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Books on the topic 'Myocardial hypertrophy'

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Published: 4 June 2021
Last updated: 20 February 2023

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1

Yang, Phillip Chung-Ming. Hypertrophic response in primary single-cell culture of adult rat myocardial cells. [New Haven: s.n.], 1989.

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2

Green, Nicola Kim. Regulation of rat myocardial gene expression by thyroid status and in experimental models of cardiac hypertrophy. Birmingham: University of Birmingham, 1991.

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3

A, Raineri, Leachman Robert D, and International School of Medical Sciences (1990 : Ettore Majorana Centre for Scientific Culture), eds. The big heart: Proceedings of a course held at the International School of Medical Sciences, Ettore Majorana Centre for Scientific Culture, Italy, 2-8 April 1990. Chur, Switzerland: Harwood Academic Publishers, 1994.

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4

Swynghedauw, B. Hypertrophie et insuffisance cardiaques. Paris: Editions INSERM, 1990.

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5

Cooklin, Michael J. The effects of hypertrophy on action potential conduction in myocardium. Manchester: University of Manchester, 1995.

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6

M, Carlson Bruce, ed. Growth and hyperplasia of cardiac muscle cells. London, U.K: Harwood Academic Publishers, 1991.

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7

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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8

Ball, Warren Todd. Expression of IGF-I and TGF[beta]-1 in cultured human myocardium insights into the role of growth factors in hypertrophic obstructive cariomyopathy. Ottawa: National Library of Canada, 1998.

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9

1929-, Ison-Franklin Eleanor L., Sandler Harold 1929-, and Hawthorne Edward William 1922-1986, eds. Myocardial hypertrophy: A symposium. Washington, D.C: Howard University Press, 1991.

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10

Ison-Franklin, Eleanor L. Myocardial Hypertrophy: A Symposium. Howard Univ Pr, 1991.

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11

Vimalesvaran, Kavitha, and Michael Marber. Myocardial Remodelling after Myocardial Infarction. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0031.

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This chapter focuses on myocardial remodelling, a process that affects the heart’s shape, structure, and function, following myocardial injury (MI). Post-MI remodelling can be divided into three phases, with the first phase 0–72 hours beginning at the time of ischaemic injury, the second phase 72 hours to 6 weeks, and the third and last phase 6 weeks and beyond. During post-infarction remodelling, hypertrophy is an adaptive response that compensates for the increased load, reduces the effect of progressive dilatation, and balances contractile function. The chapter discusses the factors involved in ventricular remodelling and its association with heart failure progression. The effects of therapies designed to prevent or attenuate post-infarction left ventricular remodelling, with reference to the pathophysiological mechanisms involved, are then considered. Therapies specifically discussed include angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), β‎-adrenoreceptor blockers, and aldosterone receptor antagonists.
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12

Cate, Folkert J. ten, 1948-, ed. Hypertrophic cardiomyopathy: Clinical recognition and management. New York: Dekker, 1985.

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13

Tata, Nazneen. Molecular chronobiology of myocardial hypertrophy and the chronotherapeutic effects of captopril. 2006.

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14

Giorgio, Baroldi, Camerini F, Goodwin John F, and Italian Study Group on Cardiomyopathies., eds. Advances in cardiomyopathies. Berlin: Springer-Verlag, 1990.

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15

Zoccali, Carmine, Davide Bolignano, and Francesca Mallamaci. Left ventricular hypertrophy in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0107_update_001.

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Alterations in left ventricular (LV) mass and geometry and LV dysfunction increase in prevalence from stage 2 to stage 5 in CKD. Nuclear magnetic resonance is the most accurate and precise technique for measuring LV mass and function in patients with heart disease. Quantitative echocardiography is still the most frequently used means of evaluating abnormalities in LV mass and function in CKD. Anatomically, myocardial hypertrophy can be classified as concentric or eccentric. In concentric hypertrophy, the muscular component of the LV (LV wall) predominates over the cavity component (LV volume). Due to the higher thickness and myocardial fibrosis in patients with concentric LVH, ventricular compliance is reduced and the end-diastolic volume is small and insufficient to maintain cardiac output under varying physiological demands (diastolic dysfunction). In those with eccentric hypertrophy, tensile stress elongates myocardiocytes and increases LV end-diastolic volume. The LV walls are relatively thinner and with reduced ability to contract (systolic dysfunction). LVH prevalence increases stepwisely as renal function deteriorates and 70–80% of patients with kidney failure present with established LVH which is of the concentric type in the majority. Volume overload and severe anaemia are, on the other hand, the major drivers of eccentric LVH. Even though LVH may regress after renal transplantation, the prevalence of LVH after transplantation remains close to that found in dialysis patients and a functioning renal graft should not be seen as a guarantee of LVH regression. The vast majority of studies on cardiomyopathy in CKD are observational in nature and the number of controlled clinical trials in these patients is very small. Beta-blockers (carvedilol) and angiotensin receptors blockers improve LV performance and reduce mortality in kidney failure patients with LV dysfunction. Although current guidelines recommend implantable cardioverter-defibrillators in patients with ejection fraction less than 30%, mild to moderate symptoms of heart failure, and a life expectancy of more than 1 year, these devices are rarely offered to eligible CKD patients. Conversion to nocturnal dialysis and to frequent dialysis schedules produces a marked improvement in LVH in patients on dialysis. More frequent and/or longer dialysis are recommended in dialysis patients with asymptomatic or symptomatic LV disorders if the organizational and financial resources are available.
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16

Cardim, Nuno, Denis Pellerin, and Filipa Xavier Valente. Hypertrophic cardiomyopathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0042.

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Hypertrophic cardiomyopathy is a common inherited heart disease caused by genetic mutations in cardiac sarcomeric proteins. Although most patients are asymptomatic and many remain undiagnosed, the clinical presentation and natural history include sudden cardiac death, heart failure, and atrial fibrillation. Echocardiography plays an essential role in the diagnosis, serial monitoring, prognostic stratification, and family screening. Advances in Doppler myocardial imaging and deformation analysis have improved preclinical diagnosis as well as the differential diagnosis of left ventricular hypertrophy. Finally, echocardiography is closely involved in patient selection and in intraoperative guidance and monitoring of septal reduction procedures. This chapter describes the pathophysiology, clinical presentation, role of echocardiography, morphological features, differential diagnosis, diagnostic criteria in first-degree relatives, echo guidance for the treatment of symptomatic left ventricular outflow tract obstruction, and follow-up and monitoring of patients with hypertrophic cardiomyopathy.
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17

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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18

Kaprielian, Roger. Molecular and cellular mechanisms associated with cardiac hypertrophy following myocardial infarction in rats: Studies on ion channels and intracellular calcium. 2000.

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19

Maron, Barry J. Diagnosis and Management of Hypertrophic Cardiomyopathy. Wiley & Sons, Limited, John, 2007.

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20

Reckman, Yolan J., and Yigal M. Pinto. The role of non-coding RNA/microRNAs in cardiac disease. 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/9780198757269.003.0031.

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In the past two decades, our knowledge about non-coding DNA has increased tremendously. While non-coding DNA was initially discarded as ‘junk DNA’, we are now aware of the important and often crucial roles of RNA transcripts that do not translate into protein. Non-coding RNAs (ncRNAs) play important functions in normal cellular homeostasis and also in many diseases across all organ systems. Among the different ncRNAs, microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) have been studied the most. In this chapter we discuss the role of miRNAs and lncRNAs in cardiac disease. We present examples of miRNAs with fundamental roles in cardiac development (miR-1), hypertrophy (myomiRs, miR-199, miR-1/133), fibrosis (miR-29, miR-21), myocardial infarction (miR-15, miR17~92), and arrhythmias/conduction (miR-1). We provide examples of lncRNAs related to cardiac hypertrophy (MHRT, CHRF), myocardial infarction (ANRIL, MIAT), and arrhythmias (KCNQ1OT1). We also discuss miRNAs and lncRNAs as potential therapeutic targets or biomarkers in cardiac disease.
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21

Myocardial structure and function differences between steroid using and non-steroid using elite powerlifters and endurance athletes. 1989.

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22

Myocardial structure and function differences between steroid using and non-steroid using elite powerlifters and endurance athletes. 1992.

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23

Hypertrophic Cardiomyopathy. Univ of Tokyo Press, 1989.

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24

Paneni, Francesco, and Massimo Volpe. Co-morbidity (HFrEF and HFpEF): hypertension. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198784906.003.0415_update_001.

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Hypertensive heart disease is a major cause of heart failure (HF) and mortality. Hypertension precedes HF occurrence in 75% of cases, and carries a sixfold increase in HF risk as compared to non-hypertensive individuals. Most importantly, a minority of patients survive 5 years after the onset of hypertensive HF. In hypertensive patients, the heart may present different patterns of adaptive remodelling: concentric remodelling, concentric hypertrophy, and eccentric hypertrophy. Although most hypertensive patients are at high risk of developing concentric hypertrophy, a growing proportion of subjects display a concentric-to-eccentric progression eventually leading to left ventricular dilation and systolic dysfunction. Several factors including myocardial ischaemia, ethnicity, genetic background, history of diabetes, and blood pressure pattern may significantly influence the pathway from hypertension to left ventricular dilation. Patients with a concentric hypertrophy usually develop HF with preserved ejection fraction (HFpEF), whereas those with an eccentric (dilated) phenotype develop HF with reduced ejection fraction (HFrEF). Lowering blood pressure has a striking effect in reducing the risk of HF. Although available antihypertensive drugs are all successful in lowering blood pressure, angiotensin-converting enzyme inhibitors, angiotensin receptor blocker (ARBs), and diuretics are more effective than other drug classes in preventing HF. The combination of the neprilysin inhibitor sacubitril with the ARB valsartan (LCZ696) has recently been shown to be highly effective in reducing HF-related outcomes in hypertensive subjects. An individualized treatment scheme taking into account blood pressure levels, type of HF (HFpEF or HFrEF), and relevant co-morbidities (i.e. renal disease, diabetes) is currently the best approach to improve morbidity and mortality in hypertensive patients with HF.
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25

Maron, Barry J., and Lisa Salberg. Hypertrophic Cardiomyopathy: For Patients, Their Families and Interested Physicians. Wiley & Sons, Incorporated, John, 2008.

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26

Maron, Barry J., and Lisa Salberg. Hypertrophic Cardiomyopathy: For Patients, Their Families and Interested Physicians. Wiley & Sons, Incorporated, John, 2008.

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27

Pierard, Luc A., and Lauro Cortigiani. Stress echocardiography: diagnostic and prognostic values and specific clinical subsets. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0015.

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Stress echocardiography is a widely used method for assessing coronary artery disease, due to its high diagnostic and prognostic value. While inducible ischaemia predicts an unfavourable outcome, its absence is associated with a low risk of future cardiac events. The method provides superior diagnostic and prognostic information than standard exercise electrocardiography and perfusion myocardial imaging in specific clinical subsets, such as women, hypertensive patients, and patients with left bundle branch block. Stress echocardiography allows effective risk assessment also in the diabetic population. The evaluation of coronary flow reserve of the left anterior descending artery by transthoracic Doppler adds diagnostic and prognostic information to that of standard stress test. Stress echocardiography is indicated in the cases when exercise electrocardiography is unfeasible, uninterpretable or gives ambiguous result, and when ischaemia during the test is frequently a false-positive response, as in hypertensive patients, women, and patients with left ventricular hypertrophy. Viability detection represents another application of stress echocardiography. The documentation of a large amount of viable myocardium predicts improved ejection fraction, reverse remodelling, and improved outcome following revascularization in patients with ischaemic cardiomyopathy. Moreover, stress echocardiography can aid significantly in clinical decision-making in patients with valvular heart disease through dynamic assessment of primary or secondary mitral regurgitation, transvalvular gradients, and pulmonary artery systolic pressure, as well as before vascular surgery due to the excellent negative predictive value. Finally, stress echocardiography allows effective risk stratification in patients with hypertrophic cardiomyopathy through evaluation of inducible ischaemia, coronary flow reserve, and intraventricular gradient.
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28

London, Gerard M. Cardiovascular complications in end-stage renal disease patients. Edited by Jonathan Himmelfarb. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0268.

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Cardiovascular complications are the predominant cause of death in patients with end-stage renal disease (ESRD). The high incidence of cardiovascular complications results from pathology present before ESRD (generalized atherosclerosis, diabetes, hypertension) and an additive effect of multiple factors including haemodynamic overload and metabolic and endocrine abnormalities more or less specific to uraemia or its treatment modalities. These disorders are usually associated and can exacerbate each other. While ischaemic heart disease is a frequent cause of cardiac death, heart failure and sudden death are the most frequent causes of death in ESRD. Cardiomyopathy of overload with development of left ventricular hypertrophy and fibrosis are the most characteristic alterations and major determinants of prognosis. Left ventricular hypertrophy may result in systolic and/or diastolic dysfunction and is a risk factor for arrhythmias, sudden death, heart failure, and myocardial ischaemia. Arterial disease, whether due to atherosclerosis or arteriosclerosis (or both), represents a major contributory factor to the cardiovascular complications. Arterial disease may result in ischaemic complications (ischaemic heart disease, peripheral artery diseases) or arterial stiffening with direct consequences on left ventricular afterload, decreased coronary perfusion, and microvascular abnormalities (inward remodelling and microvessel rarefaction).
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29

Maron, Barry J., and Lisa Salberg. Hypertrophic Cardiomyopathy: For Patients, Their Families and Interested Physicians. Blackwell Publishing Professional, 2002.

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30

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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31

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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32

De Sutter, Johan, Piotr Lipiec, and Christine Henri. Heart failure: preserved left ventricular ejection fraction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0028.

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Nearly half of all patients with heart failure present with a preserved left ventricular ejection fraction (HFPEF). HFPEF is a pathophysiologically and clinically heterogeneous disease with an overall similar outcome to heart failure patients with a reduced ejection fraction. It is predominantly seen in elderly patients and comorbidities such as obesity, diabetes, hypertension, a sedentary lifestyle, and myocardial ischaemia play important roles in its development. In this chapter the conventional echocardiographic hallmarks of HFPEF including a preserved ejection fraction, left ventricular hypertrophy, left atrial dilatation, diastolic dysfunction, and pulmonary hypertension are presented. For the evaluation of left ventricular diastolic dysfunction, it is important to keep in mind that no single echocardiographic parameter is sufficiently accurate and reproducible to be used in isolation to make a diagnosis of diastolic dysfunction. The value of newer techniques including three-dimensional echocardiography and longitudinal strain assessment for the diagnosis and follow-up of HFPEF patients are promising but require further evaluation. As exercise-induced dyspnoea may be the first manifestation of HFPEF, the role of exercise echo (or diastolic stress testing) with evaluation of exercise-induced changes in left ventricular filling pressure and pulmonary artery systolic pressure is also presented. This chapter ends with a discussion on the echocardiographic parameters that can be used for risk stratification and follow-up of HFPEF patients.
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33

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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34

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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35

Goodwin, John F., and Eckhardt G. J. Olsen. Cardiomyopathies: Realisations and Expectations. Springer, 2011.

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36

Goodwin, John F. Cardiomyopathies: Realisations and Expectations. Springer, 1993.

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37

Olsen, Eckhardt G. J., and John F. Goodwin. Cardiomyopathies: Realisations and Expectations. Springer London, Limited, 2012.

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38

F, Goodwin John, and Olsen E. G. J, eds. Cardiomyopathies: Realisations and expectations. Berlin: Springer-Verlag, 1993.

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39

Goodwin, John F. Cardiomyopathies: Realisations and Expectations. Springer, 1993.

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40

D, Slaughter Graham R. Characterization and identification of the dual-lineage kinase, MUK/DLK in rat myocardium: A possible role in cardiac growth and hypertrophy. 2002.

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41

Andrade, Maria João, and Albert Varga. Stress echocardiography: methodology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0012.

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Stress echocardiography is the combination of echocardiography with a physical, pharmacological, or electrical stress. Good quality images are absolutely necessary and a quad-screen format should be applied for comparative analysis. Different stress echo protocols can be used in different pathologies. Exercise echocardiography has the advantages of its wide availability, low cost, and versatility for the assessment of various cardiac conditions. The most usual pathologies are suspected or known ischaemic heart disease, mitral and aortic valve diseases, hypertrophic cardiomyopathy, and pulmonary hypertension. Among exercise-independent stresses, dobutamine and dipyridamole are the most frequently used. Dobutamine is widely accepted for the evaluation of myocardial viability. The two tests have comparable accuracy for the detection of coronary artery disease. Ergonovine echo is highly feasible, accurate, and safe for the diagnosis of coronary vasospasm. High-rate pacing is especially appropriate in patients with a permanent pacemaker because non-invasive diagnosis of coronary artery disease in these patients is an extremely difficult task.
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42

Cortigiani, Lauro, and Eugenio Picano. Stress echocardiography. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199599639.003.0013.

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Stress echocardiography is a widely used method for assessing coronary artery disease, due to the high diagnostic and prognostic value. While inducible ischaemia predicts an unfavourable outcome, its absence is associated with a low risk of future events. The evaluation of coronary flow reserve by Doppler adds prognostic information to that of standard stress test. Stress echocardiography is indicated in cases when exercise testing is unfeasible, uninterpretable, or gives ambiguous result, and when ischaemia during the test is frequently a false positive response, as in hypertensives, women and patients with left ventricular hypertrophy. Viability detection represents another application of stress echocardiography. The documentation of viable myocardium predicts an improved outcome following revascularization in ischaemic and following resynchronization therapy in idiopathic cardiomyopathy. Moreover, stress echocardiography can aid significantly in clinical decision making in patients with valvular heart disease through dynamic assessment of mitral insufficiency, transvalvular gradients and pulmonary artery systolic pressure. Among the various stress modalities, exercise is safer than pharmacologic stress, in which major complications are three times more frequent with dobutamine than with dipyridamole. Stress echocardiography provides similar accuracy than perfusion scintigraphy but a substantially lower cost, without environmental impact and with no radiation biohazards for the patient.
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43

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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