Key result
A 72-year-old woman with multiple autoimmune comorbidities developed Takotsubo cardiomyopathy triggered by sepsis, with left ventricular ejection fraction recovering from 35% to 60-65% at 10 weeks with conservative management.
Why the study?
The pathophysiologic mechanisms of Takotsubo cardiomyopathy remain unclear, though emerging evidence suggests accompanying systemic inflammatory activation may play a causal role.
Case Report (n=1)
This case report highlights a potential immune-mediated pathophysiology of Takotsubo cardiomyopathy, suggesting that chronic inflammatory states may predispose patients to the condition.
TCM with multiple autoimmune comorbidities supports inflammatory pathophysiology; leaves open causality and requires prospective validation before practice change.
Background: Takotsubo cardiomyopathy (TCM) is an under-recognized cardiovascular syndrome, leading to myocardial infarction and left ventricular systolic dysfunction, in the absence of detectable coronary artery lesion. The pathophysiologic mechanisms underlying the condition remain unclear. Whilst previously believed to be a result of circulating high levels of catecholamines due to preceding severe emotional or physical stress, giving it its colloquial name of 'broken heart syndrome', newer evidence suggesting accompanying systemic inflammatory activation hints at a mechanism of acute stress encounters serving as the trigger for an enhanced systemic and hence myocardial inflammation. Case summary: In this report, we present a 72-year-old female patient presenting to ED with sepsis, whose echocardiogram upon admission showed the entire mid and apical segments of the left ventricle as akinetic, with residual contractility only on the basal segments, suggestive of TCM as a likely diagnosis. This is on a backdrop of a complex history of autoimmune and chronic inflammatory comorbidities, including type 1 diabetes, asthma, sarcoidosis, primary biliary cholangitis, Sjogren's syndrome, and type 3 cryoglobulinaemia. Discussion: In line with previous reports, this adds to the evidence base for the potential immune-mediated pathophysiology of TCM, highlighting inflammatory activation as causative as opposed to consequential to TCM, given its greater propensity for development of the disease in low-grade chronic inflammatory states. This identifies an understudied aspect of its aetiology, warranting further clinical and mechanistic investigation with implications for treatment and prophylaxis. Additionally, this highlights an important differential for acute myocardial infarction, in patients with underlying chronic inflammatory and autoimmune diseases.
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Chen et al. (2025) conducted a case report in Takotsubo cardiomyopathy (n=1). Conservative management was evaluated on Left ventricular ejection fraction recovery. A 72-year-old woman with multiple autoimmune comorbidities developed Takotsubo cardiomyopathy triggered by sepsis, with left ventricular ejection fraction recovering from 35% to 60-65% at 10 weeks with conservative management.
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