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J Am Coll Cardiol, 2005; 46:741-742, doi:10.1016/j.jacc.2005.05.047 (Published online 27 July 2005).
© 2005 by the American College of Cardiology Foundation
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CORRESPONDENCE: LETTER TO THE EDITOR

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Hisham Dokainish, MD, Manu Pillai, MD, Sabina A. Murphy, MPH, Peter M. DiBattiste, MD, Marc J. Schweiger, MD, Amir Lotfi, MD, David A. Morrow, MD, MPH, Christopher P. Cannon, MD, Eugene Braunwald, MD, Nasser Lakkis, MD* for the TACTICS-TIMI-18 Investigators

* Ben Taub General Hospital, Baylor College of Medicine, Cardiology, Houston, TX 77030 (Email: nlakkis{at}bcm.tmc.edu).


We thank Drs. Bybee and Rihal for their valuable comments regarding our study (1). The major point of our publication is that patients presenting with symptoms suggestive of acute coronary syndrome (ACS) who are troponin positive on admission without evidence of significant epicardial coronary artery disease (CAD) on angiography have a worse prognosis than do those who are troponin negative without significant epicardial disease. In our discussion we recognized that the mechanisms conferring this adverse prognosis are not known. Notwithstanding that, we agree with the comments of Drs. Bybee and Rihal that transient left ventricular apical ballooning syndrome (TLVABS) should be included as a potential explanation for troponin positivity in some of our patients, especially women. It is intriguing to note that the underlying mechanism(s) that account for TLVABS remain unknown. Some of the mechanisms, which we suggested in our study, to explain troponin positivity in the absence of significant epicardial coronary disease may be the same ones responsible for TLVABS, namely coronary vasospasm (2), microvascular ischemia (2), acute myocarditis (3), plaque erosions (4), and others such as emotional stress with possible excessive sympathetic stimulation (5).

We would also like to thank Dr. Leibowitz for his interest in our study. We agree with his comments that the number of patients with positive troponin and no significant epicardial coronary disease on angiography is small. Therefore, as we noted in our Study Limitations section that "the results should be interpreted with caution."

To validate the results of our study, we have analyzed the event rate in all patients included in the TACTICS study who were either troponin-T or -I positive on admission, and who underwent coronary angiography either because they were randomized to the invasive arm or randomized to the conservative arm and subsequently underwent coronary angiography. In this analysis, 57 patients were troponin positive without significant epicardial CAD. Of these patients, one died, two had reinfarction, and four were rehospitalized for ACS. Therefore, the composite event rate was 10.5% at six months compared to no events in the group of patients who were troponin negative without significant epicardial disease.

It is worthwhile to mention also that no statistical differences existed in the incidence of congestive heart failure or LV ejection fraction between the group of patients without epicardial coronary disease with or without troponin positivity on admission (2 of 95 patients vs. 3 of 32 patients; p = NS) and (60.5% vs. 58.3%; p = NS), respectively.

In conclusion, large prospective studies are definitely needed to validate these potentially important results, which have a significant impact on patients presenting with ACS.


    References
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 References
 
1. Dokainish H, Pillai M, Murphy SA, et al. Prognostic implications of elevated troponin in patients with suspected acute coronary syndrome but no critical epicardial coronary disease: a TACTICS-TIMI-18 substudy J Am Coll Cardiol 2005;45:19-24.[Abstract/Free Full Text]

2. Abe Y, Kondo M, Matsuoka R, Araki M, Dohyama K, Tanio H. Assessment of clinical features in transient left ventricular apical ballooning J Am Coll Cardiol 2003;41:737-742.[Abstract/Free Full Text]

3. Dec GW, Waldman H, Southern J, Fallon JT, Hutter AM, Palacios IF. Viral myocarditis mimicking acute myocardial infarction J Am Coll Cardiol 2001;37:786-792.[Abstract/Free Full Text]

4. Farb A, Burke AP, Tang AL. Coronary plaque erosion without rupture into lipid core: a frequent cause of coronary thrombosis in sudden cardiac death Circulation 1996;93:1354-1363.[Abstract/Free Full Text]

5. Sharkey SW, Lesser JR, Zenovich AG, et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States Circulation 2005;111:472-479.[Abstract/Free Full Text]


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Myocardial Infarction in the Absence of Obstructive Epicardial Coronary Disease
Kevin A. Bybee and Charanjit S. Rihal
J. Am. Coll. Cardiol. 2005 46: 740. [Full Text] [PDF]




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