Billman, G.E., Nishijima, Y., Belevych, A.E., Terentyev, D., Xu, Y., Haizlip, K.M., Monasky, M.M., Hiranandani, N., Harris, W.S., Gyorke, S., Carnes, C.A. and Janssen, P.M.L. (2010) Effects of dietary omega-3 fatty acids on ventricular function in dogs with healed myocardial infarctions: in vivo and in vitro studies. American Journal of Physiology—Heart and Circulatory Physiology, 298, H1219-H1228. doi:10.1152/ajpheart.01065.2009

has been cited by the following article:

• TITLE: Effects of omacor® on left ventricular remodelling consecutive to post myocardial infarction special issue-myocardial infarction

  AUTHORS: Bruno Le Grand

  KEYWORDS: Left Ventricular Remodelling; Myocardial Infarction; OMACOR®

  JOURNAL NAME: World Journal of Cardiovascular Diseases, Vol.3 No.5A, August 23, 2013

  ABSTRACT: Ventricular remodelling is the main trigger of the development of heart failure. Therefore, the reduction of structural remodelling is known to prevent the development of heart failure. The aim of the present study was to investigate the effects of OMACOR?, a well known mixture of EPA and DHA in an experimental model of heart failure induced by occlusion of left descending coronary artery and the reperfusion within 2 months. After a long term treatment of 2 months; OMACOR? (100 mg/kg) statistically significantly reduced the expansion of infarcted zone (35% ± 4%, P ± 3% in the vehicle group). The phosphorylation of Cx43 as biomarker of the cardiac remodelling was visualised by immunofluorescence in rat’s heart at the end of the study. In the vehicle-infarcted group, a significant de-phosphorylation of Cx43 was observed (8.2 ± 1.0 u.a, n = 8 compared to 11.8 ± 1.3 u.a in the sham group, n = 9) confirming a remodelling process in the infarcted group. In the group treated with OMACOR?,the de-phosphorylation of Cx43 was no longer observed compared to the sham group (16.4 ± 2.9 u.a, n = 9, NS). The present results demonstrate that a long term treatment with OMA-COR? reduced the infarcted size in experimental models of heart failure and that these anti-remodelling effects are due at least in part by resynchronizing the gap junction activity.