Takotsubo cardiomyopathy is a syndrome with distinctive features that mimics acute myocardial infarction at clinical presentation; symptoms are acute chest pain and dyspnea, and ST-segment elevations can be seen on electrocardiograms. Cardiac catheterization should reveal a characteristic left ventricular wall-motion pattern without evidence of obstructive atherosclerotic coronary disease.
Dote et al. first described this syndrome in Japanese patients; the name relates to the peculiar shape of the left ventricle, which resembles an octopus-fishing pot called a Takotsubo, and can be visualized by end-systolic ventriculography. This cardiomyopathy is becoming increasingly recognized around the world,[2,3,4,5,6,7] and clinicians should include it in the differential diagnosis of patients presenting with a suspected acute coronary syndrome.
Elevations in the levels of creatine phosphokinase and troponin are typically less than those observed in acute anterior STEMI,[4,5,7] but this difference cannot be used to exclude an acute coronary syndrome.
Echocardiography revealed akinesis of the apex and the mid-ventricle as well as basal hyperkinesis, wall-motion abnormalities extending beyond the region supplied by one coronary artery. This feature is characteristic of Takotsubo cardiomyopathy, whereas wall-motion abnormalities observed in acute myocardial infarction are often more localized. Myocardial viability is preserved in Takotsubo cardiomyopathy, which can be demonstrated using cardiac MRI. Although nonobstructive atherosclerotic lesions have been observed with this condition, they have all been smaller than 50% of the luminal diameter, as in the case described here. Interestingly, Ibanez et al. suggest that this cardiomyopathy might result from a transient LAD obstruction caused by a ruptured artherosclerotic plaque located proximally in a large LAD that extends to the diaphragmatic surface of the left ventricle. They observed this phenomenon on intravascular ultrasonograms of five patients. Takotsubo cardiomyopathy might, therefore, be an acute coronary syndrome arising in patients with an unusual LAD anatomy. Early reperfusion follows, resulting in a widely stunned, rather than infarcted myocardium. Takotsubo cardiomyopathy has, however, been observed in patients without this type of LAD anatomy,[3,4] bringing into question whether this pathophysiology is involved in all cases.
Most data regarding treatment have been derived by observing patients initially treated for STEMI, and diagnosed later as having Takotsubo cardiomyopathy. Since differentiation between this cardiomyopathy and an acute coronary syndrome is often difficult at initial presentation, we tend to treat patients conservatively to avoid complications that might arise by failing to treat an anterior wall myocardial infarction. Patients receive aspirin, β-blockers, angiotensin-converting-enzyme inhibitors, cardiac catheterization and intravenous diuretics if needed.
1)Dote K et al. (1991) Myocardial stunning due to simultaneous multivessel coronary spasm: a review of 5 cases. J Cardiol 21: 203-214
2)Tsuchihashi K et al. (2001) Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan. J Am Coll Cardiol 38: 11-18
3)Kurisu S et al. (2002) Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. Am Heart J 143: 448-455
4)Desmet WJR et al. (2003) Apical ballooning of the left ventricle: first series in white patients. Heart 89: 1027-1031
5)Bybee KA et al. (2004) Clinical characteristics and thrombolysis in myocardial infarction frame counts in women with transient left ventricular apical ballooning syndrome.