Sirs, A 59-year-old woman with a history of arterial hypertension was admitted with acute chest pain. ECG did not reveal abnormalities (Fig. 1, panel a), cardiac biomarkers remained within normal ranges, and transthoracic echocardiography (TTE) showed regular cardiac function. Multislice computed tomography (CT) confirmed Stanford type B aortic dissection (panel b, AO aorta) also indicating normal end-diastolic dimensions of the right and left heart (panel c, RV right ventricle, LV left ventricle). Nine days after an uneventful clinical course, the patient developed chest pain again with subsequent dyspnoea and cyanosis. She was intubated and mechanically ventilated using bilevel positive airway pressure with an inspiratory positive airway pressure of 25 mbar and an expiratory positive airway pressure of 8 mbar; initial fraction of inspired oxygen was 0.5. The first blood gas revealed satisfactory oxygenation and metabolic acidosis due to a rise in serum lactate (pH 7.26, pO2 166 mmHg, pCO2 40.7 mmHg, base excess 4.7 mmol/L, lactate 5.1 mmol/L). Vasopressor therapy with norepinephrine (initial dose of 0.7 lg/kg/min) was initiated because of pronounced hemodynamic instability. The ECG immediately prior to intubation showed sinus tachycardia with new S1/Q3 pattern and complete right bundle branch block (panel d). Troponin T slightly elevated up to a maximum of 0.27 lg/L. TTE now revealed right ventricular dilatation up to 58 mm with akinesia of the right ventricular free wall and the apex with only mild tricuspid regurgitation which did not allow for reliable estimation of right ventricular pressure. Central venous pressure (CVP) was elevated initially up to 18 mmHg. CT was performed for suspected pulmonary embolism but neither central nor peripheral emboli were detectable (panel e). CT also confirmed severe end-systolic dilatation of the right ventricle (panel f). Any progress of aortic dissection or signs of pneumonia were not found. The patient rapidly recovered clinically, mechanical ventilation and vasopressor therapy could be stopped after 20 h. Right ventricular function as assessed by TTE, CVP, and ECG (panel g) were normalized within 4 days. Subsequently, atherosclerotic coronary artery disease (CAD) was excluded by left heart catheterization (panel h). Cardiac magnetic resonance imaging (MRI) on day 6 after the index event did not reveal late enhancement suggestive for structural myocardial abnormalities such as edema, necrosis or fibrosis. MRI confirmed normalization of right ventricular diameter and function (panel i). With respect to the clinical course and the actual findings we consider that this patient suffered from an isolated right ventricular manifestation of stress-induced (‘‘Tako-Tsubo’’) cardiomyopathy. In accordance with this assumption the patient presented typical features: a stressor (recurrent chest pain after aortic dissection 9 days before), changes on the ECG, elevation of cardiac markers, rapid recovery, and exclusion of other causes such as pulmonary embolism, CAD, or any other structural cardiac abnormality [1–3]. Stress-induced cardiomyopathy most often affects the left ventricle [4] or in up to one-fourth of the patients both C. Burgdorf (&) P. W. Radke H. Schunkert V. Kurowski Department of Internal Medicine II, University Hospital Schleswig-Holstein, Campus Lubeck, Ratzeburger Allee 160, 23538 Lubeck, Germany e-mail: christof.burgdorf@uk-sh.de