Prognostic value of C-reactive protein and cardiac troponin I in primary percutaneous interventions for ST-elevation myocardial infarction.

BACKGROUND: The rise in cardiac troponin I after ST-elevation myocardial infarction treated by primary percutaneous coronary interventions (PCIs) is predictive of infarct size and left ventricular ejection fraction (LVEF). However, the comparative value of C-reactive protein (CRP) and troponin I for infarct size evaluation and the respective relationships between these biomarkers and mortality have not been investigated. METHODS: We studied 87 patients who underwent primary PCI for ST-elevation myocardial infarction. Concentrations of troponin I and CRP were measured before and for 72 hours after PCI. Infarct size was measured by the cumulative release of alpha-hydroxybutyrate deshydrogenase during the 72 hours after PCI (QHBDH72) and by delayed radionuclide LVEF (at 4.6 +/- 1.7 weeks). RESULTS: Concentrations of CRP at peak and at 24, 48 and 72 hours, and of troponin I at 6 and 72 hours, correlated with QHBDH72 and LVEF. In single variable analysis, at a mean follow-up of 42 +/- 8 months, Killip score of 3 to 4, CRP at baseline and at 48 hours, and troponin I at 6 and 72 hours were related to mortality. By multiple variable analysis, Killip score (OR 9.9, CI 1.6-58.8) and troponin I at 72 hours (OR 9.43, CI 2.1-43.5) were the only independent predictors of mortality. CONCLUSIONS: Plasma concentrations of CRP and troponin I after PCI were related to infarct size and mortality. However, Killip class and troponin I at 72 hours were the only independent predictors of mortality at long-term follow-up.

Troponin I concentrations following primary percutaneous coronary intervention predict large infarct size and left ventricular dysfunction in patients with ST-segment elevation acute myocardial infarction.

The aim of this study was to investigate the ability of troponin I (cTnI) levels to predict myocardial infarction size in patients with ST-segment elevation acute myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). In 87 patients with STEMI undergoing primary PCI, serial plasma concentrations of cTnI and alpha-hydroxybutyrate deshydrogenase (HBDH) were measured before PCI and over the following 72 h. Enzymatic infarct size was estimated by the cumulative release of HBDH during the 72 h following PCI (QHBDH72). Delayed radionuclide left ventricular ejection fraction (LVEF) was measured in 63 patients. While cTnI concentrations at admission did not correlate with QHBDH72 or with LVEF, from the 3rd to the 72nd h following PCI, they did correlated with QHBDH72 (P<0.001; R: 0.76-0.86) and with LVEF (P<0.001; R: -0.42 to -0.50). Receiver-operator characteristic (ROC) curve analysis showed that admission concentrations of cTnI could not predict either a large infarct size (i.e., QHBDH72>10 g-eq l(-1)) or a low LVEF (i.e., LVEF<40%). However, 6 h and up until 72 h after PTCA, cTnI concentrations were predictive of large enzymatic infarct size (sensitivity: 91 and 95%, specificity: 90 and 87%, respectively) and of LVEF under 40% (sensitivity: 75 and 77%, specificity: 90 and 78%, respectively). Thus, our study suggests that in contrast with admission cTnI concentration, cTnI levels following primary PCI represent a reliable tool for predicting large enzymatic infarct size and may help in selecting patients with a high risk of low LVEF at 1 month.