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Books on the topic 'Cardiomyopathie dilatée'

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Published: 4 June 2021
Last updated: 6 July 2024

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1

Sinagra, Gianfranco, Marco Merlo, and Bruno Pinamonti, eds. Dilated Cardiomyopathy. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-13864-6.

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2

V, Unverferth Donald, ed. Dilated cardiomyopathy. Mount Kisco, N.Y: Futura Pub. Co., 1985.

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3

Figulla, Hans-Reiner, Reinhard Kandolf, and Bruce McManus, eds. Idiopathic Dilated Cardiomyopathy. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77891-9.

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4

T, Cooper Leslie, ed. Myocarditis: From bench to bedside. Totowa, N.J: Humana Press, 2003.

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5

1952-, Engelmeier Richard S., and O'Connell John B, eds. Drug therapy in dilated cardiomyopathy and myocarditis. New York: Dekker, 1988.

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6

Salemy, Shahram. Reduction ventriculoplasty for dilated cardiomyopathy: The Batistaprocedure. [New Haven Conn: s.n.], 1999.

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7

Sinagra, Gianfranco. Dilated Cardiomyopathy: From Genetics to Clinical Management. Cham: Springer Nature, 2019.

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8

Schultheiss, H. P., and Michel Noutsias. Inflammatory cardiomyopathy (DCMi): Pathogenesis and therapy. Basel: Birkhäuser, 2010.

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9

1949-, Figulla H. R., Kandolf R. 1949-, McManus Bruce M, and International Symposium on Idiopathic Dilated Cardiomyopathy (1992 : Baden-Baden, Germany), eds. Idiopathic dilated cardiomyopathy: Cellular and molecular mechanisms, clinical consequences. Berlin: Springer-Verlag, 1993.

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10

The heart disease sourcebook. Los Angeles: Lowell House, 1997.

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11

Jin, Ou. Molecular studies on the detection of enteroviral RNA genome in cultured cells and endomyocardial biopsies from patients with myocarditis and dilated cardiomyopathy. Ottawa: National Library of Canada, 1990.

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12

Rigo, Fausto, Covadonga Fernández-Golfín, and Bruno Pinamonti. Dilated cardiomyopathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0043.

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Dilated cardiomyopathy (DCM) is characterized by a globally dilated and dysfunctioning left ventricle (LV). Therefore, echocardiographic diagnostic criteria for DCM are a LV end-diastolic diameter greater than 117% predicted value corrected for age and body surface area and a LV ejection fraction less than 45% (and/or fractional shortening less than 25%). Usually, the LV is also characterized by a normal or mildly increased wall thickness with eccentric hypertrophy and increased mass, a spherical geometry (the so-called LV remodelling), a dyssynchronous contraction (typically with left bundle branch block), and diastolic dysfunction with elevated LV filling pressure. Other typical echocardiographic features of DCM include functional mitral and tricuspid regurgitation, right ventricular dysfunction, atrial dilatation, and secondary pulmonary hypertension. Several echocardiographic parameters, measured both at baseline and at follow-up, are valuable for prognostic stratification of DCM patients. Furthermore, re-evaluation of echocardiographic parameters during the disease course under optimal medical therapy is valuable for tailoring medical treatment and confirming indications for invasive treatments at follow-up. The stress echo can play a pivotal role in the different phases of DCM helping us in stratifying the prognosis of these patients. Finally, familial screening is an important tool for early diagnosis of DCM in asymptomatic patients.
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13

Katritsis, Demosthenes G., Bernard J. Gersh, and A. John Camm. Dilated cardiomyopathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199685288.003.0850_update_004.

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Epidemiology, aetiology, pathophysiology, diagnosis, and therapy of patients with dilated cardiomyopathy are discussed. Recommendations on the use of CRT and ICD therapy by the ACC/AHA and ESC are presented.
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14

Seth, Ashok. Dilated Cardiomyopathy. Elsevier - Health Sciences Division, 2008.

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15

Merlo, Marco, Bruno Pinamonti, and Gianfranco Sinagra. Dilated Cardiomyopathy. Saint Philip Street Press, 2020.

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16

Arbustini, Eloisa, Valentina Favalli, Alessandro Di Toro, Alessandra Serio, and Jagat Narula. Classification of cardiomyopathies. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0348.

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For over 50 years, the definition and classification of cardiomyopathies have remained anchored in the concept of ventricular dysfunction and myocardial structural remodelling due to unknown cause. The concept of idiopathic was first challenged in 2006, when the American Heart Association classification subordinated the phenotype to the aetiology. Cardiomyopathies were classified as genetic, acquired, and mixed. In 2008, the European Society of Cardiology proposed a phenotype-driven classification that separated familial (genetic) from non-familial (non-genetic) forms of cardiomyopathy. Both classifications led the way to a precise phenotypic and aetiological description of the disease and moved away from the previously held notion of idiopathic disease. In 2013, the World Heart Federation introduced a descriptive and flexible nosology—the MOGE(S) classification—describing the morphofunctional (M) phenotype of cardiomyopathy, the involvement of additional organs (O), the familial/genetic (G) origin, and the precise description of the (a)etiology including genetic mutation, if applicable (E); reporting of functional status such as American College of Cardiology/American Heart Association stage and New York Heart Association classification (S) was left optional. MOGE(S) is a bridge between the past and the future. It allows description of comprehensive phenotypic data, all genetic and non-genetic causes of cardiomyopathy, and incorporates description of familial clustering in a genetic disease. MOGE(S) is the instrument of precision diagnosis for cardiomyopathies. The addition of the early and unaffected phenotypes to the (M) descriptor outlines the clinical profile of an early affected family member; the examples include non-dilated hypokinetic cardiomyopathy in dilated cardiomyopathy and septal thickness (13–14 mm) in hypertrophic cardiomyopathy classes.
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17

Lancellotti, Patrizio, and 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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18

Rahimi, Kazem. Heart muscle disease (cardiomyopathy). Edited by Patrick Davey and 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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19

Kamra, Komal, and Glyn D. Williams. Cardiomyopathy and Heart Failure. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0012.

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Congenital heart disease and cardiomyopathy are common causes of heart failure in children. Among cardiomyopathies, dilated cardiomyopathy is the most common cause of heart transplant in children. These patients with end-stage heart failure secondary to cardiomyopathy present for multiple interventions requiring anesthesia and may be challenging to manage because of their hemodynamic instability. Thoughtful, collaborative planning and execution of perioperative care is recommended to optimize patient outcomes. This includes good understanding of the patient’s clinical status and the relevant cardiac pathophysiology. Also, an appreciation of the implications of heart failure therapies and the invasive procedures for which the patient requires anesthesia care.
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20

Sinagra, Gianfranco, Marco Merlo, and 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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21

Characterization and Clinical Management of Dilated Cardiomyopathy. MDPI, 2021. http://dx.doi.org/10.3390/books978-3-03943-762-7.

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22

Merlo, Marco, Bruno Pinamonti, and Gianfranco Sinagra. Dilated Cardiomyopathy: From Genetics to Clinical Management. Springer International Publishing AG, 2019.

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23

Johnson, Cameron. Dilated Cardiomyopathy: An Issue of Cardiology Clinics. Murphy & Moore Publishing, 2022.

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24

Merlo, Marco, Bruno Pinamonti, and Gianfranco Sinagra. Dilated Cardiomyopathy: From Genetics to Clinical Management. Springer International Publishing AG, 2020.

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25

Publications, ICON Health. The Official Patient's Sourcebook on Dilated Cardiomyopathy. Icon Health Publications, 2002.

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26

Karatasakis, G., and G. D. Athanassopoulos. Cardiomyopathies. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199599639.003.0019.

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Echocardiography is a key diagnostic method in the management of patients with cardiomyopathies.The main echocardiographic findings of hypertrophic cardiomyopathy are asymmetric hypertrophy of the septum, increased echogenicity of the myocardium, systolic anterior motion, turbulent left ventricular (LV) outflow tract blood flow, intracavitary gradient of dynamic nature, mid-systolic closure of the aortic valve and mitral regurgitation. The degree of hypertrophy and the magnitude of the obstruction have prognostic meaning. Echocardiography plays a fundamental role not only in diagnostic process, but also in management of patients, prognostic stratification, and evaluation of therapeutic intervention effects.In idiopathic dilated cardiomyopathy, echocardiography reveals dilation and impaired contraction of the LV or both ventricles. The biplane Simpson’s method incorporates much of the shape of the LV in calculation of volume; currently, three-dimensional echocardiography accurately evaluates LV volumes. Deformation parameters might be used for detection of early ventricular involvement. Stress echocardiography using dobutamine or dipyridamole may contribute to risk stratification, evaluating contractile reserve and left anterior descending flow reserve. LV dyssynchrony assessment is challenging and in patients with biventricular pacing already applied, optimization of atrio-interventricular delays should be done. Specific characteristics of right ventricular dysplasia and isolated LV non-compaction can be recognized, resulting in an increasing frequency of their prevalence. Rare forms of cardiomyopathy related with neuromuscular disorders can be studied at an earlier stage of ventricular involvement.Restrictive and infiltrative cardiomyopathies are characterized by an increase in ventricular stiffness with ensuing diastolic dysfunction and heart failure. A variety of entities may produce this pathological disturbance with amyloidosis being the most prevalent. Storage diseases (Fabry, Gaucher, Hurler) are currently treatable and early detection of ventricular involvement is of paramount importance for successful treatment. Traditional differentiation between constrictive pericarditis (surgically manageable) and the rare cases of restrictive cardiomyopathy should be properly performed.
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27

Leonski, Joseph. Peripartum and Dilated Cardiomyopathies: Prevalence, Risk Factors and Treatment. Nova Science Publishers, Incorporated, 2018.

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28

Leonski, Joseph. Peripartum and Dilated Cardiomyopathies: Prevalence, Risk Factors and Treatment. Nova Science Publishers, Incorporated, 2018.

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29

Figulla, H. R., and R. Kandolf. Idiopathic Dilated Cardiomyopathy: Cellular and Molecular Mechanisms, Clinical Consequences. Springer-Verlag Telos, 1993.

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30

Figulla, H. R. Idiopathic Dilated Cardiomyopathy: Cellular and Molecular Mechanisms, Clinical Consequences. Springer, 1993.

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31

McManus, Bruce, Hans-Reiner Figulla, and Reinhard Kandolf. Idiopathic Dilated Cardiomyopathy: Cellular and Molecular Mechanisms, Clinical Consequences. Springer, 2011.

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32

McManus, Bruce, Hans-Reiner Figulla, and Reinhard Kandolf. Idiopathic Dilated Cardiomyopathy: Cellular and Molecular Mechanisms, Clinical Consequences. Springer London, Limited, 2012.

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33

Karon, Barry L., and Naveen L. Pereira. Heart Failure and Cardiomyopathies. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0046.

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Heart failure is a clinical syndrome characterized by the inability of the heart to maintain adequate cardiac output to meet the metabolic demands of the body while still maintaining normal or near-normal ventricular filling pressures. Heart failure may be present at rest, but often it is present only during exertion as a result of the dynamic nature of cardiac demands. For correct treatment of heart failure, the mechanism, underlying cause, and any reversible precipitating factors must be identified. Typical manifestations of heart failure are dyspnea and fatigue that limit activity tolerance and fluid retention leading to pulmonary or peripheral edema. The most recent proposed categorization divided the cardiomyopathies into primary and secondary cardiomyopathies, and the primary disorders are further subdivided as genetic, acquired, or mixed. Although this proposal takes into account our progressive understanding of this heterogeneous group of disorders, the previous phenotypic classification of dilated, hypertrophic, and restrictive diseases still provides utility in day-to-day understanding and management of these disorders.
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34

Noutsias, Michel, and 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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35

Noutsias, Michel, and Bernhard Maisch. Myocarditis and pericarditis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0058_update_001.

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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 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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36

Publications, ICON Health. Dilated Cardiomyopathy - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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37

Bass, Cristina, Barbara Bauce, and Gaetano Thiene. Arrhythmogenic right ventricular cardiomyopathy: diagnosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0360.

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Arrhythmogenic cardiomyopathy is a heart muscle disease clinically characterized by life-threatening ventricular arrhythmias and pathologically by an acquired and progressive dystrophy of the ventricular myocardium with fibrofatty replacement. The clinical manifestations of arrhythmogenic cardiomyopathy vary according to the ‘phenotypic’ stage of the underlying disease process. Since there is no ‘gold standard’ to reach the diagnosis of arrhythmogenic cardiomyopathy, multiple categories of diagnostic information have been combined. Different diagnostic categories include right ventricular morphofunctional abnormalities (by echocardiography and/or angiography and/or cardiovascular magnetic resonance imaging), histopathological features on endomyocardial biopsy, electrocardiogram, arrhythmias, and family history, including genetics. The diagnostic criteria were revised in 2010 to improve diagnostic sensitivity, but with the important prerequisite of maintaining diagnostic specificity. Quantitative parameters have been put forward and abnormalities are defined based on the comparison with normal subject data. A definite diagnosis of arrhythmogenic cardiomyopathy is achieved when two major, or one major and two minor, or four minor criteria from different categories are met. The main differential diagnoses are idiopathic right ventricular outflow tract tachycardia, myocarditis, sarcoidosis, dilated cardiomyopathy, right ventricular infarction, congenital heart diseases with right ventricular overload, and athlete’s heart. Among diagnostic tools, contrast-enhanced cardiovascular magnetic resonance is playing a major role in detecting subepicardial-midmural left ventricular free wall involvement, even preceding morphofunctional abnormalities. Moreover, electroanatomical mapping is an invasive tool able to detect early right ventricular free wall involvement in terms of low-voltage areas. Both techniques are increasingly used in the diagnostic work-up although are not yet part of diagnostic criteria.
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38

Garcia-Pavia, Pablo, and Fernando Dominguez. Left ventricular non-compaction: genetics and embryology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0362.

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Left ventricular non-compaction (LVNC) is a rare disorder that is considered an ‘unclassified cardiomyopathy’ by the European Society of Cardiology. Several different gene mutations related to LVNC have been identified, involving sarcomeric, cytoskeletal, Z-line, ion channel, mitochondrial, and signalling proteins. However, there is broad genetic overlap between LVNC and other inherited cardiac diseases such as dilated cardiomyopathy and hypertrophic cardiomyopathy. LVNC could also be part of multisystemic genetic entities such as Barth syndrome, or accompany congenital heart defects.
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39

Michels, Virginia V. Genetics. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0276.

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Genetic factors play a role in the development of many types of human disease. Genetic determinants may be chromosome abnormalities (Down syndrome, Kleinfelter syndrome, Turner syndrome), single gene defects (dilated and hypertrophic cardiomyopathies, Ehlers-Danlos syndrome, Marfan syndrome, neurofibromatosis, tuberous sclerosis, Gaucher disease, cystic fibrosis, sickle cell disease), mitochondrial mutations (MELAS, MERRF, Kearns-Sayre syndrome), or epigenetic or multifactorial factors. Genetics testing methods are also reviewed.
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40

Sheppard, Mary N. Myocardial non-compaction. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0026.

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Isolated left ventricular non-compaction is a controversial entity which has only been reported in the past 30 years. It is becoming more frequently diagnosed due to the use of echocardiography and MRI. It can present in fetal life, infancy, childhood, and adult life. Clinically, the patient can present with cardiac arrhythmias, cardiac failure, systemic emboli due to thrombosis within the ventricles, and sudden death. It can be a genetic entity associated with mutations in many genes associated with hypertrophic cardiomyopathy, dilated cardiomyopathy, and arrhythmogenic cardiomyopathy. It is a rare entity found at autopsy and is more common in children than adults. In the past the prognosis has been considered worse in children then in adults. Treatment is usually empirical, dealing with the cardiac failure, arrhythmias, and thromboemboli.
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41

Codd, Mary B. Epidemiology and natural history of idiopathic dilated and hypertrophic cardiomyopathy: A population-based study in Olmsted County, Minnesota. 1995.

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42

Sarcoplasmic reticulum calcium ATPASE (SRCA) gene expression in myocardial biopsies in dilated cardiomyopathy and suspected myocarditis: Molecular/physiologic. Ottawa: National Library of Canada, 1998.

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43

D’Andrea, Antonello, André La Gerche, and 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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44

Cicala, Roger. Heart Disease Sourcebook: A Complete Guide from Preconception to Postdelivery. McGraw-Hill Education, 1998.

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45

Turc, Guillaume, David Calvet, and Jean-Louis Mas. Cardiac aetiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0005.

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Cardiac aetiology accounts for approximately 20% of strokes in young adults. Although atrial fibrillation is a leading cause of stroke in the general population, it is uncommon in young adults. In such patients, more diverse causes of ischaemic stroke are observed, including valvular heart diseases, infective endocarditis, Libman–Sacks endocarditis, dilated cardiomyopathies, congenital heart diseases, myocardial infarction, and intracardiac tumours. Patent foramen ovale is commonly observed in young adults with ischaemic stroke, but this association may be incidental in a sizeable proportion of patients. Young adults who are the most likely to have a stroke-related patent foramen ovale are also those with the lowest recurrence risk.
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46

Voigt, Jens Uwe, Peter Søgaard, and Emer Joyce. Heart failure: left ventricular dyssynchrony. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0026.

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Echocardiography plays a pivotal role in the management of patients with dilative cardiomyopathy and conduction disease, particularly in the setting of cardiac resynchronization therapy (CRT). Current CRT guidelines recommend the echocardiographic assessment of left ventricular size and function. Furthermore, echocardiography has the potential of analysing regional myocardial mechanics with high temporal resolution and without radiation burden or danger for the patient. Assessment of left ventricular dyssynchrony has therefore become the next challenge. Besides the visual approaches, newer methods of functional imaging such as tissue Doppler and speckle tracking allow the exact quantification of regional myocardial function. This chapter reviews the current status of left ventricular dyssynchrony assessment by echocardiography and introduces emerging techniques which can better link conduction abnormalities and mechanical events and, thus, potentially improve clinical decision-making in this field.
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47

Foggensteiner, Lukas, and Philip Beales. Bardet–Biedl syndrome and other ciliopathies. Edited by 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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