Publication
Interrelationships among platelet-activating factor and lipoprotein-associated phospholipase A2 activity and traditional cardiovascular risk factors
Publisher:
Wiley
Date:
20-12-2023
DOI:
10.1002/BIOF.1928
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 A 2 (Lp‐PLA 2 ) 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‐PLA 2 , 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‐PLA 2 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‐PLA 2 , 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‐PLA 2 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‐PLA 2 , 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.