Cardiac Left Ventricular Hypertrophy [electronic resource] /

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.

Saved in:
Bibliographic Details
Main Authors: Keurs, H. E. D. J. Ter. editor., Schipperheyn, J. J. editor., SpringerLink (Online service)
Format: Texto biblioteca
Language:eng
Published: Dordrecht : Springer Netherlands, 1983
Subjects:Medicine., Cardiology., Medicine & Public Health.,
Online Access:http://dx.doi.org/10.1007/978-94-009-6759-5
Tags: Add Tag
No Tags, Be the first to tag this record!
id KOHA-OAI-TEST:176566
record_format koha
institution COLPOS
collection Koha
country México
countrycode MX
component Bibliográfico
access En linea
En linea
databasecode cat-colpos
tag biblioteca
region America del Norte
libraryname Departamento de documentación y biblioteca de COLPOS
language eng
topic Medicine.
Cardiology.
Medicine & Public Health.
Cardiology.
Medicine.
Cardiology.
Medicine & Public Health.
Cardiology.
spellingShingle Medicine.
Cardiology.
Medicine & Public Health.
Cardiology.
Medicine.
Cardiology.
Medicine & Public Health.
Cardiology.
Keurs, H. E. D. J. Ter. editor.
Schipperheyn, J. J. editor.
SpringerLink (Online service)
Cardiac Left Ventricular Hypertrophy [electronic resource] /
description 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.
format Texto
topic_facet Medicine.
Cardiology.
Medicine & Public Health.
Cardiology.
author Keurs, H. E. D. J. Ter. editor.
Schipperheyn, J. J. editor.
SpringerLink (Online service)
author_facet Keurs, H. E. D. J. Ter. editor.
Schipperheyn, J. J. editor.
SpringerLink (Online service)
author_sort Keurs, H. E. D. J. Ter. editor.
title Cardiac Left Ventricular Hypertrophy [electronic resource] /
title_short Cardiac Left Ventricular Hypertrophy [electronic resource] /
title_full Cardiac Left Ventricular Hypertrophy [electronic resource] /
title_fullStr Cardiac Left Ventricular Hypertrophy [electronic resource] /
title_full_unstemmed Cardiac Left Ventricular Hypertrophy [electronic resource] /
title_sort cardiac left ventricular hypertrophy [electronic resource] /
publisher Dordrecht : Springer Netherlands,
publishDate 1983
url http://dx.doi.org/10.1007/978-94-009-6759-5
work_keys_str_mv AT keurshedjtereditor cardiacleftventricularhypertrophyelectronicresource
AT schipperheynjjeditor cardiacleftventricularhypertrophyelectronicresource
AT springerlinkonlineservice cardiacleftventricularhypertrophyelectronicresource
_version_ 1756264155162083328
spelling KOHA-OAI-TEST:1765662018-07-30T22:55:17ZCardiac Left Ventricular Hypertrophy [electronic resource] / Keurs, H. E. D. J. Ter. editor. Schipperheyn, J. J. editor. SpringerLink (Online service) textDordrecht : Springer Netherlands,1983.engLeft 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.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.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.Medicine.Cardiology.Medicine & Public Health.Cardiology.Springer eBookshttp://dx.doi.org/10.1007/978-94-009-6759-5URN:ISBN:9789400967595