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      Cardiac Remodeling: Concepts, Clinical Impact, Pathophysiological Mechanisms and Pharmacologic Treatment

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          Abstract

          Cardiac remodeling is defined as a group of molecular, cellular and interstitial changes that manifest clinically as changes in size, mass, geometry and function of the heart after injury. The process results in poor prognosis because of its association with ventricular dysfunction and malignant arrhythmias. Here, we discuss the concepts and clinical implications of cardiac remodeling, and the pathophysiological role of different factors, including cell death, energy metabolism, oxidative stress, inflammation, collagen, contractile proteins, calcium transport, geometry and neurohormonal activation. Finally, the article describes the pharmacological treatment of cardiac remodeling, which can be divided into three different stages of strategies: consolidated, promising and potential strategies.

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          Most cited references46

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          Pathological ventricular remodeling: mechanisms: part 1 of 2.

          Despite declines in heart failure morbidity and mortality with current therapies, rehospitalization rates remain distressingly high, substantially affecting individuals, society, and the economy. As a result, the need for new therapeutic advances and novel medical devices is urgent. Disease-related left ventricular remodeling is a complex process involving cardiac myocyte growth and death, vascular rarefaction, fibrosis, inflammation, and electrophysiological remodeling. Because these events are highly interrelated, targeting a single molecule or process may not be sufficient. Here, we review molecular and cellular mechanisms governing pathological ventricular remodeling.
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            Role of oxidative stress in cardiac hypertrophy and remodeling.

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              Oxygen, oxidative stress, hypoxia, and heart failure.

              A constant supply of oxygen is indispensable for cardiac viability and function. However, the role of oxygen and oxygen-associated processes in the heart is complex, and they and can be either beneficial or contribute to cardiac dysfunction and death. As oxygen is a major determinant of cardiac gene expression, and a critical participant in the formation of ROS and numerous other cellular processes, consideration of its role in the heart is essential in understanding the pathogenesis of cardiac dysfunction.
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                Author and article information

                Journal
                Arq Bras Cardiol
                Arq. Bras. Cardiol
                abc
                Arquivos Brasileiros de Cardiologia
                Sociedade Brasileira de Cardiologia
                0066-782X
                1678-4170
                January 2016
                January 2016
                : 106
                : 1
                : 62-69
                Affiliations
                [01]Faculdade de Medicina de Botucatu, São Paulo, SP - Brazil
                Author notes
                Mailing Address: Leonardo Antônio Mamede Zornoff, Faculdade de Medicina de Botucatu. Departamento de Clínica Médica, Rubião Jr. Postal Code 18618-970, Botucatu, SP - Brazil. E-mail: lzornoff@ 123456fmb.unesp.br , lzornoff@ 123456cardiol.br
                Article
                10.5935/abc.20160005
                4728597
                26647721
                df89b26f-b4a1-4bc8-8dac-174c27bbb384

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 25 August 2015
                : 25 September 2015
                : 15 September 2015
                Categories
                Review Article

                ventricular remodeling,heart failure,medication therapy management,ventricular dysfunction / physiopathology

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