536584 research-article2014
PRF0010.1177/0267659114536584PerfusionLiang et al.
Original paper
Dynamic left ventricular outflow tract obstruction in apical ballooning syndrome (Takotsubo cardiomyopathy)
Perfusion 2015, Vol. 30(1) 82–84 © The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0267659114536584 prf.sagepub.com
JJ Liang,1 CD Janish,1 KG Bishu2 and GS Reeder2
Abstract Patients with apical ballooning syndrome may develop dynamic left ventricular outflow obstruction due to systolic anterior motion of the mitral valve leaflet and secondary functional mitral regurgitation, causing decreased cardiac output and hypotension. If suspected, bedside echocardiography will quickly confirm this complication. Positive inotropic/chronotropic agents should be avoided as they may exacerbate outflow tract obstruction, resulting in further hemodynamic compromise. Keywords Takotsubo; apical ballooning syndrome; hypotension; systolic anterior motion; mitral regurgitation; dynamic outflow tract obstruction
Background While hypotension in patients with apical ballooning syndrome (ABS) is usually due to profound systolic left ventricular (LV) dysfunction, additional factors may be contributory. We present the case of a post-menopausal woman who developed hypotension due to dynamic LV outflow tract obstruction in the setting of ABS.
Case Presentation A 73-year-old woman with hypertension presented to the emergency department for evaluation of acute onset substernal chest pain and dyspnea. Pain began while at rest and worsened with exertion. On arrival, she was hypotensive, with a blood pressure of 92/53 mmHg. Her oxygen saturation was below 90%, but improved with 2 litres oxygenation via nasal cannula. Physical examination revealed a systolic ejection murmur, elevated jugular venous pressure and diffuse rales. Electrocardiography demonstrated sinus tachycardia, but there were no ST-segment or T-wave changes to suggest myocardial ischemia. Three hundred and twenty-five milligrams of aspirin were administered and her blood pressure improved with a crystalloid fluid bolus. Troponin T was elevated at 0.51 ng/mL (normal
PRF0010.1177/0267659114536584PerfusionLiang et al.
Original paper
Dynamic left ventricular outflow tract obstruction in apical ballooning syndrome (Takotsubo cardiomyopathy)
Perfusion 2015, Vol. 30(1) 82–84 © The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0267659114536584 prf.sagepub.com
JJ Liang,1 CD Janish,1 KG Bishu2 and GS Reeder2
Abstract Patients with apical ballooning syndrome may develop dynamic left ventricular outflow obstruction due to systolic anterior motion of the mitral valve leaflet and secondary functional mitral regurgitation, causing decreased cardiac output and hypotension. If suspected, bedside echocardiography will quickly confirm this complication. Positive inotropic/chronotropic agents should be avoided as they may exacerbate outflow tract obstruction, resulting in further hemodynamic compromise. Keywords Takotsubo; apical ballooning syndrome; hypotension; systolic anterior motion; mitral regurgitation; dynamic outflow tract obstruction
Background While hypotension in patients with apical ballooning syndrome (ABS) is usually due to profound systolic left ventricular (LV) dysfunction, additional factors may be contributory. We present the case of a post-menopausal woman who developed hypotension due to dynamic LV outflow tract obstruction in the setting of ABS.
Case Presentation A 73-year-old woman with hypertension presented to the emergency department for evaluation of acute onset substernal chest pain and dyspnea. Pain began while at rest and worsened with exertion. On arrival, she was hypotensive, with a blood pressure of 92/53 mmHg. Her oxygen saturation was below 90%, but improved with 2 litres oxygenation via nasal cannula. Physical examination revealed a systolic ejection murmur, elevated jugular venous pressure and diffuse rales. Electrocardiography demonstrated sinus tachycardia, but there were no ST-segment or T-wave changes to suggest myocardial ischemia. Three hundred and twenty-five milligrams of aspirin were administered and her blood pressure improved with a crystalloid fluid bolus. Troponin T was elevated at 0.51 ng/mL (normal
