A new study led by researchers at The University of Alabama at Birmingham (UAB) revealed that the lipid compound Resolvin D1 is capable of reducing prolonged inflammation and heart failure in mice models after a heart attack. The study was recently published in the Journal of Molecular and Cellular Cardiology and is entitled “Resolvin D1 activates the inflammation resolving response at splenic and ventricular site following myocardial infarction leading to improved ventricular function.”
The Centers for Disease Control and Prevention estimates that approximately 5.1 million individuals in the United States suffer from heart failure, a condition that is responsible for one in every nine deaths. About half of the individuals with heart failure die within five years after the diagnosis.
In a heart attack, cardiac muscle cells suffer damage and die. In this situation, the body’s immune system reacts through inflammation, a beneficial response that removes dead cells and promotes the repair in the injured site. Prolonged, unresolved inflammation, on the other hand, can significantly contribute to the development of heart failure after myocardial infarction (heart attack).
Inflammation can be counteracted by resolvins, a family of bioactive lipid products naturally generated in the human body through omega-3 fatty acid transformation. Resolvin D1 (RvD1) in particular, is the product of the docosahexaenoic omega-3 fatty acid, which is especially found in fish oil. In this study, researchers assessed the role of resolvin D1 (RvD1) in inflammation in post-myocardial infarction. Two forms of RvD1 were tested: the free acid form (RvD1) and a more stable form incorporated into liposomes (Lipo-RvD1).
Researchers analyzed the left ventricle, which is the major pumping chamber of the heart, and splenic remodeling after myocardial infarction, as splenocytes (immune cells stored in the spleen) have been shown to be involved in the heart failure that follows an infarction. The team used mice in which the levels of RvD1 were boosted through an injection of Lipo-RvD1 or RvD1 three hours after the induced heart attack.
The team found that mice that received RvD1 boost, either free or as Lipo-RvD1, showed reduced heart failure, with less left ventricle enlargement and improved function, less lung edema (fluid in the lung) and less collagen deposition, when compared to mice that received a control saline solution. In the spleen, researchers found that the levels of pro-resolving mediators that help resolve inflammation, such as RvD1, RvD2, Maresin 1 (MaR1) and Lipoxin A4 (LXA4) were increased in RvD1 injected mice 5 days after myocardial infarction. RvD1 administration was also found to reduce macrophage density, an important type of immune cells, and stimulate early resolution of inflammation. Collagen deposition was also reduced, thus reducing fibrosis and stabilizing the extracellular matrix of the heart.
The research team concluded that RvD1 and Lipo-RvD1 are able to promote the resolution of prolonged inflammation initiated by myocardial infarction, this way delaying the onset of heart failure. “Thus, Resolvin D1 has the potential to delay heart failure but still requires long-term studies in order to prove its utilization in chronic heart failure management,” explained the study’s senior author Dr. Ganesh Halade in a news release. “This paper is the first to show resolvin’s effect on heart failure.”
