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baseline 1h 3h 12h 24h

Time from Presentation

Fig. 3. Evolution of ST2 serum levels over 24 h after presentation for AMI. Each line represents 1 of228 patients in TIMI 14 study who had serum samples available at all five time points. Peak values occurred at 12 h in most patients, although some patients with particularly high levels had peak values at 24 h. (Reproduced from ref. 20.)

baseline 1h 3h 12h 24h

Time from Presentation

Fig. 3. Evolution of ST2 serum levels over 24 h after presentation for AMI. Each line represents 1 of228 patients in TIMI 14 study who had serum samples available at all five time points. Peak values occurred at 12 h in most patients, although some patients with particularly high levels had peak values at 24 h. (Reproduced from ref. 20.)

To determine the relationship between ST2 serum levels and clinical outcome in AMI, we assayed serum for ST2 from patients with ST-elevation MI enrolled in the Thrombolysis in Myocardial Infarction (TIMI 14) and ENTIRE (TIMI 23) trials (20). TIMI 14 evaluated the combination of fibrinolytics with abciximab, a glycoprotein IIb/IIIa antagonist (21,22). Serum samples were available at 1, 3, 12, and 24 h after enrollment. TIMI 23 was designed to evaluate the low molecular weight heparin enoxaparin as adjunctive anti-thrombin therapy with various forms ofpharmacological reperfusion (23). Serum samples were available at baseline (enrollment). Measurement of ST2 in TIMI 14 showed that although ST2 serum concentration is elevated at the time of presentation in patients with MI compared with healthy subjects, peak levels are achieved 12 h after presentation and begin to decline by 24 h in most patients (Fig. 3). This observation is useful for understanding the potential of ST2 as a marker of hemodynamic stress in AMI and is in agreement with the rapid induction of ST2 mRNA expression in cultured cardiac myocytes.

Interestingly, higher baseline ST2 levels were associated with adverse clinical outcome at 30 d. Dichotomized at the median, elevated levels of ST2 were associated with higher mortality through 30 d of follow-up (p = 0.0009) (Fig. 4), and the risk of death or combined death/heart failure increased in a stepwise fashion according to quartiles ofST2. In multivariable analysis that included traditional indicators of risk in AMI, increasing concentration of ST2 was an independent predictor of death at 30 d. Establishing ST2 as a novel

Fig. 4. Probability of death through 30 d after presentation with STEMI stratified by serum ST2 level at baseline. (Reproduced from ref. 20.)

10 20 Follow-up (days)

Fig. 4. Probability of death through 30 d after presentation with STEMI stratified by serum ST2 level at baseline. (Reproduced from ref. 20.)

biomarker that offers prognostic information in patients with AMI. The findings also suggest a potential role for ST2 to modulate the inflammatory response following hemodynamic stress after MI.

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