Abstract
We have previously reported that pulsatile mechanical stretch in vitro induced rapid secretion of vascular endothelial growth factor (VEGF) by cultured cardiac myocytes and that the stretch-induced secretion of VEGF was mainly mediated by secretion of transforming growth factor (TGF)-β1 by cardiac myocytes in an autocrine fashion. To investigate whether tachycardia-induced mechanical overload increases serum levels of VEGF and TGF-β1, we investigated the serum levels of VEGF and TGF-β1 in patients with atrial fibrillation undergoing defibrillation therapy. The serum VEGF level before defibrillation was significantly increased in 13 out of 20 patients (89.48±16.09 pg/ml [mean±SE]). After defibrillation, the serum VEGF level in these 13 patients significantly (p=0.019) decreased (65.04±16.61 pg/ml [mean± SE]), although it increased slightly in one patient. The serum TGF-β1 level before defibrillation therapy (13.01±1.97 pg/ml [mean±SE]) in these 12 patients also decreased after defibrillation therapy (11.47±2.06 pg/ml [mean±SE]). The changes in serum VEGF level significantly correlated with those in the serum TGF-β1 level in these 12 patients (r=0.73, p<0.05, n=12). Our data suggest that tachyarrhythmia-induced mechanical overload can increase the serum VEGF level, which can be a useful clinical marker for relative myocardial oxygen shortage in such patients. (Jpn Heart J 2000; 41: 27-32)
