Chen Yuqing, Cuthbert Joseph, Khan Labib, Malaczynska-Rajpold Katarzyna
School of Clinical Medicine, University of Cambridge, Addenbrooke's Hospital NHS Foundation Trust, Hills Rd, Cambridge CB2 0SP, UK.
Lister Hospital, East and North Hertfordshire NHS Trust, Coreys Mill Lane, Stevenage SG1 4AB, UK.
Eur Heart J Case Rep. 2025 Apr 17;9(5):ytaf193. doi: 10.1093/ehjcr/ytaf193. eCollection 2025 May.
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.
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.
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.
应激性心肌病(TCM)是一种未被充分认识的心血管综合征,在没有可检测到的冠状动脉病变的情况下,可导致心肌梗死和左心室收缩功能障碍。该病的病理生理机制尚不清楚。虽然以前认为它是由于先前严重的情绪或身体应激导致循环中儿茶酚胺水平升高所致,因此有了通俗名称“心碎综合征”,但新证据表明伴随的全身炎症激活暗示了急性应激事件作为全身炎症进而心肌炎症增强的触发机制。
在本报告中,我们介绍了一名72岁女性患者,因脓毒症就诊于急诊科,入院时超声心动图显示左心室整个中间段和心尖段运动减弱,仅基底段有残余收缩力,提示可能诊断为应激性心肌病。这是在自身免疫性和慢性炎症合并症的复杂病史背景下发生的,包括1型糖尿病、哮喘、结节病、原发性胆汁性胆管炎、干燥综合征和3型冷球蛋白血症。
与先前的报告一致,这增加了应激性心肌病潜在免疫介导病理生理学的证据基础,强调炎症激活是应激性心肌病的病因而非结果,因为在低度慢性炎症状态下该病更易发生。这确定了其病因学中一个研究不足的方面,需要进一步进行临床和机制研究,以指导治疗和预防。此外,这突出了潜在慢性炎症和自身免疫性疾病患者急性心肌梗死的一个重要鉴别点。