Clinical Case An 89-year old lady presented with symptoms of chest pain and dyspnea, without a significant cardiovascular history, regular medical therapy nor any cardiac risk factors. The electrocardiogram (ECG) demonstrated hyper-acute T waves, and moderate troponin T elevation which peaked at 998 ng/ml. Transthoracic echocardiography (TTE) demonstrated apical ballooning, with hyperdynamic function of the basal left ventricle (LV). These findings were suggestive of a diagnosis of Takotsubo’s cardiomyopathy (TTC), further supported by the coronary angiogram, which confirmed the absence of obstructive coronary artery disease. Notably, her symptoms had not occurred in the setting of emotional or physical stress. The initial recovery was uncomplicated, with no recurrence of symptoms, arrhythmias or cardiac failure. Five days after her presentation, she suddenly experienced severe chest pain and dyspnea associated with profound hypotension. The ECG demonstrated widespread, deep T wave inversion which had evolved over the preceding days, without new ischaemic ST segment changes. Bedside TTE demonstrated severe eccentric mitral regurgitation (MR) with an anteriorly directed jet, not present on earlier TTE, and a hyperdynamic LV. Stability was re-established with intravenous vasopressors, and subsequently with an intra-aortic balloon pump. Transoesophageal echocardiography to evaluate the aetiology of the acute MR demonstrated rupture of the antero-medial papillary muscle with a resultant flail posterior mitral valve leaflet. She was managed with a palliative, non-surgical approach following consideration of her advanced age, frailty, and wishes, and passed away the following day. Discussion TTC is characterized by transient LV impairment, typically due to apical ballooning, with a modest troponin elevation and ECG changes that can mimic acute myocardial infarction. There is, however, an absence of obstructive coronary artery disease. It is most common in post-menopausal females. The overall prognosis is favourable, but can be complicated by cardiac failure, ventricular arrhythmias, and thrombo-embolic phenomena, which carry a significant in-hospital mortality. Rarely, acute MR due to systolic anterior motion of the mitral valve with LV outflow tract obstruction can complicate TTC. Acute MR due to papillary muscle rupture, as in this case, is unusual and has only been reported on a few occasions. The mechanism is not well understood as this pathology is usually found in the context of myocardial infarction, which is excluded on coronary angiography as part of the diagnostic evaluation TTC. Two potential mechanisms have been proposed. As is the case in dilated cardiomyopathy, dilatation of the LV in TTC may create abnormal tension on the tendinae chordae and papillary muscle, or microvascular ischaemia, which has been postulated as a cause for TTC, either of which may then lead to spontaneous papillary muscle rupture. Abstract P1297 Figure.