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J Am Coll Cardiol, 2002; 39:181-182
© 2002 by the American College of Cardiology Foundation
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LETTER TO THE EDITOR

Reply

Kazufumi Tsuchihashi, MD, PhDa

a Second Department of Internal Medicine, Sapporo Medical University School of Medicine, S-1, W-16, Chuo-ku, Sapporo 060-0061, Japan

tsuchiha{at}sapmed.ac.jp


We appreciate the interest of Castro et al. in our recent clinical study on a heart syndrome with transient left ventricular (LV) apical ballooning without coronary artery stenosis mimicking acute myocardial infarction (AMI) (1). As first reported by Satoh et al. (2) and Dote et al. (3) and as pointed out by Castro et al., coronary vasospasm under various underlying disorders, including administration of adrenergic drugs, might be considered as an initial etiological basis of this novel syndrome. However, we defined this syndrome as: 1) suspected AMI based on persistent chest symptoms or electrocardiogram (ECG) changes (ST-T changes, abnormal Q-wave formation); 2) transient LV ballooning confirmed by left ventriculography (LVG) and/or echocardiography (which is generally mismatched with the magnitude of creatine kinase release and with the area perfused by a single coronary artery); and 3) confirmed normal epicardial artery (luminal narrowing of <50% in all three coronary arteries) within 48 h of onset. Actually, no case exhibited vasospasm during manifestation symptoms or ECG changes. Also, autopsy findings in some cases were different from those of myocardial ischemia (4). Therefore, the possibility of transient ischemia including vasospasm as a initiating factor of this syndrome could not be ruled out; however, we speculate that vasospasm is not a main cause. Important etiologic bases suspected from our study will be vigorous stress (cathecholamine exposure) (5,6), dynamic midventricular obstruction due to basal hypercontraction (7), and/or secondary myocardial ischemia by apical ballooning (increased wall tension). However, as already mentioned in the discussion (1), our study was a retrospective investigation, and there are several limitations. Further cases therefore should be investigated to determine regional and racial differences.


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1. Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. J Am Coll Cardiol. 2001;38:11–18[Abstract/Free Full Text]

2. Satoh H, Tateishi H, Uchida T, et al. Stunned myocardium with specific (tsubo-type) left ventriculographic configuration due to multivessel spasm. Kodama K, Haze K, Hori M. Clinical Aspect of Myocardial Injury: From Ischemia to Heart Failure. Tokyo: Kagakuhyouronsya; 1990. p. 56–64 in Japanese

3. Dote K, Sato H, Tateishi H, et al. Myocardial stunning due to simultaneous multivessel spasms: a review of 5 cases. in Japanese with English abstractJ Cardiol. 1991;21:203–214[Medline]

4. Kawai S, Suzuki H, Yamaguchi H, et al. Ampulla cardiomyopathy ("Takotsubo" cardiomyopathy)—reversible left ventricular dysfunction with ST-segment elevation. Jpn Circ J. 2000;64:156–159[CrossRef][Medline]

5. Pavin D, Le Breton H, Daubert C. Human stress cardiomyopathy mimicking acute myocardial syndrome. Heart. 1997;78:509–511[Abstract/Free Full Text]

6. Sharkey SW, Shear W, Hodges M, Herzog CA. Reversible myocardial contraction abnormalities in patients with an acute noncardiac illness. Chest. 1998;114:98–105[Abstract/Free Full Text]

7. Villareal RP, Achari A, Wilansky S, Wilson JM. Anteroapical stunning and left ventricular outflow tract obstruction. Mayo Clin Proc. 2001;76:79–83[Abstract]





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