Mental Stress and Heart Disease

A heart attack is usually the end result of a process that has been going on for many years. This process involves the build up of fatty materials within the blood vessel wall, called atherosclerosis. These fatty materials (i.e., the atherosclerotic plaque) are separated from the blood stream by a protective fibrous cap. Most heart attacks occur when this cap cracks and exposes the fatty materials to the blood. The blood clot that forms as a result of the reaction between the blood and fatty materials can occlude a coronary artery completely. There is evidence that the process of building up atherosclerotic plaque and the cracking of the cap are influenced by inflammation. Therefore, heart disease is now rightly regarded as an inflammatory disorder of the blood vessels. Patients with rheumatoid arthritis have a high risk of developing heart disease, but we still do not know the reasons for this. It is possible that the inflammation that affects the joints also affects the blood vessels.

As inflammation plays an important role in heart disease, the high levels of inflammation commonly found in patients with rheumatoid arthritis might explain their higher risk for a heart attack. We now know that stressful events, like missile attacks and earthquakes can trigger heart attacks. Studies have examined how stressful events could cause heart attack. In these studies, the working of the heart is examined while the participants perform a mental stress task (e.g., adding numbers or performing a speech in front of an audience). Researchers from the School of Sport and Exercise Sciences at the University of Birmingham in collaboration with the Rheumatology Department of the Dudley Group of Hospitals NHS Trust are one of the first groups to conduct a study to examine the effect of mental stress on the heart’s activity in patients with rheumatoid arthritis.

Twenty-one patients with rheumatoid arthritis and 10 patients with osteoarthritis participated in this study. Blood pressure and heart rate were measured during an initial rest and then during a mental stress task. The stress task required participants to add numbers under time pressure, and to make it more stressful a buzzer was used to let the patient know when they made a mistake. A blood sample was taken at the end of the rest period and immediately following the stress task. These blood samples were analysed to monitor a possible inflammatory response to the stress task. The responses to the mental stress task in patients with rheumatoid arthritis were compared to those in patients with osteoarthritis. Osteoarthritis is a disease that affects the joints, but is not characterised by inflammation. It was found that the mental stress task caused an increase in blood pressure and heart rate in both patient groups. There was a difference between patient groups in the inflammatory response to the stress task, measured by C-Reactive Protein (CRP). In patients with rheumatoid arthritis CRP increased following the stress task, whereas no such increase was seen in patients with osteoarthritis.

When the patients with rheumatoid arthritis were classified further depending on the disease activity on the day of the test, CRP only increased in patients with rheumatoid arthritis with high disease activity, characterised by high inflammation. CRP is an inflammatory marker that is known to play a role in heart disease, from atherosclerotic plaque build up to the breaking of the cap over the atherosclerotic plaque. Patients with high levels of CRP have a higher risk for a heart attack, and a high level of CRP after a heart attack increases the risk for another heart attack. Thus, CRP is an established risk factor for heart disease and, as such, it is routinely measured in patients with suspected heart disease.

In conclusion, our study found that a mental stress task caused an increase in CRP in patients with rheumatoid arthritis with active disease. Disease activity has been previously related to the risk for heart disease; patients with active disease had a higher risk for a heart attack than patients with inactive disease. Thus, it is possible that the CRP increase during stress might contribute to the increased risk for heart attacks in patients with rheumatoid arthritis with active disease. Further research is underway in order to explore these findings further.

• Patients with rheumatoid arthritis are at increased risk for heart attacks
• Heart disease is an inflammatory disease
• Mental stress is a known trigger for heart attack
• A brief mental stress task induced increases in blood pressure and heart rate in patients with rheumatoid arthritis and osteoarthritis
• Patients with rheumatoid arthritis with high disease activity showed an increase in C-Reactive Protein, an inflammatory marker and established risk factor for heart attacks
• This specific inflammatory reaction might be one of the reasons for the increased susceptibility for heart attacks in patients with rheumatoid arthritis