Left ventricular hypertrophy (LVH) is usually considered to be a compen satory adjustment of heart muscle to an inreased work load. LVH develops in the course of valvular or congenital heart disease, or when part of the myocardium is damaged by long-standing ischemia or infarction. In the hypertrophied heart the muscle fibers increase in size, not in number. The fibers are found to contain a larger number of myofibrils and the cell organelles are larger. From epidemiologic studies it is known that even mild LVH is associated with myocardial ischemia, ventricular arrhythmias, and sudden cardiac death. Most cases of LVH show focal degenerative tissue changes including cellular atrophy, myofibrillar disorganization, interstitial fibrosis, and loss of intracellular connections. Myocardial dysfunction develops and, unlike the functional adaptive changes found in pure hypertrophy, is not reversible by surgical treatment of the valvular heart disease or medical correction of hypertension. Interstitial fibrosis, intracellular changes of musc Ie cells, and loss of contract ile tissue lead to poor mechanical function and undoubtedly increase the risk of ischemia, arrhythmias, or sudden death, a well-recognized problem in patients with a variety of heart diseases. Even When successfully treated, the patients may remain at risk if the compensatory hypertrophy is not fully reversed. Epidemiologic studies conducted in the Framingham population in the early 1950' s demonstrated LVH according to electrocardiographic criteria in 1. 5% of the population; 2% of the population had LVH according to chest X-ray criteria.
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Section 1: Prevalence and risks of left ventricular hypertrophy.- Epidemiologic features of left ventricular hypertrophy in normotensive and hypertensive subjects.- Sensitivity of echocardiography for detection of left ventricular hypertrophy.- Determinants and modulators of left ventricular structure.- Section 2: Etiology and functional aspects at the cellular level.- Relationship between cardiac work and cardiac growth: some general thoughts on cardiac hypertrophy.- Myocardial cell properties and hypertrophy.- Section 3: Etiology and functional aspects of the hypertrophied heart.- Some functional consequences of left ventricular hypertrophy in hypertension.- Left ventricular hypertrophy, matching between heart and arterial system.- Assessment of the function of the hypertrophied heart.- Section 4: The coronary circulation in the hypertrophied heart.- Total and transmural perfusion of the hypertrophied heart.- Left ventricular hypertrophy and myocardial ischemia.- Coronary flow mechanics of the hypertrophied heart.- Section 5: Diagnostic developments in detection of left ventricular hypertrophy.- Electrocardiographic aspects of left ventricular hypertrophy.- Radioisotope studies in patients with left ventricular hypertrophy.- Section 6: Therapeutic aspects of left ventricular hypertrophy.- Mediators of changes in left ventricular mass during antihypertensive therapy.- Left ventricular hypertrophy in patients on chronic hemodialysis: a sign of fluid excess.- Protection of the hypertrophied heart during open-heart surgery.- Aortic valve replacement in aortic stenosis and regression of left ventricular hypertrophy.
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Taschenbuch. Condizione: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -Left ventricular hypertrophy (LVH) is usually considered to be a compen satory adjustment of heart muscle to an inreased work load. LVH develops in the course of valvular or congenital heart disease, or when part of the myocardium is damaged by long-standing ischemia or infarction. In the hypertrophied heart the muscle fibers increase in size, not in number. The fibers are found to contain a larger number of myofibrils and the cell organelles are larger. From epidemiologic studies it is known that even mild LVH is associated with myocardial ischemia, ventricular arrhythmias, and sudden cardiac death. Most cases of LVH show focal degenerative tissue changes including cellular atrophy, myofibrillar disorganization, interstitial fibrosis, and loss of intracellular connections. Myocardial dysfunction develops and, unlike the functional adaptive changes found in pure hypertrophy, is not reversible by surgical treatment of the valvular heart disease or medical correction of hypertension. Interstitial fibrosis, intracellular changes of musc Ie cells, and loss of contract ile tissue lead to poor mechanical function and undoubtedly increase the risk of ischemia, arrhythmias, or sudden death, a well-recognized problem in patients with a variety of heart diseases. Even When successfully treated, the patients may remain at risk if the compensatory hypertrophy is not fully reversed. Epidemiologic studies conducted in the Framingham population in the early 1950' s demonstrated LVH according to electrocardiographic criteria in 1. 5% of the population; 2% of the population had LVH according to chest X-ray criteria. 304 pp. Englisch. Codice articolo 9789400967618
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Taschenbuch. Condizione: Neu. This item is printed on demand - Print on Demand Titel. Neuware -Left ventricular hypertrophy (LVH) is usually considered to be a compen satory adjustment of heart muscle to an inreased work load. LVH develops in the course of valvular or congenital heart disease, or when part of the myocardium is damaged by long-standing ischemia or infarction. In the hypertrophied heart the muscle fibers increase in size, not in number. The fibers are found to contain a larger number of myofibrils and the cell organelles are larger. From epidemiologic studies it is known that even mild LVH is associated with myocardial ischemia, ventricular arrhythmias, and sudden cardiac death. Most cases of LVH show focal degenerative tissue changes including cellular atrophy, myofibrillar disorganization, interstitial fibrosis, and loss of intracellular connections. Myocardial dysfunction develops and, unlike the functional adaptive changes found in pure hypertrophy, is not reversible by surgical treatment of the valvular heart disease or medical correction of hypertension. Interstitial fibrosis, intracellular changes of musc Ie cells, and loss of contract ile tissue lead to poor mechanical function and undoubtedly increase the risk of ischemia, arrhythmias, or sudden death, a well-recognized problem in patients with a variety of heart diseases. Even When successfully treated, the patients may remain at risk if the compensatory hypertrophy is not fully reversed. Epidemiologic studies conducted in the Framingham population in the early 1950' s demonstrated LVH according to electrocardiographic criteria in 1. 5% of the population; 2% of the population had LVH according to chest X-ray criteria.Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg 304 pp. Englisch. Codice articolo 9789400967618
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