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Myeloperoxidase improves risk stratification in patients with ischemia and normal cardiac troponin I concentrations
Fred S Apple1, Stephen W Smith, Lesly A Pearce
1Department of Laboratory Medicine and Pathology, Hennepin County Medical Center, University of Minnesota School of Medicine and Minneapolis Medical Research Foundation, Minneapolis, MN 55415, USA. apple004@umn.edu
Background:
We assessed the ability of myeloperoxidase (MPO) to identify the risk for major adverse cardiac events (MACE) in patients who present with ischemic symptoms suggestive of acute coronary syndrome and have a normal cardiac troponin I (cTnI) value.
Methods:
We used Siemens (n = 400) and Abbott (n = 350) assays to measure MPO and cTnI in plasma samples from 400 patients. Event rates (myocardial infarction, cardiac death, percutaneous coronary intervention, coronary artery bypass grafting) were estimated by the Kaplan-Meier method and compared with the log-rank statistic.
Results:
At the 30-day follow-up, the adjusted hazard ratios for MACE were 3.9 (P < 0.001) for increased cTnI and 2.7 (P = 0.006) for increased MPO for the Siemens assays and were 5.5 (P < 0.001) for increased cTnI and 2.9 (P = 0.001) for increased MPO for the Abbott assays. Similar findings were observed with 6 months of follow-up. Patients who initially had a normal cTnI value and an increased Siemens MPO value demonstrated a higher rate of MACE at 30 days than those in whom both values were normal (16.1% vs 3.6%, P = 0.002) and 6 months (18.1% vs 5.0%, P = 0.002). Similarly, patients who had an increased Abbott MPO result demonstrated a higher MACE rate at 30 days (12.3% vs 3.9%, P = 0.03) and at 6 months (16.2% vs 5.1%, P = 0.01) than those with normal values.
Conclusions:
A combination of MPO and cTnI allowed the identification of a greater proportion of patients at risk for MACE than the use of cTnI alone. Increased MPO values remained predictive of future cardiac events even when the cTnI value was normal.
Insights
Myeloperoxidase (MPO) aids in identifying major adverse cardiac events (MACE) risk, even with normal cardiac troponin I (cTnI) levels. This biomarker combination improves risk stratification for acute coronary syndrome patients.
Area of Science:
- Cardiology
- Biomarker Discovery
- Clinical Diagnostics
Background:
- Assessing risk for major adverse cardiac events (MACE) is crucial in patients with ischemic symptoms.
- Cardiac troponin I (cTnI) is a standard biomarker, but its utility is limited in some acute coronary syndrome presentations.
- Myeloperoxidase (MPO) is investigated as a potential complementary biomarker for risk stratification.
Purpose of the Study:
- To evaluate the predictive ability of myeloperoxidase (MPO) for major adverse cardiac events (MACE).
- To determine if MPO can identify MACE risk in patients with normal cardiac troponin I (cTnI) levels.
- To compare the diagnostic performance of MPO and cTnI assays from different manufacturers.
Main Methods:
- Plasma samples from 400 patients presenting with ischemic symptoms were analyzed.
- Myeloperoxidase (MPO) and cardiac troponin I (cTnI) levels were measured using Siemens and Abbott assays.
- Event rates for MACE (myocardial infarction, cardiac death, revascularization) were estimated using Kaplan-Meier analysis and compared with log-rank tests.
Main Results:
- Increased MPO levels were significantly associated with higher MACE risk (adjusted HRs 2.7-2.9, P < 0.006) across both assay types.
- MPO predicted MACE even in patients with normal cTnI values, showing significantly higher event rates (12.3-16.1%) compared to those with normal MPO and cTnI (3.6-3.9%).
- Findings were consistent at 30-day and 6-month follow-ups, indicating sustained predictive value.
Conclusions:
- Myeloperoxidase (MPO) improves the identification of patients at risk for major adverse cardiac events (MACE) beyond cTnI alone.
- Elevated MPO levels are predictive of future cardiac events, particularly in patients with normal cTnI.
- The combination of MPO and cTnI offers enhanced risk stratification for acute coronary syndrome.
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