Key result
Admission cardiac troponin T ≥0.1 μg/L in STEMI patients undergoing primary PCI was associated with higher 9-month mortality (14% vs 3.9%, P=0.005) and a 3.2-fold risk of incomplete reperfusion.
Why the study?
Does admission troponin T level predict clinical outcomes and reperfusion success in STEMI patients undergoing primary PCI?
Cohort (n=140)
Does admission troponin T level predict clinical outcomes and reperfusion success in STEMI patients undergoing primary PCI?
Elevated admission troponin T in STEMI patients undergoing primary PCI predicts higher mortality and worse epicardial and myocardial reperfusion.
Answers are grounded in this paper and cite their sources.
May aid risk stratification after primary PCI; leaves open whether troponin thresholds should guide therapy in prospective trials.
BACKGROUND: In ST-segment elevation myocardial infarction, a troponin T >/=0.1 microg/L on admission indicates poorer prognosis despite early reperfusion. To evaluate the underlying reason, we studied the value of cardiac troponin T (cTnT) for prediction of outcomes, epicardial blood flow, and myocardial reperfusion after primary percutaneous intervention. METHODS AND RESULTS: Patients (n=140) admitted within 12 hours after onset of symptoms were stratified by admission cTnT. Epicardial and myocardial reperfusion were graded by the TIMI score and by measurement of relative increases of myoglobin, cTnT, and creatine kinase (CK)-MB 60 minutes after recanalization, respectively. cTnT was positive in 64 patients (45.7%) and was associated with longer median time intervals to admission (5.5 versus 3.5 hours, P<0.001) and higher mortality rates after 30 days (12.5% versus 3.9%, P=0.06) and 9 months (14% versus 3.9%, P=0.005). cTnT independently predicted a 3.2-fold risk for incomplete epicardial reperfusion (P=0.03). In addition, cTnT >/=0.1 microg/L was associated with more severely impaired myocardial perfusion despite normal epicardial flow, as indicated by lower 60-minute ratios of myoglobin (2.6 versus 7.6, P=0.007), cTnT (6.6 versus 29.2, P<0.001), and CK-MB (3.5 versus 21.4, P=0.002) and a tendency for less resolution of ST-segment elevations (54% versus 60%, P=0.08). CONCLUSIONS: cTnT predicts poorer clinical outcomes, lower rates of postprocedural TIMI 3 flow, and more severely compromised myocardial perfusion despite normal epicardial flow. Thus, a cTnT-positive patient may require more aggressive adjunctive therapy when treated by percutaneous coronary intervention. The impact of preexisting or evolving microvascular dysfunction and the effect of therapies that target myocardial perfusion require further prospective evaluation.
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Giannitsis et al. (2001) conducted a cohort in Acute ST-Segment Elevation Myocardial Infarction (n=140). Admission cardiac troponin T ≥0.1 μg/L vs. Admission cardiac troponin T <0.1 μg/L was evaluated on 9-month mortality (p=0.005). Admission cardiac troponin T ≥0.1 μg/L in STEMI patients undergoing primary PCI was associated with higher 9-month mortality (14% vs 3.9%, P=0.005) and a 3.2-fold risk of incomplete reperfusion.
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