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Interrelationships among platelet-activating factor and lipoprotein-associated phospholipase A2 activity and
Carolyn J English1, Anna E Lohning1, Hannah L Mayr1,2,3
1Bond University, Faculty of Health Sciences and Medicine, Bond University, Robina, Queensland, Australia.
Insights
Novel inflammatory markers, platelet-activating factor (PAF) and lipoprotein-associated phospholipase A2 (Lp-PLA2), show distinct correlations with cardiovascular disease (CVD) risk factors compared to C-reactive protein (hsCRP). These findings suggest varying roles in atherogenic pathways.
Area of Science:
- Cardiovascular Science
- Inflammation Biology
- Biomarker Research
Background:
- Cardiovascular disease (CVD) risk is traditionally assessed using blood lipids and C-reactive protein (hsCRP).
- Emerging research highlights novel pro-inflammatory markers, platelet-activating factor (PAF) and lipoprotein-associated phospholipase A2 (Lp-PLA2), as potential indicators of vascular damage, even without traditional risk factors.
Purpose of the Study:
- To investigate the relationship between circulating PAF, Lp-PLA2, hsCRP, and established CVD risk factors.
- To explore potential differences in the atherogenic pathways involving these inflammatory markers.
Main Methods:
- Cross-sectional study of 100 adults with variable CVD risk.
- Measurement of fasting inflammatory markers (PAF, Lp-PLA2, hsCRP) and lipid profiles (Total, HDL, LDL cholesterol, triglycerides).
- Assessment of blood pressure, body mass index (BMI), and waist circumference; statistical analysis using linear and multiple regressions.
Main Results:
- PAF showed unexpected correlations: positive with HDL cholesterol and negative with Total:HDL cholesterol, systolic blood pressure, BMI, and waist circumference.
- Lp-PLA2 strongly correlated positively with LDL and non-HDL cholesterol.
- hsCRP demonstrated strong positive correlations with Total:HDL cholesterol, BMI, and waist circumference.
Conclusions:
- PAF, Lp-PLA2, and hsCRP are implicated in CVD pathophysiology.
- The distinct correlation patterns suggest these markers may be involved in different atherogenic pathways.
- Further research is warranted to elucidate the specific roles of PAF and Lp-PLA2 in CVD development.
Abstract:
Traditionally cardiovascular disease (CVD) risk has been assessed through blood lipids and inflammatory marker C-reactive protein (hsCRP). Recent clinical interest in novel pro-inflammatory markers platelet-activating factor (PAF) and lipoprotein-associated phospholipase A2 (Lp-PLA2 ) recognizes that vascular damage can exist in the absence of traditional risk factors. This cross-sectional study investigated the potential relationship between circulating PAF, Lp-PLA2 , hsCRP, and traditional risk factors for CVD. One hundred adults (49 ± 13 years, 31% male) with variable CVD risk were recruited. Fasting inflammatory markers PAF, Lp-PLA2 and hsCRP and total, high-density lipoprotein (HDL), low-density lipoprotein (LDL) cholesterol, and triglycerides were measured. Blood pressure, body mass index, and waist circumference were measured. Medical and physical activity data were self-reported. Linear and multiple regressions were performed. PAF, Lp-PLA2 , and hsCRP independently correlated with several CVD risk factors. PAF was correlated significantly with risk factors in an unexpected way; there was a medium positive correlation between PAF and HDL cholesterol (r = 0.394, p < 0.001) and medium negative correlations with Total:HDL cholesterol; (r = -0.436, p < 0.001) systolic blood pressure; (r = -0.307, p = 0.001); BMI (r = -0.381, p < 0.001); and waist circumference (r = -0.404, p < 0.001). There were large positive correlations between Lp-PLA2 and LDL (r = 0.525, p < 0.001) and non-HDL cholesterol (r = 0.508, p < 0.001). There were large positive correlations between hsCRP and Total:HDL cholesterol (r = 0.524, p < 0.001); BMI (r = 0.668, p < 0.001); and waist circumference (r = 0.676, p < 0.001). PAF, Lp-PLA2 , and hsCRP are implicated in the pathophysiology of inflammation in CVD; however, the relationships between each marker and traditional risk factors were different suggesting they may be involved in different atherogenic pathways.
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