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Lipoprotein-associated Phospholipase A2 and Coronary Heart Disease
Areti Sofogianni1, Stelina Alkagiet1, Konstantinos Tziomalos1
1First Propedeutic Department of Internal Medicine, Medical School, Aristotle University of Thessaloniki, AHEPA Hospital, Thessaloniki, Greece.
Insights
Lipoprotein-associated phospholipase A2 (Lp-PLA2) shows association with coronary heart disease (CHD) risk. However, evidence suggests Lp-PLA2 is not a causal factor, questioning its role as a therapeutic target for preventing CHD.
Area of Science:
- Cardiovascular Research
- Inflammation and Atherosclerosis
- Biomarker Discovery
Background:
- Inflammation is a key factor in atherosclerosis development.
- Several inflammatory markers predict coronary events, including Lp-PLA2.
- Lipoprotein-associated phospholipase A2 (Lp-PLA2) has gained attention as a potential cardiovascular risk marker.
Purpose of the Study:
- To review the role of Lp-PLA2 as a marker of coronary heart disease (CHD) risk.
- To evaluate Lp-PLA2 as a potential therapeutic target for CHD prevention.
Main Methods:
- Review of existing research on Lp-PLA2 in atherosclerosis.
- Analysis of clinical trial data for Lp-PLA2 inhibitors.
- Examination of genetic association studies related to Lp-PLA2.
Main Results:
- Elevated Lp-PLA2 mass and activity correlate with increased CHD risk in general and established CHD populations.
- Uncertainty exists regarding Lp-PLA2's added value in risk prediction models with traditional factors.
- Large trials showed no benefit from darapladib (Lp-PLA2 inhibitor) on CHD events.
- Genetic studies largely do not support Lp-PLA2 as a causal factor in atherogenesis.
Conclusions:
- Lp-PLA2 is associated with CHD risk but likely not a causal factor in atherogenesis.
- The therapeutic targeting of Lp-PLA2 for CHD prevention is questionable based on current evidence.
- Further research may be needed to clarify the precise role of Lp-PLA2 in cardiovascular disease.
Abstract:
In the last decades, the role of inflammation in the pathogenesis of atherosclerosis has been the topic of intense research. Several markers of inflammation have shown predictive value for first and recurrent coronary events in patients without and with established Coronary Heart Disease (CHD). Among these markers, lipoprotein- associated phospholipase A2 (Lp-PLA2) has recently received considerable attention. In the present review, the potential role of Lp-PLA2 as a marker of CHD risk and as a therapeutic target is discussed. Elevated Lp- PLA2 mass and activity appears to be associated with increased risk for CHD, both in the general population and in patients with established CHD. However, it is unclear whether the measurement of Lp-PLA2 improves risk discrimination when incorporated in models that include traditional cardiovascular risk factors. Moreover, the lack of effect on CHD events of darapladib, a potent, selective Lp-PLA2 inhibitor, in two large, randomized, placebo-controlled trials and the mostly negative findings of genetic association studies suggest that Lp-PLA2 is unlikely to represent a causal factor in atherogenesis. Therefore, it is doubtful whether Lp-PLA2 will constitute a therapeutic target for the prevention of CHD.
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