Chronic inflammation provokes a downward spiral in many diseases, including congestive heart failure, atherosclerosis and peripheral artery disease. A University of Alabama at Birmingham-led research team has now found that mice that are given the lipid “Resolvin D1” after experimental heart attacks have substantially reduced amounts of inflammation and 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,” Ganesh Halade, Ph.D., and his study co-authors concluded in a Journal of Molecular and Cellular Cardiology article recently published online. “This paper is the first to show resolvin’s effect on heart failure,” said Halade, an assistant professor in the Division of Cardiovascular Disease,UAB Department of Medicine.
Inflammation is the body’s immune system response to injury, such as the muscle cells that die in a heart attack. The early acute inflammation response is beneficial, removing dead cells and beginning repairs in the injured area. Lingering, ungoverned chronic inflammation, however, is harmful. Resolvin D1 is naturally produced in the body as a metabolite of one omega-3 fatty acid that is especially present in fish oil. It and other resolvins have potent anti-inflammatory effects. Resolvins are natural signaling lipids in the body; but in the mouse experiments, Halade and colleagues boosted the amount of Resolvin D1 by an injection three hours after experimental myocardial infarction. They found that the heart-attack mice that were given Resolvin D1, or a more stable Resolvin D1 protected inside liposomes, had less left ventricle enlargement, an improved left ventricle function, less lung edema and a reduced collagen deposition, as compared with heart-attack mice that received only saline. All of these indicated reduced heart failure in the Resolvin D1-treated mice.