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Cardiovascular Disease and Metabolic Syndrome
Published in Michelle Tollefson, Nancy Eriksen, Neha Pathak, Improving Women's Health Across the Lifespan, 2021
Other tests such as coronary artery calcium measurements and advanced lipid tests such as lipoprotein-associated phospholipase A2 (Lp-PLA2) continued to be studied as potential tools for CVD risk stratification in women.13
Epidemiology and prevention of coronary heart disease in older adults
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Nathan D. Wong, David Tehrani, Stanley S. Franklin
Lipoprotein-associated phospholipase A2 (Lp-PLA2), a proatherogenic inflammatory marker, has been shown to be strongly associated with risk of incident CHD in middle-aged populations (81,82). More recently, data using the Rancho Bernardo Study showed that Lp-PLA2 mass has demonstrated capabilities for predicting risk of CHD independent of traditional CHD risk factors in healthy older adults (83). Hazard ratios ranging from 1.89 to 1.75 were calculated for the highest Lp-PLA2 quartile when compared to the lowest quartile after adjusting for cumulative traditional CHD risk factors.
Beneficial Effects of Omega-3 Fatty Acids on Cardiovascular Disease
Published in Catherina Caballero-George, Natural Products and Cardiovascular Health, 2018
Estela Guerrero De León, Mahabir Prashad Gupta, Juan Antonio Morán-Pinzón
According to these mechanisms, in samples of fasting subjects showing moderate to severe hypertriglyceridemia (TGs of 500 to 2000 mg/dL), a 12-week treatment with ω–3 PUFAs revealed a significant reduction in plasma apo C III levels (Morton et al., 2016). Another randomized, double-blind, crossover study with eight-week treatment periods using high-dose EPA and DHA, demonstrated potential mechanisms by which ω–3 PUFAs may decrease the risk of coronary heart disease by reducing atherogenic apolipoproteins in individuals with elevated TGs. Treatment with 3.4 g/d of EPA and DHA significantly reduced the concentrations of both apo C III and apo B, and tended to a modest reduction of lipoprotein associated phospholipase A2 (Lp-PLA2) (Skulas-Ray et al., 2015). The effect of ω–3 PUFAs on apo B 48 has also been evaluated in animal and in vitro models where it has been shown to suppress its synthesis, with the consequent reduction of CM rich in TGs. It has been considered that this inhibition may be due to a decrease in the expression of apo B 48 and/or increased post-translational degradation (Levy et al., 2006).
The diagnostic value of lipoprotein-associated phospholipase A2 in early diabetic nephropathy
Published in Annals of Medicine, 2023
Yan Zhai, Xudong Cao, Shuye Liu, Yanna Shen
Lipoprotein-associated phospholipase A2 (Lp-PLA2), belonging to the phospholipase superfamily, can hydrolyse the phospholipid components of low-density lipoprotein (LDL) to produce lipid pro-inflammatory substances such as lyso-phosphatidylcholine (LPC) and free fatty acids (FFA) participating in the inflammatory reaction in the body [2]. Currently, a large number of studies have identified Lp-PLA2 as a strong predictive marker of cardiovascular events. Lp-PLA2 produces damaging vasoactive and inflammatory molecules, such as LPC and oxidized FFA, which promote vascular wall damage and lesions [3]. Although Lp-PLA2 is strongly associated with oxidative stress and cardiovascular complications, its role in diabetes is uncertain and its ability to act as a cardiovascular risk marker in diabetes remains controversial [4].
The use of blood biomarkers in precision medicine for the primary prevention of atherosclerotic cardiovascular disease: a review
Published in Expert Review of Precision Medicine and Drug Development, 2021
Ty Sweeney, Renato Quispe, Thomas Das, Stephen P Juraschek, Seth S. Martin, Erin D. Michos
Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an enzyme involved in the generation of pro-atherogenic and pro-inflammatory molecules that has also been associated with increased ASCVD risk [120,121]. A large case–control cohort study involving 12,819 asymptomatic men and women identified higher baseline activity of Lp-PLA2 in those who went on to suffer cardiac events than in those who did not, and prognostic information was complementary to CRP [122]. A separate analysis assessing the relationship of smoking on both Lp-PLA2 and CRP showed that both measures correlated with smoking intensity and with risk of major cardiac events, though CRP outperformed Lp-PLA2 as a risk predictor [123]. An inhibitor of Lp-PLA2, darapladib, has been developed and was tested in a randomized controlled trial for secondary prevention of CHD. As darapladib was not associated with reductions in ASCVD in this study [124], it is unlikely to play a role in primary prevention, though this has not specifically been assessed.
Recent developments in pharmacotherapy for hypertriglyceridemia: what’s the current state of the art?
Published in Expert Opinion on Pharmacotherapy, 2020
Matilda Florentin, Michael S Kostapanos, Panagiotis Anagnostis, George Liamis
Interestingly, this benefit was evident despite only a modest effect of icosapent ethyl on lipid parameters; TG and LDL-C were decreased by 19.7% and 6.6% vs placebo, respectively [92]. Also, this favorable outcome was independent of the baseline TG levels as well as of the TG reduction [92]. These observations implied that mechanisms other than lipid lowering may mediate icosapent ethyl cardiovascular benefits. In this context, icosapent ethyl may reduce the levels of cardiovascular biomarkers, such as oxidized LDL, high sensitivity C-reactive protein (hsCRP) and lipoprotein-associated phospholipase A2 (LpPLA2) levels even on top of statin treatment [93,94]. Another proposed mechanism is the anti-arrhythmic effects of EPA, whose circulating levels significantly increase by icosapent ethyl administration. This was mirrored be a reduced risk of sudden cardiac death (by 31%) and cardiac arrest (by 48%) by icosapent ethyl vs placebo in the REDUCE-IT trial [92]. However, the infrequency and the exploratory character of both these outcomes should be considered as limitations for reaching safe conclusions on that [92].