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Thematische Bibliographien / Arrhythogenic Right Ventricular Cardiomyopathy / Bücher

Bücher zum Thema „Arrhythogenic Right Ventricular Cardiomyopathy“

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Autor: Grafiati

Veröffentlicht am 22. Juni 2024

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1

Hariharan, Venkatesh. The Effects of Arrhythmogenic Right Ventricular Cardiomyopathy-Causing Proteins on the Mechanical and Signaling Properties of Cardiac Myocytes. [New York, N.Y.?]: [publisher not identified], 2014.

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2

Elliott, Perry, Kristina H. Haugaa, Pio Caso und Maja Cikes. Restrictive cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0044.

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Restrictive cardiomyopathy is a heart muscle disorder characterized by increased myocardial stiffness that results in an abnormally steep rise in intraventricular pressure with small increases in volume in the presence of normal or decreased diastolic left ventricular volumes and normal ventricular wall thickness. The disease may be caused by mutations in a number of genes or myocardial infiltration. Arrhythmogenic right ventricular cardiomyopathy is an inherited cardiac muscle disease associated with sudden cardiac death, ventricular arrhythmias, and cardiac failure. It is most frequently caused by mutations in desmosomal protein genes that lead to fibrofatty replacement of cardiomyocytes, right ventricular dilatation, and aneurysm formation.

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3

Syrris, Petros, und Alexandros Protonotarios. Arrhythmogenic right ventricular cardiomyopathy: genetics. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0359.

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Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a disorder of the heart muscle which is typically inherited in an autosomal dominant manner. It is believed to be familial in over 50% of cases. A recessive mode of inheritance has also been reported in syndromic cases with cardiocutaneous features. The classic form of the disorder is considered to be ‘a disease of the desmosome’ as pathogenic variants have been identified in five genes encoding key desmosomal proteins: plakoglobin, desmoplakin, plakophilin-2, desmoglein-2, and desmocollin-2. Mutations in these genes account for 30–50% of ARVC cases. A further eight non-desmosomal genes have also been implicated in the pathogenesis of the disorder but only account for rare cases. Studies of patients with ARVC-associated gene mutations have revealed marked genetic heterogeneity and very limited genotype–phenotype correlation. Disease expression often varies significantly amongst individuals carrying the same mutation. It has been proposed that the presence of more than one sequence variant is required to determine overt clinical disease and patients with multiple variants have a more severe phenotype compared to single variant carriers. Identification of a potentially pathogenic variant comprises a major criterion in the diagnosis of ARVC but informative integration of genetic testing into clinical practice remains challenging. Gene testing should be used to identify asymptomatic family members at risk and only aids diagnosis in cases of high suspicion for ARVC, along with other evident features of the disease already present. However, genetic findings should be used with caution in clinical practice and their interpretation must be performed in expert centres.

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4

Bass, Cristina, Barbara Bauce und 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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5

Katritsis, Demosthenes G., Bernard J. Gersh und A. John Camm. Arrhythmogenic right ventricular cardiomyopathy/dysplasia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199685288.003.0918_update_004.

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6

Touboul, Paul, und Marjaneh Fatemi. Touboul Arrhythmogenic Right Ventricular Cardiomyopathy. Wiley & Sons, Incorporated, John, 2008.

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7

(Editor), Frank I. Marcus, Andrea Nava (Editor) und Gaetano Thiene (Editor), Hrsg. Arrhythmogenic right ventricular cardiomyopathy/dysplasia: Recent Advances. Springer, 2007.

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8

Arrythmogenic Right Ventricular Cardiomyopathy: ARVC and Related Disorders. Springer, 2007.

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9

Brunckhorst, Corinna, Firat Duru und Ardan M. Saguner. Current Concepts in Arrhythmogenic Right Ventricular Cardiomyopathy / Dysplasia. Cardiotext Publishing, 2014.

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10

Brunckhorst, Corinna, Firat Duru und Ardan M. Saguner. Current Concepts in Arrhythmogenic Right Ventricular Cardiomyopathy / Dysplasia. Cardiotext Publishing, 2014.

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11

Touboul, Paul, und Marjaneh Fatemi. Arrhythmogenic Right Ventricular Cardiomyopathy (Clinical Approaches to Tachyarrhythmias, V. 17). Blackwell Publishing Limited, 2002.

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12

Arrhythmogenic right ventricular cardiomyopathy/dysplasia: Proceedings of the 1st International Symposium on [T.B.A.]. Amsterdam: Elsevier, 1997.

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13

Elliott, Perry, und Alexandros Protonotarios. Arrhythmogenic right ventricular cardiomyopathy: management of symptoms and prevention of sudden cardiac death. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0361.

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Patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) have arrhythmia-related symptoms or are identified during screening of an affected family. Heart failure symptoms occur late in the disease’s natural history. As strenuous exercise has been associated with disease acceleration and worsening of ventricular arrhythmias, lifestyle modification with restricted athletic activities is recommended upon disease diagnosis or even identification of mutation carrier status. An episode of an haemodynamically unstable, sustained ventricular tachycardia or ventricular fibrillation as well as severe systolic ventricular dysfunction constitute definitive indications for implantable cardioverter defibrillator (ICD) implantation, which should also be considered following tolerated sustained or non-sustained ventricular tachycardia episodes, syncope, or in the presence of moderate ventricular dysfunction. Antiarrhythmic medications are used as an adjunct to device therapy. Catheter ablation is recommended for incessant ventricular tachycardia or frequent appropriate ICD interventions despite maximal pharmacological therapy. Amiodarone alone or in combination with beta blockers is most effective for symptomatic ventricular arrhythmias. Beta blockers are considered for use in all patients with a definite diagnosis but evidence for their prognostic benefit is sparse. Heart failure symptoms are managed using standard protocols and heart transplantation is considered for severe ventricular dysfunction or much less commonly uncontrollable ventricular arrhythmias.

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14

Cardiac MRI in Diagnosis, Clinical Management, and Prognosis of Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia. Elsevier, 2016. http://dx.doi.org/10.1016/c2013-0-19332-4.

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15

Abidov, Aiden, Isabel Oliva und Frank I. MARCUS. Cardiac MRI in Diagnosis, Clinical Management, and Prognosis of Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia. Elsevier Science & Technology Books, 2016.

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16

Marcus, Frank I., Aiden Abidov und Isabel Oliva. Cardiac MRI in the Diagnosis, Clinical Management and Prognosis of Arrythmogenic Right Ventricular Cardiomyopathy/Dysplasia. Elsevier Science & Technology Books, 2016.

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17

Rahimi, Kazem. Heart muscle disease (cardiomyopathy). Herausgegeben von Patrick Davey und 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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18

Marcus, Frank I., Andrea Nava und Gaetano Thiene. Arrhythmogenic RV Cardiomyopathy/Dysplasia: Recent Advances. Springer London, Limited, 2007.

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19

Rigo, Fausto, Covadonga Fernández-Golfín und 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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20

Ramrakha, Punit, und Jonathan Hill, Hrsg. Heart muscle diseases. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199643219.003.0008.

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Classification 418Dilated cardiomyopathy 420Dilated cardiomyopathy: treatment 422Hypertrophic cardiomyopathy 424Hypertrophic cardiomyopathy: investigations 428Hypertrophic cardiomyopathy: treatment 430Restrictive cardiomyopathy 432Cardiac amyloidosis 434Cardiac amyloidosis: treatment 436Fabry disease 438Arrhythmogenic right ventricular cardiomyopathy (ARVC) 440ARVC: management 442Left ventricular non-compaction ...

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21

Karatasakis, G., und 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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22

D’Andrea, Antonello, André La Gerche und 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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23

Citro, Rodolfo, Laurent Davin und Daniel Rodriguez Muñoz. Takotsubo syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0046.

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Owing to its dynamic and unique nature, standard echocardiography plays a key role in the diagnostic work-up of patients suspected of takotsubo cardiomyopathy (TTC), providing distinctive features of this peculiar syndrome. Useful information for the early recognition of TTC can be derived from the discrepancy between extensive myocardial dysfunction and a modest increase in troponin levels; the detection of a ‘circumferential pattern’ of left ventricular (LV) wall motion abnormalities, which typically extend beyond the distribution of a single coronary artery; coronary flow assessment in the distal tract of the left anterior descending artery; and right ventricular (RV) involvement (biventricular ballooning). Advanced echocardiographic techniques, including speckle tracking, myocardial contrast and coronary flow studies, are providing further mechanistic and pathophysiological insights. Additionally, evaluation of both LV systolic and diastolic function along with early identification of any potential complications are crucial for clinical management and risk stratification. Comprehensive serial echocardiographic examinations should be systematically performed during the follow-up of TTC patients to monitor myocardial function recovery.

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