New research shows a relation between the muscle protein, cardiac myosin, and excess damage to the cardiovascular system during a heart attack. This prevalent protein is released into the body when a person suffers a heart attack, and researchers have now found that it can cause the blood to thicken or clot, worsening damage to heart tissue.
Cardiac myosin’s primary job is to provide the muscle-motor action that pumps blood through the heart. But, during a heart attack, the abundance of the protein can act as a procoagulant factor. Though blood clotting is the root cause of many serious cardiac events including stroke and heart attack, it wasn’t until now that researchers realized that cardiac myosin was adding to the problem.
The study led by John H. Griffin, Ph.D., a professor in the Department of Molecular Medicine at Scripps Research, spanned three years and involved researchers from multiple collaborating institutions. He spoke about the findings saying, “The real breakthrough of this study is that we’ve discovered another major biologic activity of cardiac myosin. No one had suspected it was acting as a procoagulant factor. Our findings bridge research in hematology and cardiology, showing there’s another potentially very important factor influencing the health outcomes of people with cardiac disease.”
Coagulation is Critical
Blood thickening, or coagulation, is critical for the body to prevent bleeding after an injury. When blood vessel or tissue damage occurs, many procoagulant factors cause blood to turn from a liquid into a gel, forming a blood clot and reducing blood loss. A problem can arise when the body must strike the right balance between stopping the bleeding and preventing excessive clotting, as happens in conditions such as when a blood clot causes a stroke.
“Just as with inflammation, a little coagulation is good, but too much is dangerous,” Griffin says. “While a small amount of cardiac myosin might help reduce bleeding in the heart, an excess of the protein may worsen the injury by promoting blood clots that cut off oxygen and exacerbate damage to heart tissue.”
As the first study to find a relationship between cardiac myosin and heart damage, Griffin and his team want to use this as the starting point for new research on cardiovascular disease. Long term, they envision an anticoagulant medicine that targets only cardiac myosin-driven coagulation. They believe that such a drug could theoretically be administered to patients in the hospital immediately after an acute cardiac event to prevent excess damage caused by the protein.