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Stress

The Role of Stress in Cardiovascular Disease

There is a direct link between the brain's emotional center and heart disease.

Key points

  • Takotsubo's cardiomyopathy is the cause of broken heart syndrome.
  • Patients with pre-existing psychiatric illness are at risk for Takotsubo's.
  • Emotional stress is an independent risk factor for heart disease.

On December 27, 2016, Carrie Fisher of Star Wars fame, died at the age of 60, four days after suffering a massive heart attack. Her mother, Debbie Reynolds, who had expected her at Christmas dinner, died the following day. Johnny and June Cash died within four months of each other. When June died of complications from heart surgery, no one was more devastated than Johnny Cash, her husband of many decades. When Johnny was hospitalized four months later for treatment of diabetes, his condition was poor, but not poor enough to account for his death solely based on this disease. Mary Tamm was beloved in Britain for her role in the Dr. Who television show. In 2012, she died of cancer. Just hours after delivering the eulogy at his wife’s funeral, her husband died while sitting at his computer writing thank you notes to those who had sent their condolences. Days after the catastrophic mass shooting in Uvalde, Texas the husband of a slain teacher died of a heart attack.

What explains the phenomenon of the sudden onset of a heart disorder after a significant stressor or loss of a loved one? The answer is stress cardiomyopathy, also known as Takotsubo’s cardiomyopathy. With this condition, intense emotional or physical stress causes rapid and severe heart muscle weakness. It can occur following a variety of emotional stressors such as grief, fear, or severe anger. It can also occur following numerous physical stressors to the body such as a stroke, seizure, difficulty breathing, or significant bleeding. Stress-induced heart disease has even been reported after a vigorous Zumba class.

Takotsubo’s cardiomyopathy was first reported in Japan in 1990. One of the important risk factors for Takasubo’s cardiomyopathy is being a menopausal woman. Estrogen acts as a protective hormone, and it declines during the years leading up to menopause. Other known risk factors include a history of neurological or psychiatric disorders, work-related stress, poor sleep, acting as a caregiver, and experiencing a disaster. After experiencing significant physical or psychological stress, someone who is prone to developing Takotsubo’s will suffer a change in the left ventricle—the part of the heart that is responsible for most of the heart’s work in pumping blood to the rest of the body.

While the exact mechanism of Takasubo’s remains unknown, it is clear the disease process is mediated by an excess of circulating catecholamines, a group of hormones produced by the brain, nerve tissues, and adrenal glands. The body releases catecholamines in response to emotional or physical stress. Catecholamines are produced in excess in situations perceived by the brain as catastrophic. Your body responds as if it is being threatened. This is commonly known as the “fight or flight” response. Although not yet proven, researchers believe hormones cause the dysregulation in the heart muscle itself, and possibly in the heart vessels when Takotsubo’s occurs. In a 2005 study, researchers demonstrated patients with Takotsubo’s demonstrated higher catecholamine levels in their bloodstream compared with patients who had other forms of heart attacks.

One-third of patients diagnosed with Takotsubo’s have a pre-existing psychiatric history, which is an independent risk factor. Although the cause is not yet clear, one theory suggests patients with pre-existing psychiatric illnesses have an excess of catecholamines, and their responses to stress result in an exaggerated catecholamine response. Some investigators wondered if poorly controlled psychiatric illness was the causal link rather than the diagnosis itself. There is some debate about this, and at face value it makes sense. However, the studies to date do not support this. What these studies do show unequivocally, is a direct link between the brain and the heart, and a depressed or anxious brain can cause or exacerbate cardiovascular disease.

Your amygdala is a small part of your brain, but it has a big job. It's a major processing center for emotions. Most investigators argue that stress responses arise when demands on individuals exceed their psychosocial resources or adaptive capacity. In addition, individual differences exist in how well people cope with challenges or losses in their lives. In a fascinating study at a major hospital system in Boston, researchers measured volunteers’ amygdala activity at rest using a sophisticated imaging technique. They reported that increased amygdala activity at rest was associated with blood vessel inflammation and risk of cardiovascular events over the next four years. The authors proposed that emotional stress signals a region of the amygdala to activate a portion of the nervous system which leads to the production of inflammatory white blood cells in the bone marrow. These changes may contribute to heart attack, stroke, or sudden death. This study was among the first to demonstrate a direct relationship between emotional stressors and the risk of cardiovascular events.

What are some techniques you can use to decrease stress and improve your heart health?

  • Practice Guided Meditation: It is a great way to distract yourself from the stress of day-to-day life. There are many guided meditations available online that can help you find five minutes of centered relaxation.
  • Learn Deep Breathing Techniques: Deep breathing is a great way to reduce the activation of your sympathetic nervous system, which controls the body’s response to a perceived threat. Deep breaths taken to a count of five seconds, held for two seconds, and released to a count of five seconds, can help activate your parasympathetic nervous system, which helps reduce the overall stress and anxiety you may be experiencing.
  • Exercise and Eat a Healthy Diet. Physical exercise and nutrition are two important components in how you respond to stress. When your body is healthy, your mind can be healthy, and vice versa. Physical exercise is proven to be a great stress reliever and helps to improve your overall quality of life. Nutrition is important as stress can deplete certain vitamins, such as A, B complex, C, and E. Maintaining proper nutrition not only helps your body feel better but your mind as well, which allows you to better combat stress.
  • Manage Social Media Time: Spending time on social media sites can become stressful, not only because of what we might see on them, but also because the time you are spending on social media might be best spent enjoying visiting with friends, being outside enjoying the weather, or reading a great book.
  • Maintain Your Social Connections: Humans are social beings. You need to have connections with people to feel supported. Finding a sense of community — whether at work, with a religious organization, or through shared activities, such as organized sports is important to your well-being. Enjoying a shared activity allows you to find support and foster relationships that can be supportive in difficult times.

References

A Broken Heart: A Case of Takotsubo’s Cardiomyopathy.” Cureus, vol. 13, no. 11, 2021, pp. 1–4, https://doi.org/0.7759/cureus.19933.

Mielczarek, Agnieszka, et al. “Broken Heart as Work-Related Accident: Occupational Stress as a Cause of Takotsubo Cardiomyopathy in 55-Year-Old Female Teacher – Role of Automated Function Imaging
in Diagnostic Workflow.” International Journal of Occupational Medicine and Environmental Health, vol. 28, no. 6, 7 Aug. 2015, pp. 1031–1034.

Seldenrijk, Adrie, et al. “Depression, Anxiety and 6-Year Risk of Cardiovascular Disease.” Journal of Psychosomatic Research, vol. 78, no. 2, Feb. 2015, pp. 123–129.

Awakol, Ahmed, et al. “Relation between Resting Amygdalar Activity and Cardiovascular Events: A Longitudinal and Cohort Study.” Lancet (London, England), vol. 389, no. 10071, 25 Feb. 2017, pp. 834–845.

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