to control the symptoms of CHF, promote the quality of life of the animal and increase its survival. In DCM are described changes on calcium dynamics and on cardiomyocyte apoptosis rate which justify a guarded prognosis in symptomatic treated animals. There is an intensive investigation in both veterinary and human medicine in order to find more efficacious therapeutic strategies to restore cardiac function. Gene therapy, by gene transfer, is one of the more promising approaches for this disease and has been studies under a translational research point of view. There is evidence that it allows improvement on calcium distribution and reducing of cardiomyocytes apoptosis. In this sense multiple animal and human studies are already under way.
Libros sobre el tema "Primary dilated cardiomyopathy"
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Sinagra, Gianfranco, Marco Merlo y Davide Stolfo. Dilated cardiomyopathy: clinical diagnosis and medical management. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0356.
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Dilated cardiomyopathy (DCM) is a relatively rare primary heart muscle disease with genetic or post-inflammatory aetiology that affects relatively young patients with a low-risk co-morbidity profile. Therefore, DCM represents a particular heart failure model with specific characteristics and long-term evolution. The progressively earlier diagnosis derived from systematic familial screening programmes and the current therapeutic strategies have greatly modified the prognosis of DCM with a dramatic reduction of mortality over recent decades. A significant number of DCM patients present an impressive response to pharmacological and non-pharmacological evidence-based therapy in terms of haemodynamic improvement with subsequent left ventricular reverse remodelling, which confer a favourable long-term prognosis. However, in some DCM patients the outcome is still severe. This prognostic heterogeneity is possibly related to the aetiological variety of this disease. Maximal effort towards an early aetiological diagnosis of DCM, by using all diagnostic available tools (including cardiovascular magnetic resonance imaging, endomyocardial biopsy, and genetic testing when indicated), as well as the individualized long-term follow-up appear crucial in improving the prognostic stratification and the clinical management of these patients.
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Rahimi, Kazem. Heart muscle disease (cardiomyopathy). Editado por Patrick Davey y David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0106.
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Cardiomyopathy is defined as disease of heart muscle, and typically refers to diseases of ventricular myocardium. A consensus statement of the European Society of Cardiology (ESC) working group on myocardial and pericardial diseases, published in 2007, abandoned the inconsistent and rather arbitrary classification into primary and secondary causes and based its classification on ventricular morphology and function only. This classification distinguishes five types of cardiomyopathy: dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and unclassified cardiomyopathies (such as takotsubo cardiomyopathy and left ventricular non-compaction). Each category is further subdivided into familial and non-familial causes. In a departure from the 1995 WHO classification, the ESC consensus statement excludes myocardial dysfunction caused by coronary artery disease, hypertension, valvular disease, and congenital heart disease from the definition of cardiomyopathy. The rationale for this was to highlight the differences in diagnostic and therapeutic approaches of these common diseases, and to make the new classification system more acceptable for the routine clinical use. In contrast to the American Heart Association scientific statement, the ESC definition does not consider channelopathies as cardiomyopathies. The sections on cardiomyopathy in this chapter are based on the ESC definition, with a brief reference to channelopathies.
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Lancellotti, Patrizio y Bernard Cosyns. Cardiomyopathies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713623.003.0008.
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This chapter focuses on the role of echocardiography in dilated cardiomyopathy, showing diagnostic and associated findings along with the prognostic role of echocardiography. Primary myocardial disease is inadequate hypertrophy, independent of loading conditions and often other affected structures such as mitral valve apparatus, small coronary arteries, and cardiac interstitium. Arrhythmogenic RV cardiomyopathy is fatty or fibro-fatty infiltration of the RV with apoptosis and hypertrophied trabeculae of the RV. This chapter also details diagnostic findings and progression of this condition alongside relevant echocardiographic findings. Previously known as ‘spongy heart syndrome’, left ventricular non compaction is characterized by the absence of involution of LV trabeculae during the embryogenic process. This chapter demonstrates the diagnostic findings of this condition, and looks at the diagnostic findings and complications of Takotsubo cardiomyopathy, illustrating typical, RV apical and variant views. It also shows diagnostic findings in myocarditis in both the acute phase and follow-up.
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D’Andrea, Antonello, André La Gerche y Christine Selton-Suty. Systemic disease and other conditions: athlete’s heart. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0055.
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The term ‘athlete’s heart’ refers to the structural, functional, and electrical adaptations that occur as a result of habitual exercise training. It is characterized by an increase of the internal chamber dimensions and wall thickness of both atria and ventricles. The athlete’s right ventricle also undergoes structural, functional, and electrical remodelling as a result of intense exercise training. Some research suggests that the haemodynamic stress of intense exercise is greater for the right heart and, as a result, right heart remodelling is slightly more profound when compared with the left heart. Echocardiography is the primary tool for the assessment of morphological and functional features of athlete’s heart and facilitates differentiation between physiological and pathological LV hypertrophy. Doppler myocardial and strain imaging can give additional information to the standard indices of global systolic and diastolic function and in selected cases cardiac magnetic resonance imaging may help in the diagnosis of specific myocardial diseases among athletes such as hypertrophic cardiomyopathy, dilated cardiomyopathy, or arrhythmogenic right ventricular cardiomyopathy.
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Foggensteiner, Lukas y Philip Beales. Bardet–Biedl syndrome and other ciliopathies. Editado por Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0314.
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Ciliopathies encompass a genotypically complex and phenotypically variable and overlapping series of disorders that makes the general term ‘ciliopathies’ very useful. The genes behind these conditions encode parts of the machinery of the primary cilium. This is also true of the major cystic kidney disorders autosomal dominant polycystic kidney disease and autosomal recessive polycystic kidney disease, but the ‘long tails’ of other ciliopathies are characterized by variable nephropathy (often without cyst formation), retinopathy, and effects on brain and skeletal development. Not all have substantial renal phenotypes. Bardet–Biedl syndrome (BBS) is an autosomal dominant condition characterized by obesity, retinopathy, nephropathy, and learning difficulty, but renal abnormalities are varied and end-stage renal failure occurs in only a minority. Many BBS genes have been described. Alström syndrome is a rare recessive disorder again associated with obesity and retinopathy, but also deafness and dilated cardiomyopathy. Renal failure is a common but later feature. Joubert syndrome is an autosomal dominant condition but can arise from mutations in at least 10 genes. It has a wide phenotypic variation with a common link being hypodysplasia of the cerebellar vermis and other abnormalities giving rise to the ‘molar tooth sign’ on cerebral magnetic resonance imaging scanning, associated with hypotonia in infancy, central ataxia, ocular apraxia, developmental delay, and varying degrees of cognitive impairment. Jeune syndrome is a recessive condition characterized by osteochondrodysplasia which can give rise to hypodevelopment of the chest wall known as suffocating thoracic dystrophy, in addition to other manifestations.
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Noutsias, Michel y Bernhard Maisch. Myocarditis and pericarditis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0058.
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Transition of acute myocarditis to dilated cardiomyopathy occurs in approximately 20% of patients within a follow-up period of 33 months. Recent research has revealed the adverse prognostic impact of several clinical parameters for this scenario. Acute myocarditis and its sequelae dilated cardiomyopathy and inflammatory cardiomyopathy are often caused by viral infections. Histological evaluation of endomyocardial biopsies is critical for the diagnosis of the cardiomyopathy entity and for the clinical management of around 20% of the patients. Additionally, contemporary diagnostic procedures of endomyocardial biopsies are indispensable for the selection of inflammatory cardiomyopathy patients who will likely benefit from immunosuppression or antiviral (interferon) treatment. Immunoadsorption, with subsequent immunoglobulin substitution, is a further promising immunomodulatory treatment option for dilated cardiomyopathy patients, targeting primarily the anticardiac autoantibodies. Cardiac magnetic resonance has emerged as a valuable diagnostic approach for myocarditis and pericarditis. Myocardial late gadolinium enhancement has been associated with adverse outcome and sudden cardiac death. Bridging of the first 3–6 months with a wearable cardioverter–defibrillator, until a definitive decision on the implantation of an implantable cardioverter–defibrillator, is a growingly recognized cornerstone in the clinical management of patients with acute myocarditis with depressed left ventricular ejection fraction of <40% and new-onset dilated cardiomyopathy, respectively. Acute pericarditis is labelled idiopathic or suspected viral without adequate proof of the respective aetiology. Non-steroidal anti-inflammatory drugs and colchicine are proven and safe therapeutic mainstays for pericarditis, including the first attack. Pericardiocentesis is a lifesaving treatment of cardiac tamponade. Pericardioscopy and epicardial biopsies can contribute to the aetiological differentiation of pericardial effusions.
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Noutsias, Michel y Bernhard Maisch. Myocarditis and pericarditis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0058_update_001.
Texto completoResumen
Transition of acute myocarditis to dilated cardiomyopathy occurs in approximately 20% of patients within a follow-up period of 33 months. Recent research has revealed the adverse prognostic impact of several clinical parameters for this scenario. Acute myocarditis and its sequelae dilated cardiomyopathy and inflammatory cardiomyopathy are often caused by viral infections. Histological evaluation of endomyocardial biopsies is critical for the diagnosis of the cardiomyopathy entity and for the clinical management of around 20% of the patients. Additionally, contemporary diagnostic procedures of endomyocardial biopsies are indispensable for the selection of inflammatory cardiomyopathy patients who will likely benefit from immunosuppression or antiviral (interferon) treatment. Immunoadsorption, with subsequent immunoglobulin substitution, is a further promising immunomodulatory treatment option for dilated cardiomyopathy patients, targeting primarily the anticardiac autoantibodies. Cardiac magnetic resonance has emerged as a valuable diagnostic approach for myocarditis and pericarditis. Myocardial late gadolinium enhancement has been associated with adverse outcome and sudden cardiac death. Bridging of the first 3 months with a wearable cardioverter–defibrillator, until a definitive decision on the implantation of an implantable cardioverter–defibrillator, is a growingly recognized cornerstone in the clinical management of patients with acute myocarditis with depressed left ventricular ejection fraction of <40% and new-onset dilated cardiomyopathy, respectively. Acute pericarditis is labelled idiopathic or suspected viral without adequate proof of the respective aetiology. Non-steroidal anti-inflammatory drugs and colchicine are proven and safe therapeutic mainstays for pericarditis, including the first attack. Pericardiocentesis is a lifesaving treatment of cardiac tamponade. Pericardioscopy and epicardial biopsies can contribute to the aetiological differentiation of pericardial effusions.
Capítulos de libros sobre el tema "Primary dilated cardiomyopathy"
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Pereira, Lara Elizabeth y Aftab Ahmed Ansari. "Are Autoimmune Manifestations in Human Dilated Cardiomyopathy Primary or Secondary Events?" En Diagnostic Criteria in Autoimmune Diseases, 373–78. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-285-8_68.
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Germans, Tjeerd, Massimo Lombardi, Danilo Neglia, Petros Nihoyannopoulos y Albert C. van Rossum. "Dilated cardiomyopathy". En The ESC Textbook of Cardiovascular Imaging, 468–87. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198703341.003.0035.
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Dilated cardiomyopathies either familial/genetic or non-familial/non-genetic in origin are characterized by dilatation of one or both ventricles and systolic dysfunction. The modern imaging techniques allow assessment of the primary myocardial defect as abnormalities in the structural, mechanical, metabolic, and perfusion patterns. The diagnostic and the prognostic role of the three most used imaging modalities (echocardiography, nuclear technologies, and cardiac magnetic resonance imaging) are discussed with the purpose of integrating the specific cardiac characteristics provided by each of them.
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Cappato, Riccardo. "Primary prevention of sudden death in idiopathic dilated cardiomyopathy". En ESC CardioMed, editado por Gerhard Hindricks, 2341–45. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0554.
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Idiopathic dilated cardiomyopathy is characterized by early ventricular enlargement and systolic contractile dysfunction with congestive heart failure not secondary to recognizable causes. Symptoms of congestive heart failure develop at a later stage, usually between 18 and 50 years of age, although they may occasionally occur earlier as a first manifestation of the underlying disease. Mechanisms of life-threatening arrhythmias are facilitated by subendocardial scarring, electrolyte unbalance, stretch-induced electrophysiological changes, autonomic impairment, conduction delay, or proarrhythmic effects of drug therapy. Sudden death may occur as a consequence of ventricular fibrillation, but electromechanical dissociation or bradycardia may also be a possible underlying cause. Most of the clinical characterization of idiopathic dilated cardiomyopathy is drawn from studies also enrolling patients with cardiomyopathies secondary to variable underlying conditions. Secular trends have improved the ability of early diagnosis, and the therapeutic strategies used to prevent sudden death. Among them are angiotensin-converting enzyme inhibitors, beta blockers, and mineralocorticoids/aldosterone receptor antagonists. The role of implantable cardioverter defibrillator (ICD) therapy for the primary prevention of all-cause mortality is controversial with some studies showing and others questioning the benefit of ICD in this population. Survivors of near-fatal arrhythmias have a high risk of recurrence, which may often be fatal. Idiopathic dilated cardiomyopathy contributes to less than 15% of all such patients. Previous randomized studies conducted in large heterogeneous populations showed that ICD therapy is beneficial and improves survival by about 30%. This therapy is currently recommended for all survivors of a near-fatal arrhythmia regardless of the underlying substrate.
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Cappato, Riccardo. "Primary prevention of sudden death in idiopathic dilated cardiomyopathy". En ESC CardioMed, editado por Gerhard Hindricks, 2341–45. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0554_update_001.
Texto completoResumen
In patients with dilated cardiomyopathy, the mechanisms of life-threatening arrhythmias are likely determined by subendocardial scarring, electrolyte unbalance, stretch-induced electrophysiological changes, autonomic impairment, conduction delay, or proarrhythmic effects of drug therapy. Sudden death may occur as a consequence of ventricular fibrillation, but electromechanical dissociation or bradycardia may also be a possible underlying cause. Most of the clinical characterization of idiopathic dilated cardiomyopathy is drawn from studies also enrolling patients with cardiomyopathies secondary to recognizable underlying conditions. Secular trends have improved the ability of early diagnosis, and the therapeutic strategies used to prevent sudden death. The role of implantable cardioverter defibrillator (ICD) therapy for the primary prevention of all-cause mortality is controversial with some studies showing and others questioning the benefit of ICD in this population. revious randomized studies conducted in large heterogeneous populations showed that ICD therapy is beneficial and improves survival by about 30%. This therapy is currently recommended for all survivors of a near-fatal arrhythmia regardless of the underlying substrate.
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Sinagra, Gianfranco, Marco Merlo y Davide Stolfo. "Dilated cardiomyopathy: clinical diagnosis and medical management". En ESC CardioMed, 1474–79. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0356_update_001.
Texto completoResumen
Dilated cardiomyopathy (DCM) is a relatively rare primary heart muscle disease with genetic or post-inflammatory aetiology that affects relatively young patients with a low-risk co-morbidity profile. Therefore, DCM represents a particular heart failure model with specific characteristics and long-term evolution. The progressively earlier diagnosis derived from systematic familial screening programmes and the current therapeutic strategies have greatly modified the prognosis of DCM with a dramatic reduction of mortality over recent decades. A significant number of DCM patients present an impressive response to pharmacological and non-pharmacological evidence-based therapy in terms of haemodynamic improvement with subsequent left ventricular reverse remodelling, which confer a favourable long-term prognosis. However, in some DCM patients the outcome is still severe. This prognostic heterogeneity is possibly related to the aetiological variety of this disease. Maximal effort towards an early aetiological diagnosis of DCM, by using all diagnostic available tools (including cardiovascular magnetic resonance imaging, endomyocardial biopsy, and genetic testing when indicated), as well as the individualized long-term follow-up appear crucial in improving the prognostic stratification and the clinical management of these patients.
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Kian, Waleed, Melanie Zemel, Emily H. Kestenbaum, Wafeek Alguayn, Boris Shvarts, Adam A. Sharb, Dina Levitas, Yousef Kian, Nir Peled y Alexander Yakobson. "Cardiomyopathy Etiologies, Symptoms and Management". En Cardiomyopathy - Disease of the Heart Muscle [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95566.
Texto completoResumen
Cardiomyopathy can be defined as a structural and functional myocardial disorder that is commonly genetic rather than due to coronary artery, valvular or congenital heart disease. It can be subcategorized into dilated, hypertrophic, restrictive, unclassified, and arrhythmogenic right ventricular cardiomyopathy/dysplasia. They can be further subdivided into primary and secondary cardiomyopathy. Primary includes genetics (HOCM, ARVC/D), mixed (DCM, RCM) or acquired (stress-induced, myocarditis) causes; while secondary cardiomyopathy is derived from the involvement of other organ systems. Cardiomyopathies can be identified by echocardiogram to display the anatomic and functional changes related to each subtype including systolic or diastolic dysfunction. In certain instances, cardiac-MRI or CT are used to further elucidate its specific characteristics such as fatty infiltration and focal hypertrophy. Treatment is very diverse and catered to each individual case. This will all be further elaborated on in the following chapter.
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Dinov, Borislav. "Risk stratification for sudden cardiac death in dilated cardiomyopathy". En ESC CardioMed, editado por Gerhard Hindricks, 2313–16. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0546.
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The current understanding recognizes dilated cardiomyopathy as a condition defined by cardiac enlargement that manifests clinically with symptoms of congestive heart failure. However, sudden cardiac death (SCD) can be the first clinical manifestation of the disease as well, although the main cause of death remains advanced heart failure. In patients with dilated cardiomyopathy, implantation of an implantable cardioverter defibrillator (ICD) reduced the mortality rate by approximately 30%, indicating that ventricular tachycardia and ventricular fibrillation are important causes of death. However, severe bradycardia or pulseless electrical activity can contribute as a cause of SCD as well. Since ICDs are highly efficacious in the prevention of SCD, identifying patients at highest risk of SCD is crucial for saving life, reducing associated complications, and reducing the burden of costs. However, registry data showed that the majority of sudden deaths occur in patients who do not fulfil the criteria for primary prevention with an ICD.
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M. Harvey, Evan, Murad Almasri y Hugo R. Martinez. "Genetics of Cardiomyopathy". En Cardiomyopathy - Disease of the Heart Muscle [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97010.
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Cardiomyopathies (CMs) encompass a heterogeneous group of structural and functional (systolic and diastolic) abnormalities of the myocardium and are either confined to the cardiovascular system or are part of a systemic disorder. CMs represent a leading cause of morbidity and mortality and account for a significant percentage of death and cardiac transplantation. The 2006 American Heart Association (AHA) classification grouped CMs into primary (genetic, mixed, or acquired) or secondary (i.e., infiltrative or autoimmune). In 2008, the European Society of Cardiology classification proposed subgrouping CM into familial or genetic and nonfamilial or nongenetic forms. In 2013, the World Heart Federation recommended the MOGES nosology system, which incorporates a morpho-functional phenotype (M), organ(s) involved (O), the genetic inheritance pattern (G), an etiological annotation (E) including genetic defects or underlying disease/substrates, and the functional status (S) of a particular patient based on heart failure symptoms. Rapid advancements in the biology of cardio-genetics have revealed substantial genetic and phenotypic heterogeneity in myocardial disease. Given the variety of disciplines in the scientific and clinical fields, any desired classification may face challenges to obtaining consensus. Nonetheless, the heritable phenotype-based CM classification offers the possibility of a simple, clinically useful diagnostic scheme. In this chapter, we will describe the genetic basis of dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), arrhythmogenic cardiomyopathy (ACM), LV noncompaction cardiomyopathy (LVNC), and restrictive cardiomyopathy (RCM). Although the descriptive morphologies of these types of CM differ, an overlapping phenotype is frequently encountered within the CM types and arrhythmogenic pathology in clinical practice. CMs appear to originate secondary to disruption of “final common pathways.” These disruptions may have purely genetic causes. For example, single gene mutations result in dysfunctional protein synthesis causing downstream dysfunctional protein interactions at the level of the sarcomere and a CM phenotype. The sarcomere is a complex with multiple protein interactions, including thick myofilament proteins, thin myofilament proteins, and myosin-binding proteins. In addition, other proteins are involved in the surrounding architecture of the sarcomere such as the Z-disk and muscle LIM proteins. One or multiple genes can exhibit tissue-specific function, development, and physiologically regulated patterns of expression for each protein. Alternatively, multiple mutations in the same gene (compound heterozygosity) or in different genes (digenic heterozygosity) may lead to a phenotype that may be classic, more severe, or even overlapping with other disease forms.
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Becker, Richard C. y Frederick A. Spencer. "Cardiac Chamber, Aortic, and Valvular Thromboembolism". En Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0009.
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The left-sided cardiac chambers (left atrium, left ventricle) and heart valves (mitral valve, aortic valve) (native, prosthetic) serve as potential niduses for systemic thromboembolism, including fatal or debilitating stroke. The ascending aortic is also recognized as a source for embolism (aortoembolism) and should be considered when a comprehensive patient evaluation is being undertaken. The pathogenesis of intracavitary mural thrombosis, much like venous thromboembolism, follows the construct of Virchow’s triad. The area of stasis is often provoked by chamber dilation, reduced performance, or impaired flow across an existing heart valve (e.g., left atrial dilation from mitral stenosis). Endothelial injury may follow either an acute (e.g., myocardial infarction) or chronic (e.g., dilated cardiomyopathy) cardiac process. In the case of aortoembolism, plaque rupture in areas of advanced atherosclerosis serves as the primary site for thrombus development. The third component, prothrombotic state, may be focal (areas of inflammation and necrosis) and/or systemic. Left ventricular mural thrombosis is diagnosed either echocardiographically or at the time of autopsy among patients with myocardial infarction (MI), especially in those with anterior infarction involving the ventricular apex. In large, nonrandomized clinical trials of anticoagulant therapy, researchers have reported an incidence of cerebral embolism of 2% to 4% among nontreated patients, frequently causing either severe neurologic deficits or death. Of these trials, two showed a statistically significant reduction in stroke with early anticoagulation, whereas the third trial demonstrated a positive trend (Davis and Irelant, 1986). A meta-analysis performed by Vaitkus and Barnathan (1993) supports the findings of three previous studies published in the early 1980s. The odds ratio for systemic embolism in the presence of echocardiographically demonstrated mural thrombus was 5.45 (95% confidence interval [CI] 3.02–9.83). The odds ratio of anticoagulation versus no anticoagulation in preventing embolism was 0.14 (95% CI 0.04–0.52) with an event rate difference of –0.33 (95% CI –0.50 to –0.16). The odds ratio of anticoagulation versus control in preventing mural thrombus formation was 0.32 (95% CI 0.20–0.52) and the event difference was –0.19 (95% CI 0.09–0.28).