Abstract 5078: Physical Training Reduces the Ability of Serum from Patients with Heart Failure to Induce Endothelial Cell Death
Physical training improves endothelial function and exercise capacity in patients with heart failure (HF). Serum from patients with cardiovascular diseases shows increased ability to induce apoptosis in human endothelial cells potentially contributing to the progression of atherosclerotic and endothelial dysfunction. Aim of this study was to evaluate the effect of cardiac rehabilitation on the pro-apoptotic properties of serum in patients with heart failure. Human Umbilical Vein Endothelial Cells (HUVECs) were incubated with 20% serum from 24 patients with HF (HYHA II) before and after cardiovascular rehabilitation. For apoptosis quantification, fragmented DNA was determined using Cell Death detection ELISA kit and propidium iodide (PI) staining analyzed by flow cytometry. The expression on endothelial cells of proteins involved in apoptotic pathway (bax, caspasi-3, bcl-2) was studied by Western blot analysis. Necrosis was evaluated measuring the lactate dehydrogenase released from damaged cells into the supernatant using a cytotoxicity detection kit. Serum from patients with heart failure showed a significantly greater ability to induce apoptosis (67 ± 4,6% vs 23 ± 5,2%, p<0,001) and necrosis (44 ± 3% vs 32 ± 2,1%, p<0,05) of HUVEC cells compared with controls. Cardiac rehabilitation significantly reduced the ability of patient serum to induce apoptosis (PI: 40.44% ± 3,9 vs 25.22% ± 2,6, p<0,01; ELISA: 67 ± 4,6% vs 42 ± 4,4%, p<0,001) and necrosis (44 ± 3% vs 33 ± 2%, p<0,01) of HUVEC cells compared to baseline. Moreover endothelial cells treated with serum after rehabilitation showed a significant decrease of bax expression (1,12 ± 0,06 vs 0,89 ± 0,08, p<0,05) and a significant decrease of cleaved Caspase-3 expression (0,91 ± 0,16 vs 0,72 ± 0,08, p<0.05). Serum of patients with heart failure has increased pro-apoptotic properties. Physical training reduces the ability of serum-contained factors to induce cell death of endothelial cells in patient with heart failure.