A University of Aberdeen study has found that the effects of Takotsubo cardiomyopathy – or “broken heart syndrome – can be permanent, contrary to previous research had suggested that the heart damage caused was temporary.
Severe emotional stress can prompt a sudden heart condition that poses the same sort of long-term damage as a heart attack, The Independent reports research has found. Takotsubo cardiomyopathy – or “broken heart syndrome” – affects at least 3,000 people in the UK and is typically triggered by traumatic life events such as bereavement.
During an attack, the heart muscle weakens to the point where it can no longer function as effectively.
The report says while previous research had suggested that the damage caused was temporary, scientists at the University of Aberdeen have now found that the effects can be permanent, like a heart attack.
In the study, which was funded by the British Heart Foundation (BHF), the team of doctors examined 37 Takostubo patients for an average period of two years using ultrasound and MRI scans.
They presented their findings at the American Heart Association Scientific Sessions in Anaheim, California and revealed that participants had untreatable damage to the heart’s muscle tissue which had reduced elasticity that prevented full contractions with every heartbeat.
“Takotsubo is a devastating disease that can suddenly strike down otherwise healthy people,” explained Professor Jeremy Pearson, associate medical director at BHF.
“We once thought the effects of this life-threatening disease were temporary, but now we can see they can continue to affect people for the rest of their lives.”
Pearson added that there is currently no long-term treatment in place for patients because medics had previously thought all sufferers would make a full recovery. “This new research shows there are long-term effects on heart health, and suggests we should be treating patients in a similar way to those who are at risk of heart failure,” he concluded.
Background: Takotsubo cardiomyopathy (TC) is an increasingly recognised acute heart failure syndrome following intense stress. Despite rapid and spontaneous recovery of left ventricular ejection fraction (LV EF) TC patients experience ongoing symptoms and have poor long-term prognosis. We investigated the cardiovascular phenotype of post-TC sufferers compared to matched controls in order to better understand their unexpectedly poor clinical outcome.
Methods: In a cross-sectional study we enrolled 32 patients who experienced a TC episode at least 12 months previously and 37 age, sex and co-morbidity matched controls. Subjects underwent cardiac magnetic resonance including 31P- spectroscopy, treadmill cardiopulmonary exercise testing, echocardiography, brain natriuretic peptide (BNP) testing and an array of inflammatory cytokines; patients completed the Minnesota Living with Heart Failure Questionnaire (MLHFQ).
Results: Mean age was 65±9 years in the TC group and 64±9 in the control group. In each group 97% of subjects were women. TC patients had significantly impaired cardiac energetic status compared to controls (PCr/γATP ratio 1.3±0.1 vs 1.9±0.1, p=0.001), reduced peak oxygen consumption (24±1.6 vs 30±9 mls/kg/min, p<0.001) and higher VE/VCO2 slope (31±1 vs 27±1, p=0.005). Despite normal LV EF, strain echocardiography showed impaired cardiac deformation in TC (reduced apical circumferential strain -14±1.8% vs -23±1.5%, p<0.001, and global longitudinal strain -17±3% vs -20±1%, p=0.006). Cardiac native T1 mapping was increased in TC hearts compared to controls (1264 ±10 vs 1182 ±10 msec, p<0.001). There were no significant differences in the rest, peak exercise or post-exercise BNP and only a trend for higher growth regulated protein cytokines in TC (2017±308 vs 1910±384 pg/ml, p=0.08). The majority (90%) of patients declared symptoms, scoring a median of 4 (range 0-75) in the MLHFQ.
Conclusions: We describe a new clinical phenotype in patients who suffered TC at least one year previously. This is characterized by impaired cardiac energetics and reduced maximal oxygen consumption on exercise due to significant cardiac limitation. Taken together, our findings demonstrate that post-TC patients develop a heart failure phenotype.
Caroline Scally, Amelia Rudd, Mezincescu Alice, Heather Wilsom, Janaki Srinivasan, Graham Horgan, Paul Broadhurst, Anke Henning, Dana K Dawson