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|Additional Physical Format:||Print version:|
|Material Type:||Document, Internet resource|
|Document Type:||Internet Resource, Computer File|
|All Authors / Contributors:||
J Holtz; H Drexler; H Just
|Description:||1 online resource (viii, 206 pages)|
|Contents:||Biological adaptation of the myocardium to a permanent change in loading conditions --
Role of protein kinase system in the signal transduction of stretch-mediated myocyte growth --
Sympathetic modulation of the cardiac myocyte phenotype: studies with a cell-culture model of myocardial hypertrophy --
Growth factors, growth factor response elements, and the cardiac phenotype --
Signaling mechanisms for the activation of an embryonic gene program during the hypertrophy of cardiac ventricular muscle --
Endothelial modulation of myocardial contraction: mechanisms and potential relevance in cardiac disease --
The regulation of calcium cycling in stressed hearts --
Energetics of calcium cycling in nonfailing and failing human myocardium --
Spontaneous sarcoplasmic reticulum Ca2+ release leads to heterogeneity of contractile and electrical properties of the heart --
Afterdepolarizations and triggered activity --
The contribution of nonreentrant mechanisms to malignant ventricular arrhythmias --
The potential role of Ca2+ for electrical cell-to-cell uncoupling and conduction block in myocardial tissue --
Failure of myocardial inactivation: a clinical assessment in the hypertrophied heart --
Diastolic dysfunction in pressure-overload hypertrophy and its modification by angiotesin II: current concepts --
Mechanisms of cardiac growth. The role of the rennin-angiotensin system --
Cardiac fibroblasts: function, regulation of gene expression, and phenotypic modulation --
Modulation of myocardial sarcoplasmic reticulum Ca++ -ATPase in cardiac hypertrophy by angiotensin converting enzyme?
|Responsibility:||edited by J. Holtz, H. Drexler, H. Just.|
Traditionally, cardiac hypertrophy is regarded as an adaptation of the heart to permanent mechanical overload. Regardless of the fact that many different and often unknown primary causes can result in heart failure, mechanical overload and myocardial hypertrophy is found in almost all forms of manifest chronic heart failure (apart from failure due to extramyocardial hindrances to inflow or to relaxation). However, the reactive enlargement of myocardial mass in response to an enhanced hemodynamic burden appears to be a double-edged sword. Obviously, the hypertrophy helps to reduce the enhanced ventricular wall stress in heart failure by adding contractile units to the overdistended chamber wall. However, in recent years it became clear that this adaptive hypertrophic process is rather complex and may include problematic facets. The adaptive hypertrophy includes proliferation of the nonmyocyte cardiac cells as well as substantial alterations in the phenotype of the growing myocytes due to differential changes in gene expression.
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