AIMS: The prognostic role of inflammation in peripheral arterial disease (PAD) remains to be conclusively established. Accordingly, in these patients we investigated the impact of myeloperoxidase (MPOx) and C-reactive protein on the incidence of myocardial infarction and stroke. METHODS AND RESULTS: Of 156 PAD patients, 10 had a myocardial infarction and seven a stroke, during follow-up. We used the receiver operating characteristic curve analysis and the bootstrap approach to identify the MPOx, C-reactive protein, and ankle brachial index (ABI) threshold levels that provided the best cut-off to predict the outcome. For MPOx a cut-off > or =183.7 pM was independently associated with a poor outcome (HR = 6.80, 95% CI 1.20-38.69, P = 0.031). The result remained unmodified when MPOx was used as a continuous variable (HR = 1.03, 95% CI 1.01-1.05, P = 0.031). Conversely, C-reactive protein was not a prognostic determinant in our series (HR = 0.88, 95% CI 0.60-1.29, P = 0.514). Kaplan-Meier curves for the four groups of patients delineated according to ABI and MPOx values identified using the bootstrap approach showed that the addition of MPOx measurement to ABI improved the ability to identify patients at risk for myocardial infarction and stroke. CONCLUSION: In PAD, MPOx, but not C-reactive protein, predicts an increased risk of major cardiovascular events, and adds to the prognostic value of ABI, currently the most powerful prognostic indicator in these patients.
AIMS: The prognostic role of inflammation in peripheral arterial disease (PAD) remains to be conclusively established. Accordingly, in these patients we investigated the impact of myeloperoxidase (MPOx) and C-reactive protein on the incidence of myocardial infarction and stroke. METHODS AND RESULTS: Of 156 PAD patients, 10 had a myocardial infarction and seven a stroke, during follow-up. We used the receiver operating characteristic curve analysis and the bootstrap approach to identify the MPOx, C-reactive protein, and ankle brachial index (ABI) threshold levels that provided the best cut-off to predict the outcome. For MPOx a cut-off > or =183.7 pM was independently associated with a poor outcome (HR = 6.80, 95% CI 1.20-38.69, P = 0.031). The result remained unmodified when MPOx was used as a continuous variable (HR = 1.03, 95% CI 1.01-1.05, P = 0.031). Conversely, C-reactive protein was not a prognostic determinant in our series (HR = 0.88, 95% CI 0.60-1.29, P = 0.514). Kaplan-Meier curves for the four groups of patients delineated according to ABI and MPOx values identified using the bootstrap approach showed that the addition of MPOx measurement to ABI improved the ability to identify patients at risk for myocardial infarction and stroke. CONCLUSION: In PAD, MPOx, but not C-reactive protein, predicts an increased risk of major cardiovascular events, and adds to the prognostic value of ABI, currently the most powerful prognostic indicator in these patients.
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