Led by Nipavan Chiamvimonvat, cardiologist and professor of internal medicine, a team of researchers tested a compound that inhibits the enzyme soluble epoxide hydrolase-or sEH-one of the key players in the robust immune-system response that heals tissue following an injury.
The enzyme, however, can become counterproductive after a cardiac event.
Chiamvimonvat explained that sEH increases proinflammatory lipid mediators, leading to long-term, heightened inflammatory conditions.
It also causes cells, which typically link together and provide the foundation for heart tissue, to overwork.
The outcome is scar tissue, or fibrosis, that results in an abnormal relaxation of the heart after each beat, taxing remaining heart muscle as it performs double duty and eventually leading to a decline in the heart's pumping action.
"We often see patients following a heart attack in clinic who initially respond well to current treatments, which address the initial causes of the cardiac event and try to preserve heart function," Chiamvimonvat, whose research focuses on the biological mechanisms of heart disease, said.
"Over time, though, heart function in some patients continues to worsen and can lead to heart failure. It would be ideal to have new approaches that target the cellular overproduction that leads to heart muscle stiffening and cardiac fibrosis," the researcher said.
Heart failure progressively limits oxygen throughout the body, reducing mobility, respiration and quality of life.
The study is published in the Proceedings of the National Academy of Sciences.