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1
Williams, Andrew D. Skeletal muscle in heart failure and type 2 diabetes. New York: Nova Biomedical Books, 2010.
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2
Goodwin, J. F., ed. Heart Muscle Disease. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4874-7.
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3
L, Tavazzi, and Di Prampero P. E, eds. The anaerobic threshold: Physiological and clinical significance. Basel: Karger, 1986.
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4
1962-, Laguna Pablo, ed. Bioelectrical signal processing in cardiac and neurological applications. Amsterdam: Elsevier Academic Press, 2005.
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5
Nuno, Azóia, and Dobreiro Pedra, eds. Treadmill exercise and its effects on cardiovascular fitness, depression, and muscle aerobic function. Hauppauge, N.Y: Nova Science Publisher, 2009.
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6
C, Claycomb William, Di Nardo Paolo, and New York Academy of Sciences., eds. Cardiac growth and regeneration. New York, N.Y: New York Academy of Sciences, 1995.
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7
S, Abraham, and Amitai G, eds. Calcium channel modulators in heart and smooth muscle: Basic mechanisms and pharmacological aspects : proceedings of the 33rd [i.e. 34th] Oholo Conference, Eilat, Israel, 1989. Rehovot, Israel: Balaban Publishers, 1990.
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8
L, Archer Stephen, and Rusch Nancy Jean, eds. Potassium channels in cardiovascular biology. New York: Kluwer Academic/Plenum, 2001.
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9
Wang, Tammy, Jocelyn Wong, and Anita Honkanen. Glycogen Storage Diseases. 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/9780190685157.003.0048.
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Glycogen storage diseases result from deficiencies of various enzymes or proteins in the pathways of glycogen metabolism. The reduction in effective glucose storage and/or mobilization results in hypoglycemia and accumulation of glycogen in tissues. Diagnosis can occur at any age, from infancy to adulthood, depending on the pathway affected and the degree of enzyme deficiency. The clinical presentation varies, but the most commonly affected organ systems include the heart, liver, and skeletal muscles. In addition to the morbidity that can occur from dysfunction of these organs, important anesthetic implications include administration of glucose-containing fluids to avoid hypoglycemia, monitoring for acidosis, and caution with use of depolarizing muscle relaxants because of the potential risk of hyperkalemia and rhabdomyolysis. Inheritance is commonly autosomal recessive.
10
Ramrakha, Punit, and Jonathan Hill, eds. 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 ...
11
Goodwin, J. F. Heart Muscle Disease. Springer, 2011.
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12
Goodwin, J. F. Heart Muscle Disease. Springer, 2011.
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13
Archer, Nick, and Nicky Manning. Heart muscle disease. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198766520.003.0019.
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14
Archer, Nick, and Nicky Manning. Heart muscle disease. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199230709.003.0015.
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Introduction 220Types of heart muscle disease 222Assessment 228Treatment 230Heart muscle disease in the fetus can be a 1° (often genetically determined) abnormality or 2° to another disease process in the fetus or the mother. These functional types of heart muscle disease are discussed in this chapter....
15
Goodwin, J. F. Heart Muscle Disease. Springer, 2013.
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16
F, Goodwin John, ed. Heart muscle disease. Lancaster, England: MTP Press, 1985.
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17
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.
18
Symons, Cecil, Andrew G. Mitchell, and Tom Evans. Specific Heart Muscle Disease. Elsevier Science & Technology Books, 2013.
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19
Mattsson, Gustav, and Peter Magnusson. Cardiomyopathy: Disease of the Heart Muscle. IntechOpen, 2021.
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20
Elliott, Perry, and Giuseppe Limongelli. Cardiac Aspects of INHERITED METABOLIC DISEASES. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0070.
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More than 40 inherited metabolic disorders cause heart disease, including fatty acid oxidation defects, glycogen storage disorders, lysosomal storage disorders, peroxisomal diseases, mitochondrial cytopathies, organic acidemias, aminoacidopathies, and congenital disorders of glycosylation. The pattern and severity of cardiac involvement varies between disorders but includes congenital heart diseases, heart muscle diseases, arrhythmias and sudden death, and heart failure. The majority of IMDs are multisystem diseases, but in a few cases cardiac disease is the predominant clinical feature and the main determinant of prognosis. For an increasing number of IEMs there are specific therapies designed to treat or ameliorate the effects of the underlying metabolic defect. In some cases, these therapies have an important effect on the progression of cardiac disease.
21
Cardiomyopathy - Disease of the Heart Muscle [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.91489.
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22
Mills, Gary H. Pulmonary disease and anaesthesia. Edited by Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0082.
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Respiratory adverse events are the commonest complications after anaesthesia and have profound implications for the recovery of the patient and their subsequent health. Outcome prediction related to respiratory disease and complications is vital when determining the risk:benefit balance of surgery and providing informed consent. Surgery produces an inflammatory response and pain, which affects the respiratory system. Anaesthesia produces atelectasis, decreases the drive to breathe, and causes muscle weakness. As the respiratory system ages, closing capacity increases and airway closure becomes an increasing issue, resulting in atelectasis. Increasing comorbidity and polypharmacy reduces the patient’s ability to eliminate drugs. The proportion of major operations on older frailer patients is rising and postoperative recovery becomes more complicated and the demand for critical care rises. At the same time, the population is becoming more obese, producing rapid decreases in end-expiratory lung volume on induction, together with a high incidence of sleep-disordered breathing. Despite this, many high-risk patients are not accurately identified preoperatively, and of those that are admitted to critical care, some are discharged and then readmitted to the intensive care unit with complications. Respiratory diseases may lead to increases in pulmonary vascular resistance and increased load on the right heart. Some lung diseases are primarily fibrotic or obstructive. Some are inflammatory, autoimmune, or vasculitic. Other diseases relate to the drive to breathe, the nerve supply to, or the respiratory muscles themselves. The range of types of respiratory disease is wide and the physiological consequences of respiratory support are complex. Research continues into the best modes of respiratory support in theatre and in the postoperative period and how best to protect the normal lung. It is therefore essential to understand the effects of surgery and anaesthesia and how this impacts existing respiratory disease, and the way this affects the balance between load on the respiratory system and its capacity to cope.
23
Pierce, Grant N., Pawan K. Singal, and Vincenzo Panagia. Cellular Basis of Cardiovascular Function in Health and Disease. Springer London, Limited, 2012.
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24
La Canna, Giovanni. Heart valve disease (mitral valve disease): anatomy and morphology of the mitral valve. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0034.
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The mitral valve is a complex anatomical structure that includes the valve tissue (leaflets), the left atrioventricular junction (annulus), and the valve suspension system (chordae tendineae, papillary muscles, and left ventricle). Its functional anatomy can be analysed using two- and three-dimensional transthoracic and transoesophageal echocardiography. Based on certain hallmarks (commissures, clefts), in vivo mitral valve tissue anatomy can be accurately categorized. In addition, three-dimensional reconstruction provides a quantitative model for comprehensive valve analysis. This chapter describes the anatomy and morphology of the mitral valve, including the subvalvular suspension system and functional anatomy and dynamics of the mitral annulus.
25
Singal, Pawan K. The Cellular Basis of Cardiovascular Function in Health and Disease. Springer, 2012.
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26
K, Singal Pawan, Panagia Vincenzo, and Pierce Grant N, eds. The cellular basis of cardiovascular function in health and disease. Dordrecht: Kluwer Academic Publishers, 1997.
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27
The Cellular Basis of Cardiovascular Function in Health and. Springer, 1997.
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28
Gielen, Stephan, Alessandro Mezzani, Paola Pontremoli, Simone Binno, Giovanni Q. Villani, Massimo F. Piepoli, Josef Niebauer, and Daniel Forman. Physical activity and inactivity. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0012.
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In this chapter the current evidence for regular aerobic exercise in primary prevention is discussed and recommendations for exercise interventions in the general population are given. Regular physical exercise is an established therapeutic strategy in a number of cardiovascular diseases and with stable chronic heart failure. In these disease entities moderate-intensity aerobic endurance training is the basis of most training programmes. However, high-intensity interval training is more effective in improving cardiovascular exercise capacity without any measurable additional risks. Resistance training can be used as an optional training component in patients with pronounced loss of lean muscle. In recent years new areas for application of exercise-based intervention have been explored: training interventions proved to be safe and effective in pulmonary hypertension, heart failure with preserved ejection fraction, and compensated subcritical valvular heart disease. However, in contrast to training in coronary artery disease and heart failure, the prognostic benefit is not yet established.
29
1944-1988, Robinson T. F., and Kinne Rolf K. H, eds. Cardiac myocyte-connective tissue interactions in health and disease. Basel: Karger, 1990.
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30
Kriemler, Susi, Thomas Radtke, and Helge Hebestreit. Exercise, physical activity, and cystic fibrosis. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0027.
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Cystic fibrosis (CF) is a genetic disease resulting in an impaired mucociliary clearance, chronic bacterial airway infection, and inflammation. The progressive destruction of the lungs is the main cause of morbidity and premature death. Diverse other organ systems such as heart, muscles, bones, gastro-intestinal tract, and sweat glands are often also affected and interfere with exercise capacity. Hence, exercise capacity is reduced as the disease progresses mainly due to reduced functioning of the muscles, heart, and/or lungs. Although there is still growing evidence of positive effects of exercise training in CF on exercise capacity, decline of pulmonary function, and health-related quality of life, the observed effects are encouraging and exercise should be implemented in all patient care. More research is needed to understand pathophysiological mechanisms of exercise limitations and to find optimal exercise modalities to slow down disease progression, predict long-term adherence, and improve health-related quality of life.
31
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.
32
Fletcher, Nicholas. Tremor, ataxia, and cerebellar disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0898.
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Tremors are characterized by rhythmic oscillations of one or more body parts. Although typically seen in the upper limbs, almost any area may be involved, including the trunk, head, facial muscles, and legs. Sometimes, tremor is not visible at all but may be heard or palpated, for example, in vocal or orthostatic tremor, respectively. In neurological practice, the diagnosis and treatment of tremor is an everyday problem. A common scenario is the distinction between essential tremor and Parkinson’s disease. In this chapter, the wide range of tremors are discussed, with their aetiolology, pathophysiology, diagnosis and management described.Ataxia is a term used to describe a wide range of neurological disorders affecting muscle coordination, speech and balance that reflect dysfunction of a part of the central nervous system involved in motor function. Many of ataxias have a cerebellar pathology as root cause, although it must be remembered that ataxia, clumsiness, disordered ocular motility, dysarthria, and even kinetic or intention tremor are not always caused by cerebellar disease. This chapter describes the wide range of cerebellar disorders and ataxias, as are non-cerebellar ataxias such as Friedreich’s ataxia.
33
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.
34
Iskandrian, Ami E., and Ernest V. Garcia, eds. Nuclear Cardiac Imaging. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199392094.001.0001.
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Nuclear cardiac imaging refers to cardiac radiological diagnostic techniques performed with the aid of radiopharmaceuticals, which are perfused into the myocardium as markers. These imaging studies provide a wide range of information about the heart, including the contractility of the heart, the amount of blood supply to the heart and whether parts of the heart muscle are alive or dead. This is essential information for cardiologists, and nuclear imaging has become an increasingly important part of the cardiologist's armamentarium. Chapters in Nuclear Cardiac Imaging cover historical, technical and physiological considerations, diagnosis and prognosis, conditions other than Coronary Artery Disease (CAD), advanced cardiac imaging, and challenges and opportunities. New to the fifth edition are key point summaries at the start of each chapter, clinical cases with videos, and a question and answer chapter on practical issues. This title is ideal for nuclear cardiologists in training and nuclear clinicians alike who are searching for quick answers to important clinical and technical questions.
35
Wise, Matt, and Paul Frost. Hyperthermia. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0077.
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An elevation in core body temperature due to thermoregulatory failure with a normal thermoregulatory set point is called hyperthermia. Globally, the most common heat illnesses are heat exhaustion and heat stroke, and these are major causes of morbidity and mortality. These illnesses represent a continuum of disease ranging from mild (heat exhaustion) to total (heat stroke) failure of thermoregulation. Heat exhaustion is characterized by sweating, muscle cramps, fatigue, vomiting, headaches, dizziness, and fainting. These symptoms may also occur in heat stroke but, in addition, neurological signs such as confusion, seizures, and coma predominate. While the diagnosis of these conditions may be straightforward, hyperthermia may complicate a variety of rarer illnesses, including neuroleptic malignant syndrome and drug-induced hyperthermia.
36
Gerovasili, Vasiliki, and Serafim N. Nanas. Neuromuscular Electrical Stimulation: A New Therapeutic and Rehabilitation Strategy in the ICU. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0044.
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Many critically ill patients undergo a period of immobilization with detrimental effects on skeletal muscle, effects which seem most pronounced in the first days of critical illness. Diagnosis of intensive care unit muscle weakness (ICUAW) is often made after discontinuation of sedation when significant nerve and/or muscle damage may already have occurred. Recently, there has been interest in early mobilization during the acute phase of critical illness, with the goal of preventing ICUAW. Neuromuscular electrical stimulation (NEMS) is an alternative form of exercise that has been successfully used in patients with advanced chronic obstructive pulmonary disease (COPD) and chronic heart failure. NEMS is a rehabilitation tool that can be used in critically ill, sedated patients, does not require patient cooperation, and is therefore a promising intervention to prevent muscle dysfunction in the critically ill. When applied early during the course of critical illness, NEMS can preserve muscle morphology and function. Available evidence suggests that NEMS may have a preventive role in the development of ICUAW and could even contribute to a shorter duration of weaning from mechanical ventilation. Studies are needed to evaluate the long-term effect of NEMS and to explore NEMS settings and delivery characteristics most appropriate for different subgroups of critically ill patients.
37
Fye, W. Bruce. Coronary Artery Bypass Surgery Stimulates the Growth of Angiography. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199982356.003.0015.
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Coronary artery bypass graft surgery (CABG), reported by Cleveland Clinic surgeon René Favaloro in 1969, represented a new approach to treating angina pectoris that involved operating directly on a diseased coronary artery. The strategy involved inserting a vein segment between the aorta and a coronary artery. This bypass graft carried blood to heart muscle that would normally have been supplied by a blocked coronary artery. CABG caught on quickly because it seemed to improve angina in a significant percentage of patients and produced income for surgeons and hospitals. But controversy surrounded the value of the operation, and Mayo heart specialists joined others in calling for controlled clinical trials to evaluate it. The Cleveland Clinic group initially resisted trials, claiming that their institutional experience proved that the operation was beneficial. In less than a decade, coronary bypass surgery was associated with a total annual cost of about $1 billion in America.
38
Abraham, Shlomo, and Gabriel Amitai. Calcium Channel Modulators in Heart and Smooth Muscle: Basic Mechanisms and Pharmacological Aspects: Proceedings of the 33rd Oholo Conference, eilat. VCH Publishing, 1991.
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39
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.
40
Colwell, Cynthia M. Researching Music Therapy in Medical Settings. Edited by Jane Edwards. Oxford University Press, 2015. http://dx.doi.org/10.1093/oxfordhb/9780199639755.013.16.
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Research has indicated that music therapy is effective in hospital contexts for managing pain, reducing anxiety, ameliorating social isolation, slowing the impact of cognitive or developmental regression or delays, expressing emotions, and altering physiological responses as medically needed. Music can impact physiological responses including heart rate, blood pressure, pulse oxygenation, pain indicators, respiration, muscle tension, cardiac output, and immunologic function. Participation in music therapy interventions can improve treatment adherence, reduce deleterious symptoms of diseases and effects of medical procedures, and generally enhance quality of life in an unfamiliar and potentially unappealing environment. This chapter will describe a sample of how music therapists have conducted research in medical contexts and will present ways in which such research can be planned and undertaken.
41
Schmidt, Jens. Extramuscular complications occurring in myositis. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0004.
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Extra-muscular complications affecting patients suffering from the idiopathic inflammatory myopathies (IIM) are common, and appear in recognizable patterns affecting the skin, lungs, joints, oesophagus or heart, although these complications rarely all occur simultaneously. During the initial presentation of symptoms, involvement of organs other than muscle can aid the confirmation of the correct IIM subtype. Extra-muscular manifestations can be severe and life-threatening, e.g. with respiratory or cardiac involvement. Escalations of immunosuppression and other treatment modalities will likely be required in such cases since standard immunosuppression usually is not sufficient for an effective treatment of e.g. interstitial lung disease. IIM patients should therefore be regularly checked for extra-muscular manifestations, and management altered as appropriate.
42
Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.
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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.
43
Golper, Thomas A., Andrew A. Udy, and Jeffrey Lipman. Drug dosing in acute kidney injury. Edited by William G. Bennett. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0364.
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Drug dosing in acute kidney injury (AKI) is one of the broadest topics in human medicine. It requires an understanding of markedly altered and constantly changing physiology under many disease situations, the use of the drugs to treat those variety of diseases, and the concept of drug removal during blood cleansing therapies. Early in AKI kidney function may be supraphysiologic, while later in the course there may be no kidney function. As function deteriorates other metabolic pathways are altered in unpredictable ways. Furthermore, the underlying disorders that lead to AKI alter metabolic pathways. Heart failure is accompanied by vasoconstriction in the muscle, skin and splanchnic beds, while brain and cardiac blood flow proportionally increase. Third spacing occurs and lungs can become congested. As either kidney or liver function deteriorates, there may be increased or decreased drug sensitivity at the receptor level. Acidosis accompanies several failing organs. Protein synthesis is qualitatively and quantitatively altered. Sepsis affects tissue permeability. All these abnormalities influence drug pharmacokinetics and dynamics. AKI is accompanied by therapeutic interventions that alter intrinsic metabolism which is in turn complicated by kidney replacement therapy (KRT). So metabolism and removal are both altered and constantly changing. Drug management in AKI is exceedingly complex and is only beginning to be understood. Thus, we approach this discussion in a physiological manner. Critically ill patients pass through phases of illness, sometimes rapidly, other times slowly. The recognition of the phases and the need to adjust medication administration strategies is crucial to improving outcomes. An early phase involving supraphysiologic kidney function may be contributory to therapeutic failures that result in the complication of later AKI and kidney function failure.
44
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.
45
Archer, Stephen L., and Nancy J. Rusch. Potassium Channels in Cardiovascular Biology. Springer London, Limited, 2012.
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46
Archer, Stephen L., and Nancy J. Rusch. Potassium Channels in Cardiovascular Biology. Springer, 2012.
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47
Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.
Full textAbstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
48
Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.
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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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(Editor), Stephen L. Archer, and Nancy J. Rusch (Editor), eds. Potassium Channels in Cardiovascular Biology. Springer, 2001.
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Douglas, Kenneth. Bioprinting. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780190943547.001.0001.
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Abstract: This book describes how bioprinting emerged from 3D printing and details the accomplishments and challenges in bioprinting tissues of cartilage, skin, bone, muscle, neuromuscular junctions, liver, heart, lung, and kidney. It explains how scientists are attempting to provide these bioprinted tissues with a blood supply and the ability to carry nerve signals so that the tissues might be used for transplantation into persons with diseased or damaged organs. The book presents all the common terms in the bioprinting field and clarifies their meaning using plain language. Readers will learn about bioink—a bioprinting material containing living cells and supportive biomaterials. In addition, readers will become at ease with concepts such as fugitive inks (sacrificial inks used to make channels for blood flow), extracellular matrices (the biological environment surrounding cells), decellularization (the process of isolating cells from their native environment), hydrogels (water-based substances that can substitute for the extracellular matrix), rheology (the flow properties of a bioink), and bioreactors (containers to provide the environment cells need to thrive and multiply). Further vocabulary that will become familiar includes diffusion (passive movement of oxygen and nutrients from regions of high concentration to regions of low concentration), stem cells (cells with the potential to develop into different bodily cell types), progenitor cells (early descendants of stem cells), gene expression (the process by which proteins develop from instructions in our DNA), and growth factors (substances—often proteins—that stimulate cell growth, proliferation, and differentiation). The book contains an extensive glossary for quick reference.