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- James C Coons, Megan Barnes, and Karissa Kusick.
- Allegheny General Hospital, 320 East North Avenue, Pittsburgh, PA 15212, USA. jcoons@wpahs.org
- Am J Health Syst Pharm. 2009 Mar 15;66(6):562-6.
PurposeTakotsubo cardiomyopathy is discussed as an alternative diagnosis to acute coronary syndrome (ACS) for emotionally and physically stressed patients with transient apical akinesis or dyskinesis of the left ventricle (LV) in the absence of coronary artery disease (CAD).SummaryThe name takotsubo cardiomyopathy refers to the hallmark shape of the LV during initial presentation. The apical portion of the heart balloons out, while the base of the heart has preserved systolic function. It is estimated that 0.5-2% of all patients with ACS symptoms may have takotsubo cardiomyopathy. Symptoms mimic those of a myocardial infarction (MI), and the evaluation of cardiac biomarkers, including troponin, may show a mild increase. Clinical symptoms are generally similar to ACS symptoms. While chest pain and dyspnea are most common, other features, such as cardiogenic shock, are rarer. A case example is described in which a 52-year-old white woman presented herself with complaints of chest pain and shortness of breath. She explained that the chest pain started after an argument with her supervisor. An electrocardiogram showed ST-segment elevation, and the patient was treated for ST-segment elevation MI. A left ventriculogram showed severe apical hypokinesis as well as anterolateral akinesis with a normal anterobasal segment, which led to the diagnosis of takotsubo cardiomyopathy. For patients with complications such as congestive heart failure, standard supportive care for takotsubo cardiomyopathy may include diuretics and vasodilators. In general, vasopressors and inotropes should be avoided because of the association of this syndrome with massive catecholamine release.ConclusionTakotsubo cardiomyopathy may be an alternative diagnosis to ACS for emotionally and physically stressed patients with transient-apical akinesis or dyskinesis of the LV in the absence of CAD. Because the exact pathophysiology has not been fully elucidated, the optimal management continues to evolve.
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