The syndrome, formally known as takotsubocardiomyopathy, is characterized by weakening ofthe heart’s main pumping chamber and was firstidentified in 1990 in Japan. It looks and sounds likea heart attack and is consequently often confusedfor one.
Affecting an estimated 2,500 people in the UK eachyear, the syndrome also carries a risk of complications similar to that of an actual heartattack. It is unclear what causes takotsubo, but sharp spikes in adrenaline caused by acutestress like bereavement, car accidents, earthquakes and even happy events such as weddingsare understood to drive loss of movement in part of the heart wall, which then precipitates theacute heart failure.
Two molecules – called microRNA-16 and microRNA-26a — that are linked to depression, anxiety and increased stress levels had previously been detected in the blood of takotsubopatients. Researchers assessed the impact of exposing cells from human hearts (taken fromorgans that were unsuitable for transplants) and rat hearts to the two molecules.
Afterwards, both sets of heart cells were more sensitive to adrenaline, they wrote in thejournal Cardiovascular Research.
In patients with takotsubo, the bottom of the heart stops beating, and the top of the heartbeats more, said the lead study author, Dr Liam Couch from Imperial College London. “Basically, we found the exact same thing happens when we increase the exposure to themolecules [in an experimental setting]. It reproduced exactly what happens in takotsubo, so it made it more likely for the takotsubo to occur.”
Overall, the findings appeared to link long-term stress and the dramatic takotsubo responseto a sudden shock.
However, the problem is that it is not possible, for now, to diagnose takotsubo in patientsbefore it happens, making it difficult to test whether these molecules are elevated in real-lifecases, Couch explained.
“But if we know someone’s had takotsubo, theoretically we can measure these molecules, and then predict if they’re likely to have it again, because there’s a one in five chance thatthey could have it again,” he said.
Joel Rose, chief executive of the charity Cardiomyopathy UK, said the study providedimportant insights on a less well known and poorly understood form of cardiomyopathy. “It hasthe potential to improve our understanding of who may be more susceptible to developingthe condition and subsequent improve our ability to manage its impact,” he said.
Further research is needed, said Prof Metin Avkiran, the associate medical director at theBritish Heart Foundation, to “determine if drugs that block these microRNAs could be the keyto avoiding broken hearts”.