(RxWiki News) Doctors have known that heart attack patients are at an increased risk of a future heart event, but the reason has been elusive. Now they think they know what causes that increased risk of recurrence.
Following a heart attack the body appears to experience an immune response that worsens underlying plaque buildup in the arteries, increasing the risk of another heart attack.
"Go to the hospital immediately if a heart attack is suspected."
The same also appears to hold true for strokes. Both can be caused when an artery plaque ruptures and blocks key blood vessels.
Matthias Nahrendorf, MD, PhD, of the Massachusetts General Hospital Center for Systems Biology and senior author of the study, noted that an immune response to tissue damaged by lack of oxygen can accelerate underlying disease by increasing the size and inflammation of artery plaque.
During the study researchers used a mouse model genetically programmed to develop plaque build up in the arteries. They then conducted experiments, which included inducing heart attacks.
When heart attacks were induced in the mouse model, researchers found increased activity of enzymes responsible for breaking down the fibrous plaque cap at a distance from the site of the heart attack, which could lead to another plaque rupture.
They also noticed an increased accumulation of white blood cells associated with the immune system along with other inflammatory immune cells in the artery plaque.
Other observations included increased generation of monocyte progenitors in the spleen, function changes of those immune cells, and an increased release of blood stem cells from bone marrow. The latter traveled to the spleen after increased activation of the sympathetic nervous system.
Though the study primarily focused on mice, investigators also found increased numbers of blood stem cells in the spleens of patients shortly after they died of a heart attack.
"The ancient fight-or-flight responses to injury stimulate immune cell activities that are involved in wound healing. But when the 'wound' is in the heart and caused by atherosclerosis (plaque build up), that increased activity actually accelerates the underlying disease," Dr. Nahrendorf said.
The findings could lead to new approaches for treating cardiovascular disease, including therapies directed to sites of white blood cell production, such as the bone marrow or spleen, to prevent worsening plaque build up after a heart attack.
Sarah Samaan, MD, a cardiologist with Legacy Heart Center and co-director of the Women’s Cardiovascular Institute at the Baylor Heart Hospital, called the study "fascinating." She noted that she has seen the phenomenon, but that the process has not been fully understood.
Dr. Samaan, also author of "Best Practices for a Healthy Heart: How to Stop Heart Disease Before or After It Starts," said that during a typical scenario, a patient with a suspected heart attack receives an angiogram, or images of the heart's arteries to determine whether there is a critical blockage.If so, the blockage is generally opened with a stent to prop open the blood vessel.
"A few weeks or months later, the same patient may come back in with chest pain and at that time, we find that although the stented area looks just fine, the other areas have unexpectedly become much worse," Dr. Samaan said. "This study may have an important impact on the way patients are treated after a heart attack."
The study was recently published in journal Nature.