New York University School of Medicine

“If the arteries are not badly blocked, then we have to work backward and decide: Was this a problem of blood flow to the heart muscle at all? Was it something else entirely?” said Center Director Harmony Reynolds, MD.

After recruiting patients from 16 sites throughout the U.S. and Canada, NYU researchers employed blood tests, angiograms and platelet studies, as well as sophisticated imaging techniques to get to the bottom of what could be causing the heart attacks, called myocardial infarctions with non-obstructive coronary artery disease, known to the scientific community as MINOCA. This included optical coherence tomography, “which is basically taking a very clear picture from inside the artery to see the artery wall,” Reynolds said.

“We then did cardiac MRI, which can beautifully highlight where da mage has occurred, even if that damage is not permanent,” she said. “MRI can show us traces of where injury was just starting to happen.” Using both tests, the investigators were able to find the cause of these previously unexplained heart events in 85% of cases. “Most were true heart attacks and were caused by small cholesterol plaques or blood clots, but some were not heart attack at all, and were actually inflammation of the heart muscle that imitated a heart attack.”

“The women were randomly assigned to two different interventions: an educational intervention, or training in stress management techniques. The stress intervention gave the women skills to use so they would be able to interrupt the physical consequences of emotional stress,” Dr. Reynolds said, because “stress is known to be associated with a poor prognosis after a heart attack.”

“Stress may promote heart events over the long term,” she said, adding that stress enhances platelet activity, making blood stickier and more prone to clotting. This may be the mechanism by which stress increases heart attack risk. “We know stress increases risk, but exactly how it does this has not been entirely clear.” The NYU studies found that stress increases platelet activity and makes platelets stick to, and stimulate, inflammatory cells called monocytes. This may represent a new pathway linked to stress-mediated heart disease.