Heart attack survivors are at high risk for another heart attack or stroke, but until recently, no one knew why. Now an international study led by Harvard physicians and published online in Nature has found that heart attack triggers an immune response that accelerates the development of atherosclerosis and inflammation in cholesterol-filled plaques embedded in artery walls. “It’s an ancient ‘fight-or-flight’ response to injury, but instead of healing the wound, it accelerates the underlying disease,” says senior author Dr. Matthias Nahrendorf of the Center for Systems Biology at Massachusetts General Hospital (MGH) and an assistant professor of radiology at Harvard Medical School.
During a heart attack, sympathetic nervous system activation causes stem cells to be released from the bone marrow. Stem cells induce production of monocytes and other immune cells in the spleen. These cells accumulate at yet-unruptured plaques, aggravating existing inflammation and triggering the release of enzymes that may cause those plaques to rupture.
Although most of the work was done in mice, the researchers suspect the process is identical in humans. The finding opens up novel therapeutic possibilities aimed at preventing immune system exacerbation.
“Currently, we focus on reducing risk factors. In the future, we may be able to prevent heart attacks by reducing white blood cell production in the bone marrow or spleen,” says Dr. Ralph Weissleder, director of the MGH Center for Systems Biology and a Harvard Medical School professor.