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J Am Coll Cardiol, 2006; 47:2212-2218, doi:10.1016/j.jacc.2006.01.067
(Published online 12 May 2006). © 2006 by the American College of Cardiology Foundation |
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,*
* Departments of Medical and Chemical Laboratory Diagnostics, Medical University Vienna, Vienna, Austria
Department of Angiology, Medical University Vienna, Vienna, Austria
Department of Neurology, Medical University Vienna, Vienna, Austria
Department of Cardiology, Medical University Vienna, Vienna, Austria
Manuscript received November 7, 2005; revised manuscript received January 11, 2006, accepted January 16, 2006.
* Reprint requests and correspondence: Dr. Martin Schillinger, Division of Angiology, Department of Internal Medicine II, Medical University Vienna, Waehringer Guertel 18-20, A-1090 Vienna, Austria. (Email: martin.schillinger{at}meduniwien.ac.at).
OBJECTIVES: We investigated the effect of myeloperoxidase (MPO) on progression of carotid stenosis in states of high and low high-density lipoprotein-cholesterol (HDL-C) and low-density lipoprotein-cholesterol (LDL-C) levels.
BACKGROUND: Myeloperoxidase is pivotally involved in the pathogenesis of atherosclerosis. In vitro data suggest that MPO exerts deleterious effects via oxidative modulation of lipoproteins.
METHODS: We prospectively studied 1,019 of 1,268 consecutive patients who were asymptomatic with respect to carotid artery disease. Patients underwent serial carotid ultrasound investigations at baseline and after a follow-up interval of median 7.5 months (range 6 to 9 months), categorizing carotid arteries as 0% to 29%, 30% to 49%, 50% to 69%, 70% to 89%, or 90% to 99% stenosed or occluded. The MPO, HDL-C, and LDL-C levels were measured at baseline, grouped by medians, and correlated with progression of carotid atherosclerosis.
RESULTS: Progression of carotid atherosclerosis was found in 100 of 1,019 patients (9.8%). Myeloperoxidase (p = 0.014) but not HDL-C (p = 0.95) or LDL-C (p = 0.30) were associated with progressive disease. However, MPO
310 ng/ml was significantly associated with progressive disease (adjusted odds ratio [OR] 2.57, 95% confidence interval [CI] 1.39 to 4.75) only in patients with HDL-C levels <49 mg/dl. Otherwise, in patients with higher HDL-C levels (
49 mg/dl), MPO
310 ng/ml did not predict disease progression (adjusted OR 1.42, 95% CI 0.72 to 2.78). No interaction of MPO with LDL-C was observed.
CONCLUSIONS: Myeloperoxidase was associated with progression of carotid atherosclerosis in patients with HDL cholesterol levels below 49 mg/dl.
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