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Revista chilena de cardiología

versión On-line ISSN 0718-8560

Resumen

LONIS, Alejandra et al. Cardiac remodeling in experimental cardiac failure induced by hyperlipidemia in mice. Rev Chil Cardiol [online]. 2020, vol.39, n.1, pp.24-33.  Epub 01-Abr-2020. ISSN 0718-8560.  http://dx.doi.org/10.4067/S0718-85602020000100024.

SR-B1 KO/ApoER6 1h/h mice fed a high saturated fat diet develop severe coronary atheromatosis, and cardiac failure with a high mortality rate. Cardiac remodeling under these conditions has not been well studied.

Aim:

To evaluate the time course of left ventricular function, cardiac remodeling and survival associated to the administration of an atherogenic diet.

Method:

Homozygote SR-B1 KO/ApoER6 1h/h mice received an atherogenic diet for 8 weeks. Mice receiving a normal diet served as controls. Survival rate, myocardial fibrosis, cardiomyocyte size, apoptosis and infiltration by inflammatory or mononuclear cells were compared between groups. A TUNEL technique was used to evaluate apoptosis.

Results:

A 46.7% survival reduction compared to controls was observed in the experimental group (p<0.01), due to left ventricular and atrial dilatation associated to a decrease in ejection fraction (79,3 ± 1,3% vs 66 ± 3,7%, p<0,01, respectively). Also, an increased cardiac weight, 2.6 times greater was observed in the experimental group, compared to controls. Mice receiving the atherogenic diet showed an 80% increased lung weight. There was no evident change in cardiomyocytes, but there was more (7.9 times) cardiac fibrosis (p<0.01) and 55.9 times more apoptotic cells. (p<0.01), along with a greater number of inflammatory cells and ED1 mononuclear cells.

Conclusion:

Mice receiving an atherogenic diet develop heart failure and reduced survival rate. This is associated with cardiac remodeling with underlying apoptosis an ventricular wall fibrosis. It is posible that wall edema might contribute to the observed cardiac remodeling.

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