A new study is providing what researchers are calling “unique and important insights” into potential mechanisms contributing to the Takotsubo syndrome (TTS) also known as “broken heart syndrome.”
Results from the retrospective case-control study suggest that chronically heightened stress-associated neurobiological activity may affect both the risk for, and timing of, subsequent TTS.
“The findings suggest that this stress-related acute syndrome doesn’t start simply upon exposure to a stressor, that preexisting brain wiring predates it by quite a while,” study author Ahmed Tawakol, MD, director of nuclear cardiology and co-director of the Cardiovascular Imaging Research Center at Massachusetts General Hospital and Harvard Medical School, Boston, told Medscape Medical News.
The study highlights the need to “pay close attention” to stress reduction in patients who develop TTS as they may face ongoing problems, said Tawakol.
“We should test whether reducing stress leads to health benefits in this subpopulation of patients who develop this syndrome,” he added.
The study was published online March 26 in the European Heart Journal.
TTS is a relatively rare heart failure syndrome often triggered by acute emotional or physical stressors. It usually resolves, but not always, with some patients suffering lingering effects, said Tawakol.
“We have learned that it’s not completely benign; those who have TTS are more likely to develop other cardiovascular complications including recurrences of TTS.”
From a large patient data registry, researchers identified 41 cases of TTS and 63 controls matched for age, sex, race, and health status. All participants had suspected malignancy and had undergone whole-body fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT) scanning at Massachusetts General Hospital from 2005-2019.
The median age of the study population was 67.5 years, 72% were female, and most (89.4%) were White. In the TTS group, four patients had recurrence of this condition.
About 86% of all participants had a malignancy. The authors noted that controls were “carefully” matched to those who developed TTS by type and stage of malignancy as well as malignancy treatment.
Individuals with TTS and controls had similar baseline characteristics, except autoimmune diseases were more common in the TTS group (29.3% vs 6.3%; P = .002).
The median follow-up was 2.5 years after imaging.
To examine stress-related neural activity, researchers used what they called “AmygA,” or the ratio of amygdalar metabolic activity divided by activity of regulatory brain regions.
The amygdala, which is part of the limbic system, is very active in the stress response, noted Tawakol. “The more activity in the amygdala, the greater the physiologic response to a stressor.”
But he pointed to the importance of a balance between the “pro-stress” amygdala and the “anti-stress” upper control levels of the brain, notably the prefrontal cortex.
In this study, female sex, diabetes, and chronic kidney disease were associated with higher AmygA (>mean + 1 SD).
The study linked AmygA to risk of TTS. In an adjusted logistical regression analysis, higher baseline AmygA was associated with greater odds of developing TTS (standardized odds ratio [OR] 1.64; 95% CI, 1.03 – 2.61; P = .036).
A time-adjusted Cox regression analysis showed that AmygA independently predicted subsequent TTS (standardized hazard ratio [HR] 1.643; 95% CI, 1.189 to 2.270; P = .003) after adjustment for TTS risk factors.
Thus, each standard deviation (SD) increase in AmygA was associated with a 64% increase in TTS risk, which remained significant through other multivariable adjustments.
Source : Medscape , European Heart Journal , European Heart Journal