Rol de las mitocondrias y de las especies reactivas del oxígeno en la progresión de la insuficiencia cardíaca.

GUZMÁN MENTESANA GUSTAVO; DOMÍNGUEZ RICARDO; CÓRDOBA ROQUE; BÁEZ ALEJANDRA; LO PRESTI SILVINA; RIVAROLA WALTER; PONS PATRICIA; FRETES RICARDO; PAGLINI PATRICIA

Buenos Aires

Congreso; XXVII Congreso Nacional de Cardiología.; 2009

Federación Argentina de Cardiología

Heart failure is a very important cause of morbidity and mortality throughout the world. 1 Even though the extensive studies performed in the subject, the fundamental mechanisms involved in the genesis and progression of left ventricular failure are not clearly understood.2 The development of heart failure of different aetiology, involves abnormalities at tissue and cellular levels, such as: reduction in myocardial contractility, deficit in the capacity to respond to reactive oxygen species as a consequence of cardiac ischemia, changes in ionic fluxes and electrophysiological function and fibrosis and cardiac remodelling 3, which leads to loss of cardiomyocites, and consequently changes in the ability to produce and metabolize energy.4 Several studies have proposed that cardiac cells response to oxidative stress provokes a progression of cellular changes that target the mitochondria. 2,5,6,7 It has been demonstrated that oxidative stress initiates the mitochondrial apoptotic pathway, which would be involved in the pathophysiology of ischemic heart disease and heart failure. 7The heart is an organ with high energy demand; mitochondria represent 30% of the total volume of the myocytes and provide 90% of the heart cellular energy through fatty acids, which are the primary energy substrates for cardiac muscle ATP generation through the mitochondrial oxidative phosphorylation pathway.Observations carried out in heart failure animals models of and patients propose that mitochondria would be the key to understand the beginning and progression of several heart diseases such as dilated and hypertrophic cardiac disease, ischemic and alcoholic cardiopathy, electrical disturbances and myocarditis among others. 4-8Taking into consideration that heart failure is a great public health issue, largely preventable through blood pressure control and reduction of other vascular risk factorsthat affect not only the heart, we conducted this study in order to establish the mitochondrial involvement in the heart failure, searching a link between clinical symptoms and mitochondria damage and if there is a possible parallelism between cardiac and skeletal muscle mitochondria abnormalities. The understanding of the impact of mitochondria alterations in the cardiac disease will improve the diagnosis, prognosis and the possibility of modifying the natural evolution of heart disease.