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A Pilot Study of Neurobiological Mechanisms of Stress and Cardiovascular Risk
J Douglas Bremner1,2,3, Marina Piccinelli2, Ernest V Garcia2
1Department of Psychiatry & Behavioral Sciences, Emory University School of Medicine, Atlanta, GA.
Insights
Psychological stress impacts the brain and heart, increasing coronary heart disease (CHD) risk. This study reveals how stress affects brain activity, inflammation, and myocardial ischemia in CHD patients.
Area of Science:
- Cardiovascular Disease Research
- Neuroscience
- Medical Imaging
Background:
- Coronary heart disease (CHD) is a major cause of mortality globally.
- The precise mechanisms linking psychological stress to increased CHD risk and mortality remain incompletely understood.
- Investigating the brain-heart axis in stress response is crucial for understanding CHD pathogenesis.
Purpose of the Study:
- To elucidate the mechanisms by which psychological stress influences the brain and heart, thereby increasing CHD risk.
- To assess the relationship between brain activity, peripheral organ function, and cardiac events under mental stress in CHD patients.
Main Methods:
- Coronary Heart Disease patients (N=10) underwent cardiac imaging (SPECT) at rest and during mental stress.
- Positron emission tomography (PET) with [18F]FDG was used to assess glucose uptake in the brain, heart, bone marrow, aorta, and adipose tissue.
- Comparison of glucose uptake patterns between patients with and without mental stress-induced myocardial ischemia.
Main Results:
- Patients with stress-induced ischemia exhibited increased glucose uptake in the heart, medial prefrontal cortex, and adipose tissue.
- Stress-induced activity in the medial prefrontal cortex and amygdala correlated with spleen activity.
- Increased medial prefrontal cortex activity correlated with heightened cardiac glucose uptake, indicating myocardial ischemia.
Conclusions:
- A significant link exists between brain regions mediating emotional responses to stress and peripheral organs involved in inflammation and hematopoietic activity.
- These findings highlight a potential pathway through which stress contributes to myocardial ischemia and adverse outcomes in CHD.
- Understanding this brain-heart connection offers new avenues for managing stress-related cardiovascular risk.
Objective:
Coronary heart disease is a leading cause of death and disability. Although psychological stress has been identified as an important potential contributor, mechanisms by which stress increases risk of heart disease and mortality are not fully understood. The purpose of this study was to assess mechanisms by which stress acts through the brain and heart to confer increased CHD risk.
Methods:
Coronary Heart Disease patients (N=10) underwent cardiac imaging with [Tc-99m] sestamibi single photon emission tomography at rest and during a public speaking mental stress task. Patients returned for a second day and underwent positron emission tomography imaging of the brain, heart, bone marrow, aorta (indicating inflammation) and subcutaneous adipose tissue, after injection of [18F]2-fluoro-2-deoxyglucose for assessment of glucose uptake followed mental stress. Patients with (N=4) and without (N=6) mental stress-induced myocardial ischemia were compared for glucose uptake in brain, heart, adipose tissue and aorta with mental stress.
Results:
Patients with mental stress-induced ischemia showed a pattern of increased uptake in the heart, medial prefrontal cortex, and adipose tissue with stress. In the heart disease group as a whole, activity increase with stress in the medial prefrontal brain and amygdala correlated with stress-induced increases in spleen (r=0.69, p=0.038; and r=0.69, p=0.04 respectfully). Stress-induced frontal lobe increased uptake correlated with stress-induced aorta uptake (r=0.71, p=0.016). Activity in insula and medial prefrontal cortex was correlated with post-stress activity in bone marrow and adipose tissue. Activity in other brain areas not implicated in stress did not show similar correlations. Increases in medial prefrontal activity with stress correlated with increased cardiac glucose uptake with stress, suggestive of myocardial ischemia (r=0.85, p=0.004).
Conclusions:
These findings suggest a link between brain response to stress in key areas mediating emotion and peripheral organs involved in inflammation and hematopoietic activity, as well as myocardial ischemia, in Coronary Heart Disease patients.
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