INTRODUCTION: Levels of inflammatory markers increase in patients with acute coronary syndromes (ACS) and the magnitude of the inflammatory response has been related to clinical outcomes. The release patterns and, thereby, the time point of maximal increase for multiple inflammatory markers following an ACS are not fully defined. Our purpose was to serially measure three acute phase proteins (APPs) in patients with ACS. METHODS: We prospectively enrolled 74 consecutive patients (54 men, age 62.2 ± 9.8 years) with ACS: 38 with ST-elevation acute myocardial infarction (STEMI), and 36 with non-ST-elevation acute myocardial infarction (NSTEMI) or unstable angina (UA). Peripheral levels of alpha-1 antitrypsin (A1AT), alpha-1 acid glycoprotein (A1GP) and haptoglobin (HPT) were measured on admission, and 6, 12, 24, 48, 72 hours, 7 days and 6 months after the initial evaluation. RESULTS: Baseline levels of the APPs did not differ between the two groups. A1AT, A1GP and HPT all exhibited a similar time course among NSTEMI/UA patients, all reaching maximal values at 7 days. The markers showed an earlier increase and A1AT showed earlier peaking (at 72 hours) in STEMI patients. Peak levels were higher in patients with STEMI vs. NSTEMI/UA for all three APPs (p<0.01 for A1AT and HPT, p<0.05 for A1GP). CONCLUSIONS: A1AT, A1GP and HPT levels increase significantly in patients with ACS and display different release curves in those with STEMI versus NSTEMI or UA. Knowledge of the release patterns of APPs may determine the optimal time point of measurement and thereby enhance their potential prognostic value in the setting of ACS.
INTRODUCTION: Levels of inflammatory markers increase in patients with acute coronary syndromes (ACS) and the magnitude of the inflammatory response has been related to clinical outcomes. The release patterns and, thereby, the time point of maximal increase for multiple inflammatory markers following an ACS are not fully defined. Our purpose was to serially measure three acute phase proteins (APPs) in patients with ACS. METHODS: We prospectively enrolled 74 consecutive patients (54 men, age 62.2 ± 9.8 years) with ACS: 38 with ST-elevation acute myocardial infarction (STEMI), and 36 with non-ST-elevation acute myocardial infarction (NSTEMI) or unstable angina (UA). Peripheral levels of alpha-1 antitrypsin (A1AT), alpha-1 acid glycoprotein (A1GP) and haptoglobin (HPT) were measured on admission, and 6, 12, 24, 48, 72 hours, 7 days and 6 months after the initial evaluation. RESULTS: Baseline levels of the APPs did not differ between the two groups. A1AT, A1GP and HPT all exhibited a similar time course among NSTEMI/UA patients, all reaching maximal values at 7 days. The markers showed an earlier increase and A1AT showed earlier peaking (at 72 hours) in STEMI patients. Peak levels were higher in patients with STEMI vs. NSTEMI/UA for all three APPs (p<0.01 for A1AT and HPT, p<0.05 for A1GP). CONCLUSIONS: A1AT, A1GP and HPT levels increase significantly in patients with ACS and display different release curves in those with STEMI versus NSTEMI or UA. Knowledge of the release patterns of APPs may determine the optimal time point of measurement and thereby enhance their potential prognostic value in the setting of ACS.