CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 5, November/December 2023 276 AFRICA been a research hotspot in the cardiovascular field to search for biological indicators for plaque vulnerability, combine evidencebased medicine and individualised precision medicine in clinical practice, and actively apply the easy-to-detect biological markers to clinical patients.8 Lp-PLA2, a newly discovered cardiovascular-specific inflammatory mediator, is closely related to the occurrence and development of cardiovascular events, which can facilitate the formation of atherosclerotic plaques and lead to the rupture of unstable plaques. Early examination has not only positive clinical significance for early detection of possible cardiovascular events, but also profound significance for easing the economic burden of patients and even reducing the national medical investment.9 A high correlation between the occurrence of ACS and Lp-PLA2 concentration has been found. By early monitoring of Lp-PLA2 concentration and active intervention, ACS can be prevented.10 Discovered in 1980, Lp-PLA2 is a platelet-activating factor acetyl hydrolase, synthesised and secreted by mature macrophages and lymphocytes, which can promote the hydrolysis of glycerophospholipid acyl lipid bond and lipoproteins on the cell membrane surface, ultimately generating lysophospholipase and non-esterified fatty acids. Its secretion is regulated by inflammatory mediators. After entering the blood circulation, 80% of Lp-PLA2 will bind to LDL-C to hydrolyse oxidised lecithin and produce pro-inflammatory substances. Therefore, Lp-PLA2 can contribute to inflammation and atherosclerosis. 11 As pointed out in an article in the Lancet by Zhao et al.,12 increased levels of serum Lp-PLA2 were closely associated with the risk of ACS. Mourouzis et al.13 found a close correlation between Lp-PLA2 concentration and the prognosis of ACS. Wu et al.14 showed that ACS patients had a significantly higher level of serum Lp-PLA2 (233 ± 54 μg/l) than patients without coronary artery disease (208 ± 52 μg/l), with a statistically significant difference (p < 0.01), and the Lp-PLA2 concentration was correlated with the change in LDL-C level. As proven by Jabor et al.,15 lipid-lowering therapy lowered the serum Lp-PLA 2 level while reducing the serum LDL-C level, also suggesting the correlation between Lp-PLA2 and LDL-C. Yang et al. 16 also found that Lp-PLA2 concentration was positively correlated with the occurrence of ACS. In this study, the Lp-PLA2 concentration was significantly higher in the AMI and UA groups than that in the control group, and the difference was statistically significant. This means the plasma Lp-PLA2 concentration was significantly higher in ACS, with a statistically significant difference. Moreover, the serum Lp-PLA2 concentration was positively correlated with LDL-C level. The results of this study were consistent with those obtained by the above scholars, namely that Lp-PLA2 is involved in the inflammatory response in ACS, leading to the progression of unstable plaques. It can therefore be used as a vascular inflammatory factor to monitor the occurrence of ACS, and ACS can be prevented by controlling plasma LDL-C levels. Ma et al.17 pointed out that Lp-PLA 2 concentration had no statistical correlation with the Gensini score, consistent with our findings that Lp-PLA2 concentration had no correlation with the severity of coronary artery stenosis. Besides, the serum Lp-PLA2 concentration was related to the BMI, suggesting that weight control may be beneficial to preventing ACS, which needs further study. Significant results were obtained in this study, but further research is still needed to make up for the following deficiencies. Lp-PLA2 could be used as an inflammatory marker to predict the occurrence of ACS, but the expected results were not obtained in the subgroup comparison and analysis, so further randomised clinical trials are needed. There was no correlation between Lp-PLA2 level and the severity of coronary artery stenosis, but the relationship between Lp-PLA2 concentration and stable/ unstable plaques is not described, as it is pending further research. Conclusion The Lp-PLA2 concentration was significantly higher in the AMI and UA patients than that in subjects with normal coronary angiography results, and it was positively correlated with hs-CRP levels, suggesting that Lp-PLA2 is probably an inflammatory factor related to ACS. There was a positive correlation between Lp-PLA2 concentration and LDL-C level, so it is of significance to control plasma LDL-C levels to prevent ACS. 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