Mechanisms of disease: pathologic structural remodeling is more than adaptive hypertrophy in hypertensive heart disease

Changes in the composition of cardiac tissue develop in arterial hypertension and lead to structural remodeling of the myocardium. Structural remodeling is the consequence of a number of pathologic processes, mediated by mechanical, neurohormonal and cytokine routes, occurring in the cardiomyocyte a...

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Detalles Bibliográficos
Autores: Diez-Martinez, J. (Javier)|||/items/4f3a0e43-12bf-403d-9dc7-31fab0d11d41, Gonzalez, A. (Arantxa)|||/items/9c64c0f4-66b4-4b51-8593-0e50c091a515, Lopez-Salazar, M.B. (María Begoña)|||/items/153e0e37-14b0-403e-afab-8af00c4edde0, Querejeta, R. (Ramón)|||/items/e50c385d-36de-424d-8c56-3022d68a9f98
Tipo de recurso: artículo
Fecha de publicación:2005
País:España
Institución:Universidad de Navarra
Repositorio:Dadun. Depósito Académico Digital de la Universidad de Navarra
Idioma:inglés
OAI Identifier:oai:dadun.unav.edu:10171/19965
Acceso en línea:https://hdl.handle.net/10171/19965
Access Level:acceso abierto
Palabra clave:Arterial hypertension
Collagen
Fibrosis
Left-ventricular
Hypertrophy
Descripción
Sumario:Changes in the composition of cardiac tissue develop in arterial hypertension and lead to structural remodeling of the myocardium. Structural remodeling is the consequence of a number of pathologic processes, mediated by mechanical, neurohormonal and cytokine routes, occurring in the cardiomyocyte and the noncardiomyocyte compartments of the heart. One of these processes is related to the disruption of the equilibrium between the synthesis and degradation of collagen type I and III molecules, which results in an excessive accumulation of collagen type I and III fibers in the interstitium and the perivascular regions of the myocardium. The clinical relevance of ventricular fibrosis is that it might contribute to the increased cardiac risk of patients with hypertensive heart disease. This review focuses on the mechanisms of hypertensive ventricular fibrosis and its clinical consequences. In addition, we discuss the noninvasive methods for the diagnosis of cardiac fibrosis and the therapeutic strategies aimed to promote its reduction.