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    Home»Health»Brain’s Role in Broken Heart Syndrome: How Stress-Related Brain Activity Can Temporarily Damage the Heart
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    Brain’s Role in Broken Heart Syndrome: How Stress-Related Brain Activity Can Temporarily Damage the Heart

    By Massachusetts General HospitalApril 3, 2021No Comments3 Mins Read
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    Brain Glitch Stress Disorder Concept
    New study provides insights on how stress-related brain activity can temporarily damage the heart.

    Stress-sensitive brain regions may forecast broken heart syndrome, offering new targets for prevention.

    A new study uncovers potential mechanisms that may contribute to “broken heart syndrome,” or Takotsubo syndrome (TTS), a temporary heart condition that is brought on by stressful situations and emotions. The research, which was led by investigators at Massachusetts General Hospital (MGH), indicates that a heart-brain connection likely plays a major role.

    Brain Imaging Sheds Light on Risk Factors

    For the study, published in the European Heart Journal, the team analyzed brain imaging scans from 104 patients (41 who subsequently developed TTS and 63 who did not) to determine whether increased stress-associated metabolic activity in the brain leads to an elevated risk of developing TTS. “Areas of the brain that have higher metabolic activity tend to be in greater use. Hence, higher activity in the stress-associated centers of the brain suggests that the individual has a more active response to stress,” explains senior author Ahmed Tawakol, MD, director of Nuclear Cardiology and co-director of the Cardiovascular Imaging Research Center at MGH.

    Brain Scan No TTS
    Scan of the brain of someone who did not develop TTS. Credit: European Heart Journal

    The imaging tests, which were being conducted in patients for other medical reasons, revealed that heightened activity in the brain’s amygdala predicted the development of subsequent TTS, as well as the timing of the syndrome. For example, individuals who had the highest amygdalar activity developed TTS within a year after imaging, while those with intermediate values developed TTS several years later.

    “We show that TTS happens not only because one encounters a rare, dreadfully disturbing event — such as the death of a spouse or child, as the classic examples have it. Rather, individuals with high stress-related brain activity appear to be primed to develop TTS — and can develop the syndrome upon exposure to more common stressors, even a routine colonoscopy or a bone fracture,” says Tawakol.

    Brain Scan TTS
    Scan of brain in a person who developed TTS. Credit: European Heart Journal

    Stress, Bone Marrow, and Cardiovascular Impact

    The scientists also identified a relationship between stress-related brain activity and bone marrow activity in individuals. Because bone marrow produces different types of blood cells involved with carrying oxygen, mounting immune responses, and clotting blood, stress-related brain activity may influence the activity of cells that affect cardiovascular health.

    In applying the results to the clinic, Tawakol hopes that interventions that lower stress-related brain activity will make it more difficult to develop TTS. “Studies should test whether such approaches to decrease stress-associated brain activity decrease the chance that TTS will recur among patients with prior episodes of TTS,” he says. He also underscores the need for more studies into the impact of stress reduction — or drug interventions targeting stress-related brain activity — on heart health.

    Read Stressed Brain Linked to “Broken Heart” Syndrome for more on this research.

    Reference: “Stress-associated neurobiological activity associates with the risk for and timing of subsequent Takotsubo syndrome” by Azar Radfar, Shady Abohashem, Michael T Osborne, Ying Wang, Tawseef Dar, Malek Z O Hassan, Ahmed Ghoneem, Nicki Naddaf, Tomas Patrich, Taimur Abbasi, Hadil Zureigat, James Jaffer, Parastou Ghazi, James A Scott, Lisa M Shin, Roger K Pitman, Tomas G Neilan, Malissa J Wood, Ahmed Tawakol, 26 March 2021, European Heart Journal.
    DOI: 10.1093/eurheartj/ehab029

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