Titlebook: Cardiac Fibrosis and Heart Failure: Cause or Effect?; Ian M.C. Dixon,Jeffrey T. Wigle Book 2015 Springer International Publishing Switzerl

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Testing for Multivariate Distributions, and lead to heart failure. Classically thought to be the result of myofibroblasts activated from interstitial fibroblasts endogenously present within the heart, recent research has found that there are numerous cell sources contributing to fibrosis, including various stem cell lineages found in the

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Heteroscedasticity Tests for Regressions,o mechanical load, such as in conditions of hypertension and to repair injuries after myocardial infarct. Aberrant mechanosensing and/or persistent stress results in the chronic activation of cardiac fibroblasts and other progenitors into myofibroblasts. Myofibroblasts drive the development of fibro

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Multivariate Kernel Estimators,de: widely scattered microscopic scars which have replaced myocytes lost to necrosis; and a perivascular fibrosis of intramural coronary arteries. An animal model of aldosterone/salt treatment has been used to examine the pathogenic origins of myocyte necrosis and coronary vasculopathy. A common cel

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H. Büringer,H. Martin,K.-H. Schrievere form of CVD. Despite the vast diversity of CVD forms, many disease states are associated with maladaptive remodeling of the myocardial interstitium. Elevated fibrillar collagen expression is considered to be the primary contributor to altered cardiac function based on its adverse influence on elec

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H. Büringer,H. Martin,K.-H. Schriever the heart. Cardiac hypertrophy is characterized by enlargement of the heart as a result of an increase in cardiomyocyte size and also enhanced fibrosis due primarily to phenotypic conversion of fibroblasts to myofibroblasts. Also, atherosclerosis, a disease characterized by formation of plaque with

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https://doi.org/10.1007/978-1-4684-0538-5trix components including fibrillar collagen types I and III. Increased collagen synthesis and cross-linking strengthens the myocardium but also increases wall stiffness and thereby negatively impact both diastolic (filling) and systolic (contractile) function. Myocardial fibrosis occurs secondary t

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cardiac-arrest

Lack-of-Fit Tests Based on Linear Smoothers,dely investigated MMPs. MMP-9 functions primarily by directly degrading and activating ECM structural and non-structural molecules to regulate cardiac tissue remodeling. This activity is opposed under physiological conditions by a set of endogenous inhibitors known as tissue inhibitors of metallopro