by Aly Muhammad Ladak
“Throw my heart / Against the flint and hardness of my fault / Which being dried with grief, will break to powder / And finish all foul thoughts.” In Shakespeare’s Antony and Cleopatra, the Roman soldier Enobarbus is so overcome by grief and anguish after deserting his leader that he dies of heartbreak. The notion that intense sadness or shock can cause a heart attack and death is not unique to Shakespeare – it is widespread across innumerable cultures and works of art. But is ‘dying of a broken heart’ a medical reality? Or is it best left in the hands of poets and playwrights?
The observation of otherwise-healthy individuals passing away shortly after a traumatic or saddening event – such as the loss of a loved one or the end of a relationship – has long been noted. In 1629, the city of London began recording causes of death; over the following 30 years, ‘grief’ was the singular cause of nearly 400 deaths. In the 20th century, as scientific medicine and standardized reporting became commonplace, the relationship between extreme grief and sudden cardiovascular deaths was more convincingly demonstrated. A 1967 article published in the British Medical Journal reported that the chances of someone dying increased by 600% in the year following the loss of a loved one. More recent studies have elucidated the roles of cardiovascular disease in particular – for instance, a 2014 study showed that the risk of heart and stroke mortality doubled in the 30 days following bereavement. These increases can partially be explained by behavioural changes – forgetting to take medications, neglecting self-care, and more – but this does not account for all of the difference.
For many years, we lacked a strong scientific basis for a connection between emotional trauma and heart disease. In Shakespeare’s time, the phenomenon was thought to originate from a ‘buildup of melancholy’ – not an explanation, one would hope, that holds up today. The first real evidence behind any serious correlation began in the 1980s and 1990s. One landmark study, published in 1980, looked at autopsies of homicide victims who had been ‘beaten to death’ but lacked internal injuries that were significant enough to cause death. Their hearts, however, displayed changes characteristic of extreme stress, which was sufficient to explain the deaths of 11 of the 15 victims studied. Moreover, they found signs of extremely elevated levels of stress hormones (most notably epinephrine, also known as adrenaline). This seemed to implicate stress itself as a cause of death, rather than any direct physical injury. A number of Japanese studies in the 90s outlined similar cases that were caused by emotional stress rather than physical stress, and helped clarify what physiological changes were occurring in these patients. These studies remained relatively unknown until the release of a major article in the New England Journal of Medicine in 2005. Coincidentally, it was published just before Valentine’s Day – and the wave of publicity that followed made this once-obscure condition widely known.
In the years since, scientists have slowly understood more about the cardiovascular changes associated with intense stress. The medical name for this condition is Takotsubo cardiomyopathy (or broken heart syndrome), and despite separate causes, its clinical presentation is strikingly similar to that of a heart attack: chest pains, shortness of breath, and changes in the electrical activity of the heart. A traditional heart attack (or myocardial infarction) occurs when a clot impedes blood from flowing through the coronary artery, the blood vessel which provides oxygen and nutrient-rich blood to the heart muscle. If left untreated, it causes the affected part of the heart muscle to permanently die. In Takotsubo cardiomyopathy, coronary blood flow is also stopped; however, the cause is not a blood clot, but a number of stress-related physiological changes. First, scientists have often observed that the blood vessels feeding the heart muscle in these patients are prone to vasospasms – where the muscle in the vessel wall suddenly constricts, reducing blood flow. This can be directly caused by stress-related changes, such as increases in epinephrine levels. These same chemicals can signal to the heart to increase its pumping ability, and it may do so at a rate which its blood supply cannot keep up with. In fact, the extremely high hormone levels may even be toxic to these cells. As such, one common change in anatomy associated with Takotsubo cardiomyopathy is enlargement of the left ventricle, the main ‘pump’ of the heart. However, the condition – and these anatomical and physiological changes – are typically temporary: while many are hospitalized with the condition (it accounts for 2-3% of hospital admissions that resemble a heart attack), over 97% of these patients survive, most with no long-term complications. As the acute stress gives way to a more chronic state, the dangerous changes in heart function recede.
At this point, you might be wondering whether you are likely to experience this condition. Fortunately, the answer to that is you probably aren’t. The conditions resulting in Takotsubo cardiomyopathy are rare, and the chances of a random person dying from this disease are extremely low. (It varies by demographics, though; middle-aged and elderly women account for nearly 90% of cases). Even though the disease may seem to be on the rise (reported cases in those aged 50-74 tripled from 2007 to 2017), this is largely due to increased awareness in the medical community. Nonetheless, Takotsubo syndrome helps underscore that our emotional state does not exist in isolation. Rather, our mental and emotional health is deeply intertwined with our physical health. So, this Valentine’s Day, pay homage to your beloved’s heart and to your own: remember to take care of yourself, both physically and emotionally – your heart might just thank you for it!
