Linn Elisabeth Lillerud Fosshaug has studied the biological role of omega-3 fatty acids in myocardial infarction and cardiac remodelling.
- Krill oil attenuates left ventricular dilatation after myocardial infarction in rats.
- Fatty acid composition in epicardial tissue differ between heart failure patients and controls.
- Omega-3 fatty acid derived pro-resolving lipid mediators are increased during an acute myocardial infarction.
Thesis: Adipose Tissue and Fatty Acids in Cardiovascular Disease
Candidate: Linn Elisabeth Lillerud Fosshaug
Time: October 25, 2019 at 12:30
Place: VID vitenskapelige høgskole, Diakonhjemmet: Møterom AU12
Link to university website
(1) Rats pre-treated with krill oil for 14 days before induction of myocardial infarction had significantly attenuated left ventricular dilatation seven days after the infarction, compared to controls. Echocardiography revealed that krill oil resulted in less increased heart and lung weight, matrix remodelling and inflammation. Furthermore, the levels of omega-3 fatty acids were significantly higher in the left ventricular tissue of rats pre-treated with krill oil.
(2) Interleukin-6, monounsaturated fatty acids, palmitoleic acid and fatty acid transportation are increased in epicardial tissue in patients with heart failure, whereas the omega-3 fatty acid docosahexaenoic acid is reduced. The levels of palmitoleic acids correlate with cardiac remodeling measured as NT-proBNP levels and left ventricular end-diastolic diameter.
Sixty patients who underwent cardiac surgery participated in the study, and half of them had heart failure with reduced ejection fraction. During the surgical procedure, the researchers extracted epicardial adipose tissue from the patients, in addition to subcutaneous fat. They then compared the levels of fatty acids and several other markers between the two groups of patients.
(3) Lipid mediators derived from polyunsaturated fatty acids are markedly increased immediately after onset of ST-elevation myocardial infarction. Fosshaug and co-workers compared the 15 patients with both healthy controls and patients with stable coronary artery disease. The levels declined during the following week. The results indicate that these mediators are increased to initiate repair, and strategies to boost these mechanisms may represent novel therapeutic opportunities for treatment of patients with acute myocardial infarction.
(1) Fosshaug, L. E., Berge, R. K., Beitnes, J. O., Berge, K., Vik, H., Aukrust, P., Gullestad, L., Vinge, L. E., & Øie, E. (2011). Krill oil attenuates left ventricular dilatation after myocardial infarction in rats. Lipids in health and disease, 10(1), 245.
(2) Fosshaug, L. E., Dahl, C. P., Risnes, I., Bohov, P., Berge, R. K., Nymo, S., Geiran, O., Yndestad, A., Gullestad, L., Aukrust, P., Vinge, L. E., & Øie, E. (2015). Altered levels of fatty acids and inflammatory and metabolic mediators in epicardial adipose tissue in patients with systolic heart failure. Journal of cardiac failure, 21(11), 916-923.
(3) Fosshaug, L. E., Colas, R. A., Anstensrud, A. K., Gregersen, I., Nymo, S., Sagen, E. L., Michelsen, A., Vinge, L. E., Gullestad, L., Halvorsen, B., Hansen, T. V., Aukrust, P., Dalli, J., & Yndestad, A. (2019). Early increase of specialized pro-resolving lipid mediators in patients with ST-elevation myocardial infarction. EBioMedicine, 46, 264-273.p