Patients with more activity (the purple area throughout the image at right) in the brain’s center for stress and fear were more likely to have a heart attack or stroke, compared to patients with less activity (at left).
A Mount Sinai researcher has played a key role in tracing—for the first time—the mechanisms that link stress to cardiovascular events, like heart attack or stroke. Zahi A. Fayad, PhD, Director of the Translational and Molecular Imaging Institute at the Icahn School of Medicine at Mount Sinai, was co-senior author of a paper on the research, which was published January 12, 2017, in The Lancet. The work will be expanded in a five-year project, funded by a new $7 million grant from the National Institutes of Health (NIH).
The research found that people who had more activity in an area of the brain that regulates the body’s response to stress and fear, called the amygdala, were more likely to have a heart attack or stroke than those with less activity. The findings “provide more evidence of a heart-brain connection,” Dr. Fayad says. “It may seem obvious, but until now the evidence had not been shown. We had not seen the mechanistic link.”
The Lancet paper was based on two complementary studies. One study was led by the first author of the paper, Ahmed A. Tawakol, MD, Co-Director of the Cardiac MR PET CT Program at Massachusetts General Hospital in Boston. The study analyzed data from 293 people who from 2005 to 2008 underwent positron emission tomography–computed tomography (PET/CT) brain imaging, primarily for cancer screening, using a radiopharmaceutical called FDG that measures activity in the brain, vascular system, and bone marrow. Researchers found that over the next four years, 22 of the patients had cardiovascular events. In that group, many patients had initially shown a high level of activity in the amygdala and a greater amount of inflammation in the aorta, and in the bone marrow, where new blood cells are made. The latter two factors can contribute to atherosclerosis, the hardening and narrowing of the arteries, which increases the risk for heart disease. This pathway—from emotional stress to increased white blood cells to inflammation to atherosclerosis—has been identified in animals, but until now, not in humans.
Zahi A. Fayad, PhD
The second study, conducted by Dr. Fayad’s team at the Translational and Molecular Imaging Institute, examined 13 people who were being treated for post-traumatic stress disorder at Mount Sinai’s Mood and Anxiety Disorders Program. These patients completed a questionnaire about their perceived stress levels and underwent FDG-PET/MR scans. The team found that the patients’ stress levels were linked to increased activity in the amygdala, as well as increased inflammation in the blood vessels.
In the new project, Dr. Fayad—as overall principal investigator—will work with Dr. Tawakol; the leaders of the Mood and Anxiety Disorders Program, Dennis S. Charney, MD, Anne and Joel Ehrenkranz Dean, Icahn School of Medicine at Mount Sinai, and President for Academic Affairs, Mount Sinai Health System; and Program Director James Murrough, MD, Assistant Professor of Psychiatry, and Neuroscience; and others at Mount Sinai.
The project is seeking to study three groups of patients: 80 who are being treated for PTSD; 80 who are “resilient,” with past exposure to trauma but a low perceived level of stress; and 80 who have not been exposed to trauma. It will explore the possibility that alleviating stress could not just improve patients’ psychological sense of well-being, but also improve their physical atherosclerotic health. “In the future, chronic stress can be treated as a risk factor for cardiovascular disease,” Dr. Fayad says, “so we can screen for it and manage it like other risk factors.”
A patient with high activity in the amygdala also showed inflammation in the aorta (top right) and bone marrow in the spinal column (bottom right). Another patient with low activity in the amygdala showed little or no inflammation in the aorta (top left) and bone marrow (bottom left).