CORRESPONDENCE: LETTER TO THE EDITOR
Troponin Levels and Acute Coronary Syndrome
Huseyin Yilmaz, MD* and
Ibrahim Ba arici, MD
* Akdeniz Üniversitesi Tip Fakültesi, Kardiyoloji Anabilim Dah, 07070 Antalya, Turkey (Email: hyilmaz{at}akdeniz.edu.tr).
We read with interest the recent study by Dokainish et al. (1). Both the aim and the result of the study are challenging; this is because the investigators have suggested significant prognostic evidence for troponin (Tp)-positive patients with acute coronary syndromes (ACS) but without significant coronary artery disease (CAD). As Dokainish et al. (1) suggested in the Study Limitations section, their investigation has disadvantages in being a substudy with a limited number of patients and with a limited number of patients with index event. The main finding of their study—that so-called false-positive Tp results in patients with ACS but no significant angiographic CAD—begets further attention because of a higher event rate by means of a composite end point in these patients. However, this suggestion should be interpreted cau-tiously—as mentioned in the Study Limitations—because angiography is not a gold standard for accessing atherosclerosis.
Also, because of the study design it should be remembered that all patients were treated by acetylsalicylic acid (ASA), intravenous heparin, and glycoprotein (GP) IIb/IIIa inhibitor. It is well known that patients with an elevated troponin T level and non–ST-segment elevated ACS (NSTE-ACS) have been reported to benefit particularly from antithrombotic drugs such as platelet GP IIb/IIIa antagonists and low-molecular-weight heparin (2). It is reasonable to hypothesize that the elevated troponin T levels in patients with NSTE-ACS indicate the presence of a thrombus at culprit lesions (3). As is known, a culprit lesion responsible for myocardial infarction is <50% in most cases. Thus, CAD or no-CAD classification by coronary angiography must be questioned.
Conversely, baseline creatinine (Cr) level differed between the two groups (Tp–, no-CAD vs. Tp+, no-CAD) (0.93 ± 0.56 mg/dl, 1.46 ± 2.31 mg/dl, respectively). In the original study, chronic renal failure (CRF) was an exclusion factor (serum Cr >2.5 mg/dl) (4), but in this substudy the mean Cr is high, and the standard deviation is also unexpectedly high. What could be the explanation of this high serum Cr in such a study that excludes patients with CRF? It is well established that patients with CRF have higher Tp levels even without any ACS; the difference in Cr levels may be a consequence of inadequate or slow clearance rather than excess production due to ACS in this group of patients.
It must be remembered that this study basically compares no-CAD patients with or without Tp positivity. Hence, two-way comparisons should be applied instead of four-way comparisons for statistical analysis. As a result, regarding the small event rate, the limitations previously mentioned, and our considerations for the effect of GP IIb/IIIa antagonists in borderline lesions and their effect of undiagnosed renal failure, we believe that the conclusion of the study by Dokainish et al. (1) is quite exaggerated.
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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 diseaseA TACTICS-TIMI-18 substudy. J Am Coll Cardiol 2005;45:19-24.[Abstract/Free Full Text]
2. Hamm CW, Heeschen C, Goldmann B, et al. Benefit of abciximab in patients with refractory unstable angina in relation to serum troponin T levels N Engl J Med 1999;340:1623-1629.[Abstract/Free Full Text]
3. Okamatsu K, Takano M, Sakai S, et al. Elevated troponin T levels and lesion characteristics in non-ST-elevation acute coronary syndromes Circulation 2004;109:465-470.[Abstract/Free Full Text]
4. Cannon CP, Weintraub WS, Demopoulos LA, et al. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban: TACTICS-TIMI-18 N Engl J Med 2001;34:1879-1887.
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