Bashar Jabor1, Hong Choi, Isabelle Ruel, Anouar Hafiane, Walid Mourad, Jacques Genest. 1. Cardiovascular Research Laboratories, Cardiology Division, Royal Victoria Hospital, McGill University/McGill University Health Centre, Montreal, Québec, Canada; Programme de Sciences Biomédicales, Faculté de Médecine, Université de Montréal, Montreal, Québec, Canada.
Abstract
BACKGROUND: Lipoprotein-associated phospholipase A2 (Lp-PLA2) might play a role in the formation of vulnerable atherosclerotic plaques. Its plasma distribution and mass in subjects with acute coronary syndrome (ACS) has yet to be characterized. METHODS: We compared plasma levels of Lp-PLA2 in 24 patients within 48 hours of an ACS (acute) and 12 weeks after (recovery), in 26 patients with stable coronary artery disease and in 10 normal healthy control subjects. Lp-PLA2 mass was determined using enzyme-linked immunosorbent assay. RESULTS: The ACS patients (mean age 57 ± 8.7 years) had high-sensitivity C-reactive protein (hsCRP) levels of 30.46 ± 57.57 mg/L (ACS acute) vs 1.69 ± 1.32 mg/L (ACS recovery). Plasma Lp-PLA2 levels were significantly higher in ACS acute subjects than in ACS recovery subjects (143.13 ± 60.88 ng/mL vs 88.74 ± 39.12 ng/mL; P < 0.0001). Interestingly, stable coronary artery disease patients had higher Lp-PLA2 levels than ACS recovery patients (121.72 ± 31.11 ng/mL vs 88.74 ± 39.12 ng/mL; P = 0.0018). There was a strong correlation between Lp-PLA2 and low-density lipoprotein (LDL) cholesterol (LDL-C) (r = 0.709; P < 0.0001) or changes in LDL (r = 0.449; P = 0.027), suggesting that the major determinant of plasma Lp-PLA2 is LDL-C. No significant correlations were observed between Lp-PLA2 and hsCRP or high-density lipoprotein (HDL) cholesterol. When separated using high-performance liquid chromatography, > 65%-70% of Lp-PLA2 mass was within the apolipoprotein B-containing lipoprotein fraction, with approximately 30%-35% on HDL fraction, with no significant change in distribution between ACS acute and recovery. CONCLUSIONS: Subjects with an ACS have markedly increased Lp-PLA2 levels acutely related to LDL-C levels.
BACKGROUND:Lipoprotein-associated phospholipase A2 (Lp-PLA2) might play a role in the formation of vulnerable atherosclerotic plaques. Its plasma distribution and mass in subjects with acute coronary syndrome (ACS) has yet to be characterized. METHODS: We compared plasma levels of Lp-PLA2 in 24 patients within 48 hours of an ACS (acute) and 12 weeks after (recovery), in 26 patients with stable coronary artery disease and in 10 normal healthy control subjects. Lp-PLA2 mass was determined using enzyme-linked immunosorbent assay. RESULTS: The ACS patients (mean age 57 ± 8.7 years) had high-sensitivity C-reactive protein (hsCRP) levels of 30.46 ± 57.57 mg/L (ACS acute) vs 1.69 ± 1.32 mg/L (ACS recovery). Plasma Lp-PLA2 levels were significantly higher in ACS acute subjects than in ACS recovery subjects (143.13 ± 60.88 ng/mL vs 88.74 ± 39.12 ng/mL; P < 0.0001). Interestingly, stable coronary artery diseasepatients had higher Lp-PLA2 levels than ACS recovery patients (121.72 ± 31.11 ng/mL vs 88.74 ± 39.12 ng/mL; P = 0.0018). There was a strong correlation between Lp-PLA2 and low-density lipoprotein (LDL) cholesterol (LDL-C) (r = 0.709; P < 0.0001) or changes in LDL (r = 0.449; P = 0.027), suggesting that the major determinant of plasma Lp-PLA2 is LDL-C. No significant correlations were observed between Lp-PLA2 and hsCRP or high-density lipoprotein (HDL) cholesterol. When separated using high-performance liquid chromatography, > 65%-70% of Lp-PLA2 mass was within the apolipoprotein B-containing lipoprotein fraction, with approximately 30%-35% on HDL fraction, with no significant change in distribution between ACS acute and recovery. CONCLUSIONS: Subjects with an ACS have markedly increased Lp-PLA2 levels acutely related to LDL-C levels.