Resumen

GIRALDO, Alejandro. Role of oxidative and nitrosative stress in cardiac hypertrophy and ventricular remodeling. Acta Med Colomb [online]. 2010, vol.35, n.2, pp.82-95. ISSN 0120-2448.

Objective: to review the molecular mechanisms of oxidative and nitrosative stress in the process of ventricular remodeling and the pathophysiology of heart failure. Metodology: a Medline (PubMed) search was performed using the keywords: oxidative stress, ventricular remodeling, heart failure, nitrosative stress. Cited bibliography in key papers from renowned authors in this field of research was also examined. Results: 112 articles were selected as the most relevant regarding the several systems of oxidative stress production in the cardiovascular system in addition to their relevance to the pathophysiology of heart failure. Conclusions: the stress responses of cardiomyocytes and the myocardial tissue as a whole are likely to constitute a significant aspect of the development of cardiac pathologies. Oxidative stress is a common theme in the pathophysiology of ischemic and non-ischemic cardiomyopathy. Cardiac pathologies such as heart failure are usually preceded by cardiac hypertrophy secondary, at least in part, to the generation of reactive oxygen species in cardiomyocytes. Several mechanisms have been implicated in ventricular remodeling during heart failure progression which depends on homeostatic alterations in oxidative and nitrosative stress. The discussion is centered in the exposition of recent evidence from research carried out either in vitro in cultured cardiomyocytes as well as from in vivo models of experimental cardiac pathologies. The clinical implications of this novel understanding, although very promising for the therapeutic treatment of heart failure, up until now, have failed to translate with total success to the clinical practice in several clinical trials (Acta Med Colomb 2010; 2010; 35: 82-95).

Palabras clave : heart failure; oxidative stress; ventricular remodeling; cardiac hypertrophy; NAD(P) H oxidases.

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