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Relationship of lipoprotein-associated phospholipase A2(Lp-PLA2) and periprocedural myocardial injury in patients undergoing elective percutaneous coronary intervention.

ABSTRACT: Background:Percutaneous coronary intervention (PCI) is one of the dominant methods for revascularization in patients with coronary heart disease (CHD). However, periprocedural myocardial injury (PMI) is a frequent complication following PCI and is known to be a predictor of postprocedural cardiovascular morbidity and mortality. Although several studies try to identify serum markers to predict the PMI, there is a little information about the role of lipoprotein-associated phospholipase A2 (Lp-PLA2) as a predictor of PMI. Therefore, we aimed to investigate the relationship of Lp-PLA2 levels and PMI in patients undergoing elective PCI. Methods:This study included 265 consecutive patients with normal preprocedural cardiac troponin T(cTNT) who received elective PCI. The samples for cTNT were collected at 8, 16, and 24 h after PCI to assess perioperative myocardial injury. The Lp-PLA2 and other serum lipid parameters were measured after 12 fasting hours before PCI. Results:The data suggested that the patients with preprocedural high Lp-PLA2 were strongly and independently correlated with the risk of PMI. Pearson correlation analysis showed that preprocedural Lp-PLA2 was significantly positively correlated with postprocedural cTnT elevation (r = 0.694, p < 0.05). Binary logistic regression analysis was used to analyze the risk factors of PMI, we found that Lp-PLA2 was independent risk factor for postprocedural cTnT elevation. The area under Receiver Operating Characteristic curve of Lp-PLA2 was 0.757 (95%CI 0.692 ~ 0.821, p < 0.001), the best cut-off point was 185 ng/ml, sensitivity and specificity were 65.33% and 76.32%. Conclusion:Our study demonstrated that preprocedural Lp-PLA2 was associated with postprocedural cTnT elevation and was the independent risk factor of PMI.

SUBMITTER: Yin YJ

PROVIDER: S-EPMC7256635 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature

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Relationship of lipoprotein-associated phospholipase A2(Lp-PLA2) and periprocedural myocardial injury in patients undergoing elective percutaneous coronary intervention.

Yin Yun-Jie YJ Chen Yan-Chun YC Xu Liang L Zhao Xiang-Hai XH Song Yang

International journal of cardiology. Heart & vasculature 20200526

<h4>Background</h4>Percutaneous coronary intervention (PCI) is one of the dominant methods for revascularization in patients with coronary heart disease (CHD). However, periprocedural myocardial injury (PMI) is a frequent complication following PCI and is known to be a predictor of postprocedural cardiovascular morbidity and mortality. Although several studies try to identify serum markers to predict the PMI, there is a little information about the role of lipoprotein-associated phospholipase A2 ...[more]

PMID: 32490148

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Project description:PURPOSE:GSK2647544 is a potent and specific inhibitor of lipoprotein-associated phospholipase A2 (Lp-PLA2), which was in development as a potential treatment for Alzheimer's disease (AD). In order to refine therapeutic dose predictions and confirm brain penetration, a radiolabelled form of the inhibitor, [18F]GSK2647544, was manufactured for use in a positron emission tomography (PET) biodistribution study. PROCEDURES:[18F]GSK2647544 was produced using a novel, copper iodide (Cu(I)) mediated, [18F]trifluoromethylation methodology. Healthy male subjects (n?=?4, age range 34-42) received an oral dose of unlabelled GSK2647544 (100 mg) and after 2 h an intravenous (iv) injection of [18F]GSK2647544 (average injected activity and mass were 106?±?47 MBq and 179?±?55 ?g, respectively) followed by dynamic PET scans for 120 min. Defined regions of interest (ROI) throughout the brain were used to obtain regional time-activity curves (TACs) and compartmental modelling analysis used to estimate the primary outcome measure, whole brain volume of distribution (VT). Secondary PK and safety endpoints were also recorded. RESULTS:PET dynamic data were successfully obtained from all four subjects and there were no clinically significant variations of the safety endpoints. Inspection of the TACs indicated a relatively homogenous uptake of [18F]GSK2647544 across all the ROIs examined. The mean whole brain VT was 0.56 (95 % CI, 0.41-0.72). Secondary PK parameters, Cmax (geometric mean) and Tmax (median), were 354 ng/ml and 1.4 h, respectively. Metabolism of GSK2647544 was relatively consistent across subjects, with 20-40 % of the parent compound [18F]GSK2647544 present after 120 min. CONCLUSIONS:The study provides evidence that GSK2647544 is able to cross the blood brain barrier in healthy male subjects leading to a measurable brain exposure. The administered doses of GSK2647544 were well tolerated. Exploratory modelling suggested that a twice-daily dose of 102 mg, at steady state, would provide ~80 % trough inhibition of brain Lp-PLA2 activity. TRIAL REGISTRATION:Clintrials.gov: NCT01924858.

Project description:Introduction:Lipoprotein associated phospholipase A2 (Lp-PLA2) has been explored as a potential biomarker for Cardiovascular Disease (CVD). The human Lp-PLA2 is a serine-dependent, Ca2+- independent enzyme. It gives way to oxidised free fatty acids and lysophosphatidyl choline by hydrolysing oxidised phospholipids, that leads to smooth muscle cell apoptosis, inflammatory cell chemotaxis and endothelial cell dysfunction in CVD. Owing to its role in inflammation, it may influence the development and progression of periodontitis as well. Aim:To compare the demographic variables, Gingival Index(GI), Bleeding On Probing (BOP), Probing Pocket Depth (PPD), and Clinical Attachment Level (CAL) with serum lipid profile and Lp-PLA2 level in Chronic Periodontitis (CP) subjects. Materials and Methods:A total of 75 subjects were selected and divided into three groups; based on the inclusion and exclusion criteria: Group I - 25 subjects with severe generalized CP with CAL ? 5 mm in more than 30% of sites. Group II -25 subjects with moderate generalized CD with clinical CAL 3 mm-4 mm in more than 30% of sites. Group III- 25 systemically and periodontally healthy volunteers who served as control. Clinical parameters such as Plaque Index (PI), BOP, Probing Depth (PD) and CAL, lipid profile such as Total Cholesterol (TC), Triglyceride (TG), High density Lipoprotein (HDL), Low Density Lipoprotein (LDL), Very Low Density Lipoprotein (VLDL) as well as Lp-PLA2 were assessed. One-way ANOVA and Tukey's Post-hoc test were used for data analysis. Results:Age was higher in Group I and II when compared to Group III. Group II showed a significant correlation between PI and LDL. In Group III, lower PI was significantly correlated with high HDL and low LDL and BOP was positively correlated with TG and HDL. A significant association of Lp-PLA2 was found to be higher with increase in the TG and VLDL level in Group I and Group II when compared to Group III. Conclusion:The study concluded that Lp-PLA2, TG and VLDL already being a predictor biomarker for atherosclerotic disease can be an inflammatory marker for periodontitis.

Project description:BackgroundEvidence suggests that high-dose statin pretreatment may reduce the risk of periprocedural myocardial infarction (PMI) and major adverse cardiac events (MACE) for certain patients; however, previous analyses have not considered patients with a history of statin maintenance treatment. In this meta-analysis of randomized controlled trials (RCTs), we reevaluated the efficacy of short-term high-dose statin pretreatment to prevent PMI and MACE in an expanded set of patients undergoing elective percutaneous coronary intervention.MethodsWe searched the PubMed/Medline database for RCTs that compared high-dose statin pretreatment with no statin or low-dose statin pretreatment as a prevention of PMI and MACE. We evaluated the incidence of PMI and MACE, including death, spontaneous myocardial infarction, and target vessel revascularization at the longest follow-up for each study for subgroups stratified by disease classification and prior low-dose statin treatment.ResultsTwenty-four RCTs with a total of 5,526 patients were identified. High-dose statin pretreatment was associated with 59% relative reduction in PMI (odds ratio [OR]: 0.41; 95% confidence interval [CI]: 0.34-0.49; P<0.00001) and 39% relative reduction in MACE (OR: 0.61; 95% CI: 0.45-0.83; P = 0.002). The benefit of high-dose statin pretreatment on MACE was significant for statin-naive patients (OR: 0.69; 95% CI: 0.50-0.95; P = 0.02) and prior low dose statin-treated patients (OR: 0.28; 95% CI: 0.12-0.65; P = 0.003); and for patients with acute coronary syndrome (OR: 0.52; 95% CI: 0.34-0.79; P = 0.003), but not for patients with stable angina (OR: 0.71; 95% CI 0.45-1.10; P = 0.12). Long-term effects on survival were less obvious.ConclusionsHigh-dose statin pretreatment can result in a significant reduction in PMI and MACE for patients undergoing elective PCI. The positive effect of high-dose statin pretreatment on PMI and MACE is significant for statin-naïve patients and patients with prior treatment. The positive effect of high-dose statin pretreatment on MACE is significant for patients with acute coronary syndrome.

Project description:Based on the complex pathophysiology of atherosclerosis, a large number of biomarkers that relate to lipids, inflammation, immunity, thrombosis and hemostasis, have been investigated experimentally, in epidemiologic studies and in clinical trials. Interest focuses on their potential role to aid in risk stratification, as possible surrogate markers of atherosclerosis, and potential targets for therapy. More recently, one lipid associated biomarker, lipoprotein-associated phospholipase A2 (Lp-PLA₂), has gained considerable interest. In addition to a plausible pathophysiological role by generating pro-inflammatory and pro-atherogenic compounds from oxidized LDL in the vessel wall, there is a large, fairly consistent epidemiological database indicating that increased levels of Lp-PLA2 mass or activity are associated with increased risk for cardiovascular outcomes; such data further suggest that it might improve risk stratification. In addition, clinical studies indicate that increased Lp-PLA₂ levels are associated with endothelial dysfunction. Moreover, it may also serve as an interesting therapeutic target, since a specific inhibitor of the enzyme is available with promising animal data and initial positive data in humans. Recent experimental data from a hyperlipidemic diabetic pig model strongly suggest that increased Lp-PLA2 in the vessel wall is associated with a more vulnerable plaque phenotype which can be modulated by inhibiting Lp-PLA₂ activity. A biomarker study in more than 1,000 patients with CHD over three months has demonstrated a positive effect on various inflammatory molecules. In addition, an imaging study using IVUS based modalities (greyscale, virtual histology, and palpography) together with a panel of biomarkers (IBIS-2) has been done in more than 300 patients with CHD treated over 12 months and results indicate that the progression of the necrotic core of the plaque can be retarded. Inhibition of the pro-atherogenic and pro-inflammatory effects of Lp-PLA₂ may therefore contribute to decrease the residual risk in high risk patients already on polypharmacotherapy. This hypothesis is now being tested in two large phase 3 clinical trials. Thus, Lp-PLA₂ indeed may represent a biomarker and a promising target for intervention.

Dataset Information

Relationship of lipoprotein-associated phospholipase A2(Lp-PLA2) and periprocedural myocardial injury in patients undergoing elective percutaneous coronary intervention.

Publications

Relationship of lipoprotein-associated phospholipase A2(Lp-PLA2) and periprocedural myocardial injury in patients undergoing elective percutaneous coronary intervention.

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