Affiliation:
1. Department of Cardiology, National University Heart Centre
2. Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore
3. Division of Rheumatology, University Medicine Cluster, National University Hospital, National University Health System, Singapore
Abstract
Abstract
Since its description in 1990, Takotsubo syndrome (TTS), an acute cardiac condition triggered by physical or emotional stress, has been believed to be related to catecholamine surge from overwhelming sympathetic activity. While symptomatology, biochemical features, ECG and echocardiogram alterations are largely indistinguishable from acute coronary syndrome, the absence of culprit coronary lesions often necessitates further investigations, uncovering underlying inflammatory processes. Mechanistically, animal models of TTS reveal early neutrophil infiltration followed by staged ingression of two subtypes of macrophages (M1, M2) mediating initial acute inflammatory changes (M1), followed by switching to anti-inflammatory signals (M2) that enhance myocardial tissue recovery. Here, we begin with a description of two TTS patients with primary Sjögren’s syndrome and Takayasu’s arteritis, followed by a systematic literature review that summarizes the demographic and clinical features of TTS patients with rheumatological conditions. Potential impact of disease manifestations and treatment of rheumatological conditions on TTS are critically discussed.
Publisher
Oxford University Press (OUP)
Subject
Pharmacology (medical),Rheumatology
Cited by
4 articles.
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