CONTENTS
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Prognostic relevance of troponin in
Unstable Coronary Syndromes:
Implications for Therapy
An elevated troponin level is an independant marker of adverse outcome and thrombotic microembolization in patients with unstable ischemic syndromes. [1] An analysis of 1404 patients in the TIMI IIIB trial found that troponin levels greater than 0.4 mcg/L were associated with a significantly higher mortality at 42 days compared to lower levels. (Table 1). A linear, non-threshold relationship between mortality and each 0.1 mcg/L rise in troponin was observed[2]. The prognostic information provided by troponin levels are independent of CKMB enzyme elevation, electrocardiographic changes and age, all of which are predictors of mortality.
Troponin levels should be measured at baseline and 8 hours after presentation to the emergency department. If elevated, patients should be considered for GPIIb/IIIa inhibitor treatment, as recent data confirms clinical benefit in this high-risk patient population.
Fig 1. Mortality Rates at 42 Days According to the Level of Cardiac troponin Measured at Enrollment (TIMI IIIB Trial)
Antman et al. N Engl J Med. 1996; 335: 1342-1349.
Elevated troponin levels predicts benefits of GPIIb/IIIa inhibitor therapy. Treatment with tirofiban prevents increases in Tn I levels in patients presenting with unstable ischemic syndromes.[3] In the PRISM-PLUS trial, there were no differences in baseline troponin levels between patients randomized to placebo or tirofiban. The peak Tn I level was significantly higher, however, in the heparin monotherapy group (15.5 + 29.1 ng/ml) compared to the heparin plus tirofiban group (5.2 + 8.3 ng/ml), p=0.017 (Fig. 2).
In the CAPTURE trial (c7E3 F2b antiplatelet therapy in unstable refractory angina) treatment with the GPIIb/IIIa receptor blocker abciximab reduced the risk of MI in patients with refractory unstable angina, both during the 18-24 hour period before coronary intervention and during angioplasty. For patients with troponin T levels > 0.10ng/mL, the risk of cardiac events was lower in the abciximab group, primarily due to a reduction in the rate of MI (OR, 0.23; 95% CI, 0.12 to 0.49; P <.002).
Thus, although elevated troponin levels are associated with adverse prognosis in patients with unstable ischemic syndromes, the rise in troponin can be attenuated by anti-platelet treatment. GP IIb/IIIa inhibitor therapy results in reduction of myocardial cell injury in patients with elevated troponin levels, and thus should be strongly considered in this high-risk subgroup.
Fig. 2. Tnl Levels in UA/NQWMI Patients Treated With tirobifan: PRISM-PLUS
Hahn SS et al. J Am Coll Cardiol 1998; 31(suppl A): 229A.
1. Zaachs SM, Liebbson PR, Calvin JE, et al. Unstable angina and non-Q-wave myocardial infarction: Does the clinical diagnosis have therapeutic implications? J Am Coll Cardiol 1999; 33:107-118.
2. Antman EM, Tanasijevic MJ, Thompson B, et al. Cardiac-specific Troponin-I levels to predict the risk of mortality in patients with Acute Coronary Syndrome. N Engl J Med 1996; 335:1342-1349.
3. Hahn SS, Chae R, Giuglialo R, et al. troponin levels in unstable angina/non-Q-wave myocardial infarction patients treated with tirofiban, a glycoprotein llb/llla antagonist. J Am Coll Cardiol 1998; 31 (suppl A): 229 A.
4. Hamm C, Heeschen C, Goldman B, et al. Benefit of abciximab in patients with refractory unstable angina in relation to serum troponin T levels. N Engl J Med. 1999, 340:162329.
Last modified: October 14, 1999 (PL)
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