Link between Stress Response and Cardio Vascular Risk

New Research uses imaging to obtain a first look into the mechanisms behind stress response and cardiovascular risk.

A new study reveals that people with a higher degree of activity in the stress center of the brain also have more inflammation in their arteries and are at a greater risk for cardiovascular events, which includes heart attack, stroke and death. This research is scheduled for presentation at the American College of Cardiology’s 65th Annual Scientific Session.

While there has been increasing proof of the powerful connection between stress and heart disease, fairly little is understood about the mechanisms behind this stress response and what may put somebody at risk for cardiovascular problems. This is the initial study to use medical imaging to show a feasible connection between biochemical activity in the brain and arterial inflammation. Arterial inflammation is a major aspect of atherosclerotic condition – the accumulation of plaque in the artery walls that reduces blood flow via the body and is highly predictive of future cardiovascular events and stroke.

Co-author of the study Ahmed Tawakol said,

Our research illustrates, for the initial time, a connection between activation of neural tissues – those related with fear and stress – and following heart disease events. There is a requirement to develop a better understanding in terms of the mechanism that translates stress into cardiovascular disease risk, given the occurrence and potency of stress as a risk factor.”

Data show that more the activity taking place in the amygdala (the stress center of the brain) the more the inflammation in arteries and thus a higher likelihood of having cardiovascular events. There was also a corresponding activation of the bone marrow. Bone marrow produces immune cells known as monocytes that can induce inflammation in other parts of the body.

Investigators analyzed PET/CT scans for 293 sufferers (average age of 55 years) who actually received the test between 2005 and 2008 for cancer assessment but were identified to be free of active disease. The scans helped investigators to objectively evaluate activity in regions of the brain, along with the bone marrow and arteries. Sufferers were omitted if they had proof of cancer, established cardiovascular condition or were younger than 30 years old. An hour prior to the scan, sufferers were inserted with a radioactive atom attached to a glucose molecule as a tracer; tissues that were more active would metabolize more of the glucose and shine more brightly on the scan. A radiologist who had no understanding of the patient’s history or identifying characteristics assessed the images. Activity in the amygdala was compared to other areas in the brain. Investigators then grouped sufferers based on the relative magnitude of brain stress activity.

After correcting for age, gender, and other cardiovascular risk aspects making use of the Framingham Risk Score, there was a 14-fold higher risk of cardiovascular events for every unit increase in measured brain stress activity. Over the roughly five-year study period, 35 % of the sufferers in the high-stress center activity group later experienced a cardiovascular event, in comparison to just 5 % of the low-stress center activity group.

The investigators additionally noticed that activation of the brain’s fear centers, bone marrow activation and arterial swelling may together play a role in a mechanism that provokes cardiovascular events. Tawakol said this points to the need for future studies to test whether disturbing this mechanism decreases the burden of cardiovascular disease connected with stress.

“Over the last several years, it’s become obvious that stress is not only an outcome of adversity but may by itself also be a significant cause of disease. The threats of heart problems connected to stress are on par with that for smoking, high blood pressure, high cholesterol, and diabetes, yet relatively small is done to address this risk in comparison to other risk factors,” Tawakol said. “We are optimistic research like this brings us closer to knowing how stress may result in heart disease.”

While investigators were capable to objectively evaluate stress activity in the brain, the retrospective nature of the research meant that they could not compare it to subjective measures of sufferers’ stress levels. In addition, the patient population is restricted to people who received PET/CT scans to screen for cancer.

Still, Tawakol said the research results prompt the question of whether treating stress and decreasing the activation of the fear center of the brain may result in less atherosclerotic inflammation and, eventually, decrease cardiovascular events. Larger prospective studies are required.

The study, “Greater Activity of the Brain’s Emotional Stress Center Associates With Arterial Inflammation and Predicts Subsequent CVD Events,” will be presented on April 4, 2016, at 10 a.m. CT/11 a.m. ET/4 p.m. UTC at the American College of Cardiology’s 65th Annual Scientific Session in Chicago. The meeting runs April 2-4.