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We read with great interest the article in JACCby Lindahl et al. (1)titled “Mechanisms Behind the Prognostic Value of Troponin T in Unstable Coronary Artery Disease: A FRISC II Substudy.” There is limited data on the coronary anatomy of patients with acute coronary syndromes and an elevated troponin level, and this study provides new data on this important subject.
The investigators reported that the absence of significant coronary stenosis was more frequent, and three-vessel disease or left main stenosis was less frequent without, compared with, detectable troponin T (tnT). We recently reported our findings on the prevalence of angiographically significant stenosis in patients with chest pain and an elevated troponin I (tnI) level and normal levels of creatine kinase (CK) and creatine kinase-MB fraction (CK-MB) (2). We found that an elevated tnI level with normal CK and CK-MB levels in patients with chest pain who presented within 24 h was associated with a high prevalence of angiographically significant coronary artery stenosis. Patients with an elevated tnI and normal CK and CK-MB levels had a higher prevalence of coronary stenosis ≥50% compared to the group with normal tnI and CK and CK-MB levels (80% vs. 27%; p = 0.001), and a higher prevalence of coronary stenosis ≥70% (56% vs. 27%; p = 0.027). Furthermore, those patients with an elevated tnI and normal CK and CK-MB levels had a lower prevalence of coronary stenosis ≥70% compared to the group that had both elevated tnI, CK and CK-MB levels (56% vs. 84%, p = 0.022), but there was a similar prevalence of coronary stenosis ≥50% between these two groups (80% vs. 87%, p = NS).
These angiographic findings highlight the fact that patients with acute coronary syndromes comprise a heterogeneous population with varying degrees of vessel occlusion, and they underscore several important implications in the treatment of these patients. It is noteworthy that a good number of patients who presented with “non-ST elevation myocardial infarction” on the initial 12-lead electrocardiogram (ECG) subsequently were found to have totally occluded circumflex arteries. Indeed, in the study by Lindahl et al. (1), in the group with the highest levels of tnT, occlusion of the left circumflex artery was more common than in the three other groups. Presumably, the lack of ST-segment elevation on the initial 12-lead ECG, despite the left circumflex artery total occlusion, was due to the relative insensitivity of the standard ECG in detecting voltage from the posterolateral region of the heart. Posterior wall infarction may be detected by placing additional leads in the back of the heart and finding ST-segment elevation in leads V7through V9(3,4).
Furthermore, posterior wall infarction may be inferred by reciprocal ST-segment depression leads V1through V3. Thus, in patients who present with a markedly elevated troponin, but only nonspecific ST-T wave abnormalities, special attention to ST-segment depression in the anterior leads, and perhaps the performance of additional leads V7to V9, may be warranted so as to rule out total occlusion of the artery supplying the posterior wallof the left ventricle. This practice would be similar to the performance of a right-sided 12-lead ECG in any patient who presents with an inferior wall myocardial infraction to rule out right ventricular infarction (5). Thus, patients with totally occluded left circumflex arteries would benefit from immediate triage to the cardiac catheterization laboratory for rapid revascularization. How many of the patients who presented with left circumflex artery occlusions also had ECG changes suggestive of posterior wall injury, specifically ST-segment depression in the anterior precordial leads V1through V3?
The suggestion that there is an inverted “U”-shaped curve in the risk of myocardial infarction (MI) is also important data. We agree with the investigators that this finding supports the notion that the risk for subsequent MI is dependent on the amount of remaining jeopardized myocardium. Thus, patients with the highest level of troponin have a higher risk of death at one year, but a lower incidence of reinfarction due to the smaller region of noninfarcted myocardium still at risk. We find the suggestion in the accompanying editorial by Antman (6)to be quite provocative. He alluded to the strategy of stratifying the patients into “low,” “moderate” and “high” troponin levels, and to use this stratification as a potential basis for subsequent treatment decisions regarding the use of glycoprotein IIb/IIIa inhibitors. However, clinical decision making regarding the absolute cutoff values of markedly elevated troponins, and what would constitute a “high” level, would be limited by the differences in the various available assays. Given the marked heterogeneity in the performance and interpretation of the cardiac troponin tests, and the variable time measurement points, could such a scheme be truly implemented in a clinically relevant fashion whereby the physician would be able to reliably assess what constitutes a “low” and “high” level in any given patient?
Finally, the current study found that in men and women with tnT elevation, 4% and 14%, respectively, had no significant coronary obstruction. As the investigators (1)pointed out, these findings may be due to an increase in myocardial oxygen demand or decrease in oxygen supply unrelated to significant coronary thrombosis or stenosis. These observations demonstrate the significant heterogeneity present in the various underlying etiologies of elevated troponins. It would be of interest to determine the outcome of patients with elevated troponins, but without appreciable coronary obstruction or thrombosis, as these patients would presumably have a lower event rate compared to the other groups with visible stenosis or thrombus. Were the investigators able to compare the outcomes of patients with elevated troponins but relatively “normal” coronary arteries, and what was the mean elevation of tnT in this group of patients? Although small in number, these patients would constitute an important subset of patients who present with acute coronary syndromes. If the outcomes in this group of patients with elevated troponins but relatively normal coronary arteries differed significantly from the rest of the subjects, then it would support the notion that troponin elevations are, in and of itself, not equivalent, and that it is not merely the troponin elevation, but rather the etiology behind the elevation, that makes the most difference clinically.
- American College of Cardiology Foundation
- FRISC II Investigators,
- Lindahl B,
- Diderholm E,
- Lagerqvist B,
- Venge P,
- Wallentin L
- Antman E.M