In This Video
- Ahmed Tawakol, MD, co-director of the Cardiac MR PET CT Program, focuses on the development, validation and application of novel imaging methods to non-invasively characterize atherosclerotic plaques, with a focus on plaque inflammation
- In this video, Dr. Tawakol, MD discusses the link between stress and atherosclerotic disease, and his team’s work using multimodality imaging to better understand that risk
A team of clinicians led by Ahmed A. Tawakol, MD, has found a novel pathway linking psychosocial stress to heart disease. Published in The Lancet, this study finds that brain activity in the amygdala predicts subsequent heart attacks and stroke.
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Research has shown that chronic emotional stress is associated with disease. But it was not clear until this study how stress from external circumstances translates into physical events in the body that lead to disease.
So, we had long known that there is a link between stress and disease, but what was not clear is whether or not the link was independent of other factors. For example, the link between stress and atherosclerotic disease was at first thought to be maybe associated with increased health behaviors that are putting people at increased risk for cardiovascular disease events, for example smoking or poor eating. But it turns out that that doesn't explain that risk. And so we are interested in using our multimodality imaging to better understand the risk between stress and cardiovascular disease.
The way we did that was to use advanced imaging with PET MR and PET/CT to image the brain, as well as the bone marrow and the atherosclerotic milieu to try to understand the mechanism linking stress and cardiovascular disease.
With the brain imaging were able to measure the amount of activity in the amygdala, a very important portion of the brain that is responsive to stress. For the bone marrow and arterial wall, we looked at the link between the inflammatory system with the inflammatory cell production in the bone marrow and arterial inflammation, and in 293 patients we were able to then over time assess for the development cardiovascular disease events.
What we found was that amygdalar activity very nicely predicted the development of cardiovascular disease events over the five years of follow-up. In particular, we were able to show that amygdalar activity and up-regulation of amygdalar activation was linked to increased bone marrow production as well as increase in arterial inflammation, and through mediation analysis we were able to demonstrate that in series, the amygdala, bone marrow and arterial inflammation colluded to increase the risk of cardiovascular disease.
What do we hope to accomplish going down is to better understand the system. We want to ask are there other ways that we can manipulate that system? Are there ways that we can reduce the developments of arterial inflammation that is promoted by stress and could that ultimately lead to a reduction in cardiovascular disease events?