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Published: 1 April 2023

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1

Markus, Frank I., Andrea Nava, and Gaetano Thiene, eds. Arrhythmogenic RV Cardiomyopathy/Dysplasia. Milano: Springer Milan, 2007. http://dx.doi.org/10.1007/978-88-470-0490-0.

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2

Harmon, Jordan, Tufts-New England Medical Center. Evidence-based Practice Center., and United States. Agency for Healthcare Research and Quality., eds. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md: Agency for Healthcare Research and Quality, U.S. Dept. of Health and Human Services, 2004.

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3

Harmon, Jordan, Tufts-New England Medical Center. Evidence-based Practice Center., and United States. Agency for Healthcare Research and Quality., eds. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md: Agency for Healthcare Research and Quality, U.S. Dept. of Health and Human Services, 2004.

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4

United States. Agency for Healthcare Research and Quality., ed. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md.]: Agency for Healthcare Research and Quality, 2004.

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5

Harmon, Jordan, United States. Agency for Healthcare Research and Quality., and New England Medical Center Hospital. Evidence-based Practice Center., eds. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. Rockville, Md: U.S. Dept. of Health and Human Services, Public Health Service, Agency for Healthcare Research and Quality, 2004.

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6

United States. Agency for Healthcare Research and Quality. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. Rockville, Md.]: Agency for Healthcare Research and Quality, U.S. Department of Health and Human Services, 2004.

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7

United States. Agency for Healthcare Research and Quality, ed. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md.]: Agency for Healthcare Research and Quality, 2004.

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8

United States. Agency for Healthcare Research and Quality., ed. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md.]: Agency for Healthcare Research and Quality, 2004.

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9

United States. Agency for Healthcare Research and Quality, ed. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md.]: Agency for Healthcare Research and Quality, 2004.

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10

Harmon, Jordan, Tufts-New England Medical Center. Evidence-based Practice Center, and United States. Agency for Healthcare Research and Quality, eds. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md: Agency for Healthcare Research and Quality, U.S. Dept. of Health and Human Services, 2004.

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11

United States. Agency for Healthcare Research and Quality, ed. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md.]: Agency for Healthcare Research and Quality, 2004.

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12

United States. Agency for Healthcare Research and Quality., ed. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md.]: Agency for Healthcare Research and Quality, 2004.

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13

Harmon, Jordan, Tufts-New England Medical Center. Evidence-based Practice Center, and United States. Agency for Healthcare Research and Quality, eds. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md: Agency for Healthcare Research and Quality, U.S. Dept. of Health and Human Services, 2004.

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14

Harmon, Jordan, Tufts-New England Medical Center. Evidence-based Practice Center, and United States. Agency for Healthcare Research and Quality, eds. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md: Agency for Healthcare Research and Quality, U.S. Dept. of Health and Human Services, 2004.

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15

Harmon, Jordan, Tufts-New England Medical Center. Evidence-based Practice Center., and United States. Agency for Healthcare Research and Quality., eds. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md: Agency for Healthcare Research and Quality, U.S. Dept. of Health and Human Services, 2004.

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16

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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17

Syrris, Petros, and 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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18

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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19

Katritsis, Demosthenes G., Bernard J. Gersh, and 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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20

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

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21

Marcus, Frank I., Andrea Nava, and Gaetano Thiene. Arrhythmogenic RV Cardiomyopathy/Dysplasia: Recent Advances. Springer, 2014.

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22

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

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23

Elliott, Perry, Kristina H. Haugaa, Pio Caso, and 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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24

Brunckhorst, Corinna, Firat Duru, and Ardan M. Saguner. Current Concepts in Arrhythmogenic Cardiomyopathy, Second Edition. Cardiotext Publishing, 2021.

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25

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

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26

Current Concepts in Arrhythmogenic Right Ventricular Cardiomyopathy / Dysplasia. Cardiotext Publishing, 2014.

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27

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

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28

PhD, Domenico Corrado MD, Gaetano Thiene MD, and Cristina Basso MD. Arrhythmogenic Cardiomyopathy, An Issue of Cardiac Electrophysiology Clinics. Saunders, 2011.

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29

(Editor), John A. Camm, ed. Arrhythmogenic Right Ventricular Cardiomyopathy (Clinical Approaches to Tachyarrhythmias, V. 17). Blackwell Publishing Limited, 2002.

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30

Elliott, Perry, and 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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31

Andrea, Nava, Rossi Lino, and Thiene Gaetano, eds. Arrhythmogenic right ventricular cardiomyopathy/dysplasia: Proceedings of the 1st International Symposium on [T.B.A.]. Amsterdam: Elsevier, 1997.

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32

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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33

Abidov, Aiden, Isabel Oliva, and 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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34

Nuyens, Dieter. Generation & Characterization of a Mouse Model for a Sodium Channel Based Long Qt Syndrome (Lqt3), an Inherited Arrhythmogenic Disease. Leuven University Press, 2006.

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35

Marcus, Frank I., Andrea Nava, and Gaetano Thiene. ArrhythmogenicRV Cardiomyopathy/Dysplasia. Springer, 2008.

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36

Walkey, Allan J., and Jared Magnani. Therapeutic strategy in tachyarrhythmias. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0156.

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The therapeutic approach to tachyarrhythmias in the critically-ill patient involves rapid diagnosis and haemodynamic assessment. Patients who become haemodynamically unstable due to tachyarrhythmia warrant direct current cardioversion. Effects of direct current cardioversion during critical illness are often transient unless the underlying arrhythmia precipitant is eliminated and longer-acting rate- or rhythm-controlling medications are instituted. Atrial fibrillation often responds favourably to a rate-control strategy and treatment of the underlying precipitants. After initial clinical stabilization, clinical management involves elimination of potential arrhythmogenic triggers and administration of appropriate rate or rhythm control medications. Assessment of the QT interval in patients with polymorphic ventricular tachycardia is important in determining the underlying aetiology and treatment strategy. This chapter presents an evidence-based review of the therapeutic approach to tachyarrhythmias.
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37

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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38

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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39

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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40

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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41

Fruhwald, Sonja, and Peter Holzer. Gastrointestinal motility drugs in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0040.

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Gastrointestinal motility disturbances in critically-ill patients often require treatment with prokinetic drugs. The aetiology of motility disturbances is complex, and involves electrolyte imbalances, hypervolaemia, reduced intestinal secretion, adverse effects of drugs (catecholamines, opioids, or sedatives) and disease- or treatment-related changes of microflora. However, the choice of prokinetics is narrow, and the multiplicity of pathophysiological mechanisms often limits their efficacy. Gastroparesis can be managed with gastrokinetics such as domperidone, metoclopramide and erythromycin. Their choice depends not only on efficacy, but also on adverse effect profile. The arrhythmogenic potential of domperidone limits maximum daily dose and treatment duration. Metoclopramide and erythromycin induce tachyphylaxis, which restricts treatment duration. The combination of metoclopramide and erythromycin serves as rescue therapy in severe gastroparesis. Neostigmine and laxatives are used to manage colonic paralysis, and these treatment options may eventually be extended by drug candidates, such as prucalopride, lubiprostone, and linaclotide, whose utility in the ICU awaits to be evaluated. Neostigmine’s prokinetic efficacy in colonic paralysis is limited, but well documented in patients with acute colonic pseudo-obstruction (Ogilvie syndrome). Care is advocated in dosing because higher doses of neostigmine inhibit motility. Alternative options include osmotic and stimulant laxatives, especially for prophylactic use. The opioid receptor antagonist alvimopan is used for the short-term management of post-operative ileus, while methylnaltrexone is indicated in palliative care and chronic pain management. Since its efficacy in critically-ill patients remains to be proven, the use of methylnaltrexone in the ICU is off-label and requires proper documentation.
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