Risk stratification

Several randomized trials and observational studies have contributed to a consistent body of evidence that troponin levels on admission allow for early risk stratification also in patients with STEMI (23-27) (Fig. 2). In the GUSTO III troponin T substudy with 12,666 patients enrolled, 30-d mortality rates were 15.7% in patients with positive troponin results on admission compared with 6.2% among patients with negative results (23). The predictive value ofcTnT was independent ofage, infarct location, Killip class, systolic blood pressure, and fibrinolytic agent. Two other clinical trials confirmed the adverse prognostic association of a positive cTnT or cTnI test for patients undergoing primary PCI (25,26).

There are several potential reasons for the adverse outcomes associated with increased blood concentration of cardiac troponin. First, time delays between onset of symptoms and admission are longer for troponin-positive than for troponin-negative patients. Second, complete epicardial reperfusion is obtained less frequently in patients with already elevated cardiac troponin on admission, both after fibrinolytic therapy (18,23,24,27) and after primary PCI (25,26) (Fig. 3). Third, even after restoration of TIMI 3 grade flow with primary PCI, the prognosis remains less favorable in patients with elevated cTnT levels before the procedure (20). After adjustment for time delay and other potential confound-

200 400

Time after AMI (Days) Fig. 2. Overview of clinical trials testing prognostic impact of positive troponin value on admission. TVR, target vessel revascularization.

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Time after AMI (Days) Fig. 2. Overview of clinical trials testing prognostic impact of positive troponin value on admission. TVR, target vessel revascularization.

Giannitsis (25) Matetzky (26) Frostfeldt (18)

(PCI) (PCI) (Streptokinase)

Fig. 3. Rates of successful reperfusion with either primary PCI or fibrinolytic therapy according to tro-ponin status on admission.

ers, cardiac troponin remained independently associated with morbidity, suggesting a different potential pathomechanism. Therefore, it is tempting to speculate that cardiac troponin elevation might reflect a combination of ischemic burden and actual myocardial damage and may overcome some shortcomings associated with perception of pain, ische-mic preconditioning, or collateral flow to the infarcted area (23). Moreover, episodes of thromboembolic micronecrosis, resulting in microvascular obstruction, may well precede the onset of STEMI (28).

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