Takotsubo cardiomyopathy (TC) is a recognised cause of reversible left ventricular (LV) dysfunction. It has attracted considerable attention in recent years since its presentation frequently mimics that of ST-segment elevation myocardial infarction. The exact aetiology remains ill-defined, although stress is often a precipitating factor. Recently it has emerged that stress testing can also induce TC. We report a case of TC during pharmacological (dobutamine) but not physiological (treadmill) stress echocardiography (SE) in the same patient and explore possible pathophysiological explanations for this observation. A 71 year old lady was referred for SE to investigate chronic exertional dyspnoea. She suffered from hypertension but had no other medical history. Resting echocardiography revealed mild concentric LV hypertrophy, a dilated left atrium (dimension 5.0 cm) and normal LV systolic function (biplane EF 66%). There was no significant valvular disease or pulmonary hypertension. A recent knee injury prevented exercise and thus she underwent dobutamine echocardiography (DbE) using a standard ischaemia protocol (dobutamine infused peripherally in 3-minute dose increments, starting from 10 μg/kg/min and increasing to 20, 30 and finally 40 μg/kg/min). Peak heart rate was 142 bpm (96% age-predicted maximum), peak BP 169/80 mm Hg and rate-pressure product 24140. Peak stress imaging revealed new dilatation and ballooning of the LV apex with normal contractility of the basal segments (Fig. 1A and B and online movie clip 1). One minute after ceasing dobutamine infusion, she complained of dizziness and her blood pressure fell to 94/ 50 mm Hg. Spectral (continuous wave) doppler imaging revealed significant left ventricular outflow tract obstruction (LVOTO) of almost 120 mm Hg (Fig. 1C). She did not experience chest pain and, interestingly, did not have any ischaemic ECG changes. She recovered over the next 10 min with rest and oral fluids and was allowed to go home with a plan to return for exercise SE, as the sequence of events and imaging appearances were highly suggestive of dobutamineinduced TCwith associated LVOTO rather than coronary artery disease. She returned 3 months later, once her knee had improved, and performed treadmill exercise SE. She was able to walk for 6 min and achieved similar maximum heart rate (146 bpm, 98% age-predicted maximum), blood pressure (170/70 mm Hg) and rate-pressure product (24674) to the first SE study. On this occasion, normal contractility was seen in all segments with no apical ballooning and no LVOT obstruction (Fig. 2A, B and C and online movie clip 2). The patient was reassured and has been well during follow-up. She returned 3 months later, once her knee had improved, and performed treadmill exercise SE. She was able to walk for 6 min and achieved similar maximum heart rate (146 bpm, 98% age-predicted maximum), blood pressure (170/70 mmHg) and rate-pressure product (24674) to the first SE study. On this occasion, normal contractility was seen in all segments with no apical ballooning and no LVOT obstruction (Fig. 2A, B and C and online movie clip 2). The patient was reassured and has been well during follow-up. TC is a reversible form of myocardial dysfunction, classically seen after sudden severe emotional or physical stress and of immediate clinical priority as the ECG frequently shows ST segment elevation. TC is a recognised cause of systolic anterior motion (SAM) of the mitral valve and LVOTO, which complicates up to 10% of TC cases [1]. TC, both with [2] and without [3] SAM and LVOTO, has been described during DbE though the incidence is unknown. The exact pathophysiological basis of TC remains incompletely understood, although catecholamine excess is widely accepted as a probable contributing factor. In thewesternworld, the vast majority of cases are seen in post-menopausal women, suggesting a hormonal role in the pathogenesis. Previous studies have also found that