5 edition of Functional aspects of the normal, hypertrophied, and failing heart found in the catalog.
by M. Nijhoff, Distributors for North America, Kluwer Academic Publishers in Boston, Hingham, MA
Written in English
|Statement||edited by Francis L. Abel and Walter H. Newman.|
|Series||Developments in cardiovascular medicine ;, 42, Developments in cardiovascular medicine ;, v. 42.|
|Contributions||Abel, Francis L., 1931-, Newman, Walter H., International Society for Heart Research. American Section. Meeting|
|LC Classifications||QP111.2 .F86 1984|
|The Physical Object|
|Pagination||xvi, 368 p. :|
|Number of Pages||368|
|LC Control Number||84010137|
A four chamber view (longitudinal section of the heart) may show sigmoid deformation of the hypertrophied septum Only a small portion of the left ventricle may be involved (segmental hypertrophy) and calculated left ventricular mass may be normal Any degree of wall thickness may be seen with the HCM genetic substrate. This coupling is mediated through gap junctions, such as conne which can become disorganized in the hypertrophied or failing heart, disrupting normal impulse conduction It is worth remembering that the atria are also touched by remodeling events in cardiac hypertrophy and by:
Ventricular hypertrophy (VH) is thickening of the walls of a ventricle (lower chamber) of the heart. [better source needed] Although left ventricular hypertrophy (LVH) is more common, right ventricular hypertrophy (RVH), as well as concurrent hypertrophy of both ventricles can also cular hypertrophy can result from a variety of conditions, both adaptive and lty: Cardiology. This book reviews previous investigations performed in isolated failing and nonfailing human myocardium. It provides comprehensive information on alterations in the failing human heart occurring at the levels of extracellular matrix, sarcolemma, sarcoplasmic .
The role of action potential prolongation and altered intracellular calcium handling in the pathogenesis of heart failure Alan D Wickenden a a The Centre for Cardiovascular Research, Division of Cardiology, The Toronto Hospital, The Department of Medicine and The Institute of Medical Sciences, University of Toronto, College Street, CCRW 3 Cited by: Heart failure (HF) is a clinical syndrome caused by a decline in cardiac systolic or diastolic function, which leaves the heart unable to pump enough blood to meet the normal physiological.
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Section III is primarily devoted to the mechanical aspects of the function of the heart in both hypertrophy and failure including the molecular changes in the myocyte, hypertrophied in neural control, and in inotropic responsiveness of the hypertrophied and failing heart.
Functional Aspects of the Normal, Hypertrophied, and Failing Heart Editors: Abel, Francesco, Newman, Walter H. (Eds.). Functional aspects of the normal, hypertrophied, and failing heart.
III Functional Abnormalities of the Hypertrophied and Failing Heart.- 10 Subcellular Changes in Conpensated and Failing Hypertrophied Hearts.- 11 Autonomic Neural Control of the Failing Heart.- 12 The Inotropic Responsiveness of the Failing Heart.- 13 New Inotropic Drugs.
Functional Aspects of the Normal, Hypertrophied, and Failing Heart. [Francis L Abel; Walter H Newman] -- These Proceedings are from the Fifth Annual Meeting of the American Section of the International Society for Heart Research held at Hilton Head Island, South Carolina, September 21.
In: Abel F.L., Newman W.H. (eds) Functional Aspects of the Normal, Hypertrophied, and Failing Heart. Developments in Cardiovascular Medicine, vol Springer, Boston, MACited by: 6. The structural and functional peculiarities of the hypertrophied and insufficient heart are presented for various types of hypertrophy, taking into account systolic and diastolic function.
The most important factors and failing heart book to transition from cardiac hypertrophy to failure are discussed under the aspect of their mechanical by: 1. Functional Aspects of the Normal, Hypertrophied, and Failing Heart pp | Cite as Excitation, Contraction and the Distribution of Calcium and Sodium in Smooth Muscle AuthorsAuthor: A.
Somlyo, A. Somlyo, M. Bond, T. Kitazawa, H. Shuman, A. Wasserman. In: Abel F.L., Newman W.H. (eds) Functional Aspects of the Normal, Hypertrophied, and Failing Heart. Developments in Cardiovascular Medicine, vol Springer, Boston, MAAuthor: K.
Schwartz, J. Mercadier, L. Rappaport, J. Samuel, D. Charlemagne, L. Lelievre, B. Swynghedau. The hypertrophied heart the increase in plasma renin activity occurring in rats exposed to hypoxia of the same degree and duration but with normal NaCl intake.
both with and without. The ultrastructure of mitochondria in hypertrophied but non-failing hearts was normal. The respiratory activity of mitochondria isolated from these same hearts was increased.
Profiles of granular endoplasmic reticulum and free ribosomes, widening of Z bands and distortions of intercalated discs were observed in hypertrophied hearts and were Cited by: He found that the hypertrophied heart could do more volume work or pressure work per minute than the normal heart. However, he did not relate work ''capacity" to the mass of ventricular tissue.
In his experiments the mean weights of the left ventricles (including the septum) were Gm. for normal hearts, and Gm.
for hypertrophied by: The Hypertrophied Heart Biophysical, biochemical, and morphological aspects of hypertrophy.
International Erwin Riesch Symposium,Tübingen, September 26–29, Editors: Jacob, R. (Hrsg.) Free Preview. Buy this book eBook $ price for USA in USD (gross) Buy eBook ISBN ; Digitally watermarked, DRM-free Brand: Steinkopff-Verlag Heidelberg. The decreased tension developed by failing and hypertrophied heart muscle can be related to an intrinsic weakness of the muscle rather than an abnormal position on a basically normal length-tension curve, thus allowing re- jection of the hypothesis that the decreased contractility of failing heart muscle is due to its operation along the Cited by: 2.
[Na +] i transport in and out of cardiac myocytes. Several transporters facilitate Na + entry into cardiac myocytes (Fig. 1), with Na + channels and NCX being the most important quantitatively in the normal heart.
Other transporters however may become prominent in producing Na + overload under pathophysiological conditions. For example, the activity of NHE and NBC is increased greatly Cited by: wall stress and permit normal cardiovascular function at rest (i.e.
compensated growth). However, function in the hypertrophied heart may eventually decompensate, leading to left ventricle dilation and heart failure.6 In contrast, physiological hypertrophy does not decompensate into dilated cardiomyopathy or heart failure.4,5Cited by: Heart hypertrophy is a condition where the muscular wall of the heart becomes thickened.
The heart wall is a muscle. It can thicken as a result of high blood pressure do to the heart having to pump against a higher blood pressure or it can thicken due to valvular problems especially when.
Reports demonstrating benefit from inhibition of cardiac hypertrophy despite persistence of the initiating stimulus have been short term (≈10% to 15% of a normal mouse lifespan); long-term targeting of hypertrophy in a heart with increased wall stress might still result in by: Recent studies call into question the necessity of hypertrophic growth of the heart as a “compensatory” response to hemodynamic stress.
These findings, coupled with recent progress in dissecting the molecular bases of hypertrophy, raise the prospect of suppressing hypertrophy without provoking circulatory by: What you can do. To promote heart health: Include physical activity in your daily routine. Try walking, swimming or other activities you enjoy.
Regular moderate physical activity can help you maintain a healthy weight and lower your heart disease risk. In: Abel F.L., Newman W.H. (eds) Functional Aspects of the Normal, Hypertrophied, and Failing Heart.
Developments in Cardiovascular Medicine, vol Springer, Boston, MAAuthor: Niels Haugaard, Marilyn E. Hess. Alterations in myocyte Ca 2+ regulation are centrally involved in the reduced contractility reserve of the hypertrophied or failing heart.1, 2, 3 Although contraction and Ca 2+ transient amplitudes of failing ventricular myocytes are near or above normal at slow pacing rates, the positive inotropy normally induced by increased heart rate or Cited by: 1.
Author(s): Abel,Francis L,; Newman,Walter H; International Society for Heart Research. American Section. Meeting,(5th: Hilton Head Island, S.C.) Title.15 During ischemic heart conditions, glucose becomes the prevalent source of energy for myocardial tissue À both in chronically hypertrophied and normal hearts.
16 In severely ischemic.