Abstract Background Takotsubo cardiomyopathy (TCM) is an under-recognised 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 remains 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 (LV) as akinetic, with residual contractility only on the basal segments, suggestive of Takotsubo Cardiomyopathy (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 Takotsubo cardiomyopathy, 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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