Asian Journal of Advanced Research and Reports

Takotsubo Syndrome, also known as “broken heart syndrome,” is a reversible acute cardiac condition that commonly mimics acute coronary syndrome and predominantly affects post-menopausal women following emotional or physical stress. Although traditionally considered to occur in the absence of coronary artery disease, recent evidence shows that significant coronary lesions may coexist with TTS, making multimodal imaging essential for accurate diagnosis and appropriate management. A 72-year-old woman with hypertension and dyslipidaemia presented with acute chest pain following an emotional stressor. ECG showed anterior ST-segment elevation, activating the STEMI pathway. High-sensitivity troponin T was mildly elevated at 840 ng/L — notably modest relative to the extent of ECG changes. Emergency coronary angiography revealed a 60% mid-LAD stenosis without thrombus or plaque rupture. Left ventriculography demonstrated the pathognomonic apical ballooning configuration with basal hyperkinesis, extending well beyond the territory of the mid-LAD lesion. Echocardiography confirmed moderate LV dysfunction (LVEF 40%) with apical and mid-ventricular akinesia across multiple coronary territories. Cardiac MRI within 48 hours showed myocardial oedema without late gadolinium enhancement, definitively excluding myocardial infarction and confirming the diagnosis of Takotsubo syndrome. A conservative strategy was adopted — beta-blockade, ACE inhibition, and aspirin monotherapy — without percutaneous coronary intervention. LVEF recovered completely to 60% at six weeks, and the patient remained asymptomatic at three months. This case illustrates a diagnostically treacherous and increasingly recognised clinical scenario: the coexistence of Takotsubo syndrome (TTS) and significant coronary artery disease (CAD). Historically considered mutually exclusive, contemporary registry data — including the InterTAK Registry — demonstrate that obstructive CAD coexists with TTS in up to 15% of cases, predominantly involving the LAD. The key diagnostic principle is the anatomical-functional mismatch: when wall motion abnormalities extend beyond the territory of the identified coronary lesion, an ischaemic mechanism alone cannot account for the clinical picture, and TTS must be actively considered. Cardiac MRI, with its ability to confirm myocardial oedema without necrosis, is decisive in resolving this uncertainty. Recognising this overlap prevents unnecessary revascularisation and ensures appropriate supportive management. Complete cardiac recovery, as demonstrated in our patient, confirms the excellent prognosis achievable when the correct diagnosis is established promptly.