Job strain could be harming your heart
People who have high-stress jobs — such as assembly line workers — may be more likely to develop A-fib.
This was the conclusion of a new Swedish study on work stress, now published in the European Journal of Preventive Cardiology.
The researchers define “high-strain jobs” as those that are “psychologically demanding” but give job-holders little control “over the work situation.”
Examples include bus driving, nursing, and working on assembly lines.
Previous studies have linked work stress to coronary heart disease, but whether there is also a link to atrial fibrillation (A-fib) is less clear.
According to first study author Eleanor I. Fransson, who is an associate professor of epidemiology at Jönköping University in Sweden, A-fib “is a common condition with serious consequences and therefore it is of major public health importance to find ways of preventing it.”
A-fib and consequences
A-fib affects millions of people in the United States. It occurs when the upper two chambers of the heart (the atria) beat abnormally and disrupt blood flow to the lower two chambers (the ventricles).
The condition, which can be temporary or permanent, raises the risk of stroke. A person with A-fib has a four to five times higher risk of having a stroke than a person without it.
As well as irregular heartbeat, individuals with A-fib might also experience: chest pain, palpitations (a fluttering or pounding sensation in the heart), shortness of breath, feeling lightheaded, and “extreme fatigue.”
However, some people with A-fib may have no symptoms and not even realize that they have it.
Each year in the U.S., A-fib is responsible for over 750,000 hospital admissions and contributes to 130,000 deaths. Deaths in which A-fib is a contributory or primary cause have been increasing for the past 20 years.
The costs associated with A-fib are substantial. Overall, the burden in the U.S. amounts to $6 billion per year. The average annual medical bill for treating an individual with A-fib is $8,705 higher than for those without it.
To assess work stress, Prof. Fransson and team used a measure of job strain that is based on the job demands-control model. It is one of the “most widely studied” models of work stress.
It is based on the idea that the effect of job demands on the strain that people experience is “buffered” by the amount of control that they have over their work.
For their study, the researchers used a Swedish questionnaire based on the model. It comprises five items on job demands and six on control.
The questions ask, for example, whether the individual:
- has “to work very hard or very fast”
- experiences conflicting demands in the job
- has enough time to complete tasks
- has to complete lots of repetitive tasks
- is able to decide which tasks to do and how to do them
Link between job strain and A-fib
The researchers used data on 13,200 individuals who constituted a “representative sample of the working population” of Sweden. They were recruited in 2006, 2008, and 2010 to take part of the Swedish Longitudinal Occupational Survey of Health (SLOSH).
None of the participants had A-fib — or a history of the disorder — when they joined the study. Neither did they have a history of heart failure or heart attack.
They were all employed, and they all completed a battery of questionnaires when they entered the study. These were sent out by post and included the usual demographic questions plus others about health, lifestyle, and work.
The study followed the group for a median of 5.7 years. Using national registers, the researchers identified 145 cases of A-fib during this period.
Analysis of the SLOSH data — after adjusting for age, gender, and education — showed that job strain was linked to an almost 50 percent raised risk of A-fib.
The risk stayed the same when the team further adjusted the results to take into account the effect of exercise, smoking, blood pressure, and body mass index (BMI).
Stress, heart health, and the amygdala: Links explained
Breaking research explains why stress can contribute to poor heart health.
Psychological stress carries with it a wealth of ills. In fact, excessive stress is known to contribute to a range of conditions, including hypertension (high blood pressure), ulcers, asthma, and irritable bowel syndrome.
It also has a well-documented impact on heart health. Some of this negative influence could be due to coping mechanisms – such as drinking alcohol or smoking tobacco – but there also appears to be a direct link between elevated stress levels and heart complaints.
Although this relationship is common knowledge to medical researchers and laypeople alike, the exact physiological processes behind it have remained difficult to unpick.
How can an emotion that is constructed in the brain influence the physical health of the heart?
“While the link between stress and heart disease has long been established, the mechanism mediating that risk has not been clearly understood.”
Dr. Ahmed Tawakol, lead author
Studies in animals have found that stress increases the manufacture of white blood cells in bone marrow. This, in turn, leads to an increase in inflammation. How this fits into the full picture is yet to be understood.
Stress, inflammation, and heart health
Researchers from Massachusetts General Hospital (MGH) and Icahn School of Medicine at Mount Sinai (ISMMS) in New York designed a double-pronged investigation to gain insight into this fascinating question.
The results, published this week in The Lancet, provide new information regarding the links between cardiac health and psychological stress.
Dr. Tawakol’s paper describes two studies that aimed to combat the same problem in a similar way. The first study, conducted at MGH, analyzed positron emission tomograph (PET) and computed tomography (CT) scans of nearly 300 individuals. The scans utilized a radiopharmaceutical called fluorodeoxyglucose (FDG), which can simultaneously measure activity in the brain and the level of inflammation in arteries.
All participants were healthy at the time of the scan and had information in their medical records of at least three additional clinical visits within the following 5 years.
The second study was carried out at the Translational and Molecular Imaging Institute at ISMMS. This smaller study involved 13 participants with a history of post-traumatic stress disorder (PTSD). The researchers assessed their current levels of perceived stress and carried out FDG-PET scans.
In the larger MGH study, 22 participants experienced a cardiovascular event – such as stroke, angina, or a heart attack – during the follow-up period.
Dr. Tawakol and his team were able to show an association between the likelihood of a cardiac event and a specific part of the brain: the amygdala, a region known to be involved in emotional processing.
Stress and the amygdala
High levels of activity in the amygdala at the start of the study were associated with an increased risk of experiencing a cardiac event. Even after adjusting for other cardiovascular risk factors and atherosclerosis, the association was significant. The link became even stronger when the analysis only took into account more serious cardiac events.
They also showed that activity in the amygdala could predict the timing of the events. Higher levels of activity at baseline were associated with the occurrence of cardiac events sooner in time.
Greater activity levels in the amygdala were also associated with increased metabolism in regions of the body responsible for creating blood cells (bone marrow and spleen) and an increase in arterial inflammation.
The results from the smaller ISMMS study add weight to the MGH findings. Participants’ stress levels were, again, significantly associated with activity in the amygdala and arterial inflammation.
“This pioneering study provides more evidence of a heart-brain connection, by elucidating a link between resting metabolic activity in the amygdala, a marker of stress, and subsequent cardiovascular events independently of established cardiovascular risk factors. We also show that amygdalar activity is related to increased associated perceived stress and to an increased vascular inflammation and hematopoietic activity.”
Zahi A. Fayad, Ph.D., co-senior author
Further research will help to deepen our understanding of the so-called amygdala-bone marrow-arterial axis. In the future, medications that target this mechanism may be useful for controlling or minimizing cardiovascular disease. The findings also underscore the importance of addressing stress in order to reduce health risks.
As Dr. Tawakol says: “It would be reasonable to advise individuals with increased risk of cardiovascular disease to consider employing stress-reduction approaches if they feel subjected to a high degree of psychosocial stress.”