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Cardiology Tako-Tsubo Syndrome Tako-Tsubo Syndrome with Cardiogenic Shock and Left Ventricular Outflow Tract Obstruction Diagnosis On physical examination blood pressure was 100/60 mmHg, pulse rate 64 bpm, a 3/6 apical systolic murmur was heard, and there were signs of peripheral hypo-perfusion. Fluid therapy with intravenous saline was initially administered. The 12-lead electrocardiogram exhibited sinus rhythm with minor ST-segment elevation in V1-V2 without additional significant repolarization changes. The chest X-ray showed signs of alveolar edema without cardiomegaly. The cTnI was 8.11 ng/cc normal <0.012, NT-proBNP 18.300 pg/cc normal <900 for this age, and D-Dimer 4452 mcg/l normal <494. A multislice CT scan study excluded an aortic dissection and a pulmonary embolism. Treatment Shortly after admission, the patient became very dyspneic, cyanotic, and stuporous, with oxygen desaturation and hypotension (80/40 mmHg) despite IV fluid therapy. Orotracheal intubation was performed and dopamine infusion was immediately started. A transthoracic echocardiogram showed an extensive apical akinesia with a left ventricular ejection fraction (LVEF) around 20% and mild mitral regurgitation. Because of the hemodynamic instability a Swan-Ganz catheter was inserted in the pulmonary artery. The systolic right ventricular and pulmonary artery pressures were 44 mmHg, the mean pulmonary artery wedge pressure 25 mmHg, and the cardiac Patient History An 83-year-old hypertensive woman arrived in our emergency room complaining of acute chest pain and dyspnea, after a physical and psychologically stressful event. Her past medical history was otherwise irrelevant. index 1.7 L/min/m2, thus confirming the diagnosis of cardiogenic shock. An urgent coronary angiography disclosed no significant coronary stenosis. The angiographic LVEF was 35% and there was a wide akinesia of the mid and apical segments of the LV, with hyperkinesia of the basal areas and moderate mitral regurgitation (Fig. 1A and B). The mid-segment of the left anterior descending coronary artery showed systolic milking and also the first and second septal branches collapsed during systole (Fig. 1C and D). At the apical LV the systolic pressure was 160 mmHg and the end-diastolic pressure 28 mmHg. On withdrawing the catheter there was an intermediate LV chamber with systolic pressures of 110 mmHg, similar to those obtained within the ascending aorta (110/60 mmHg) (Fig. 2). A peak-to-peak systolic gradient of 50 mmHg existed between the apical LV and the ascending aorta or the intermediate LV chamber. Thus, we found a systolic gradient at the level of the mid LV cavity without any significant gradient across the aortic valve. Because of these findings the dopamine infusion was withdrawn resulting in an increase of the arterial pressure and an improvement of the peripheral perfusion. IV metoprolol was started further resulting in a significant clinical and hemodynamic improvement (cardiac index 2.1 L/min/ m2 and pulmonary artery wedge pressure 20 mmHg). Forty eight hours later the patient was extubated and transferred to the cardiology ward without signs of heart failure. Courtesy of Roberto MartÍn-Reyes, MD Department of Cardiology, FundaciÓn Jiménez Díaz, Madrid, Spain 42  AXIOM Innovations | December 2013 | www.siemens.com/angiography


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