CENTRO DE INVESTIGACIONES CARDIOVASCULARES "DR. HORACIO EUGENIO CINGOLANI"
Unidad Ejecutora - UE
congresos y reuniones científicas
Physiologic cardiac hypertrophy: impact of its development upon a model od pathologic hypertrophy
ENNIS IL; NOLLY MB; PINILLA OA; GARCIARENA CD; CARRANZA VB; PIAGGIO MR; ESCUDERO EM; CINGOLANI
Buenos Aires, Argentina
Congreso; 16th World Congress of Cardiology; 2008
World Heart Federation
Pathologic cardiac hypertrophy (CH) is an independent risk factor for cardiovascular morbidity and mortality. It usually leads to heart failure development. On the other hand, cardiac hypertrophy induced by intense and periodical execersise training is an adaptive response of the myocardium to the increase haemodinamic demand and of course it does not represent a risk factor. The aim of the present work was to analize in spontaneously hypertensive rats (SHR) the effect of intense exercise trainning (swiming, 90 min/day, 5 days a week during 2 months) upon CH and cardiac function. Male SHR (5 month of age) were randomly assigned to a control group (C, no physical training) or the excersice group (E, swimming rutine). Echocardiographic studies of each animal were performed at day 1 and day 60 of the protocol. At the end of the protocol the animals were euthanized and hearts kept for histological , biochemical and molecular analizys. The 60 day swimming rutine induced a significant increase in left ventricular mass determined by ecochardiography (3.02±0.07 in E vs. 2.76±0.07 mg/g in C; p<0.02), however in the excersised animals a significant reduction in the expression of molecular markers of CH was detected by real time RT-PCR: atrial natriuretic peptide (ANP, C: 100±19; E: 41±10 %, p<0.05) and myosin light chain-2 (MLC-2, C: 100±8; E: 61±9 %; p<0.05). Moreover, exercise training improved cardiac function when measured by the mid-ventricular shortening (C: 32.12±1.01; E: 36.03±1,34; p<0.05). The histological study revealed a significant reduction in collagen fraction in the exercised animals. In conclusion, our results suggest that intense and programmed exercise training is capable of inducing physiological CH even in the presence of pathologic CH, leading to an improvement in the histology, molecular pattern and yet more important in contractility. This finding could be clinically relevant in the prevention of heart failure in patients with pathologic CH.