Value Of Lipoprotein-associated Phospholipase A2 Research Articles

Risk factors of atherosclerotic tissue types in single-vessel and intermediate coronary lesions: a cross-sectional study

BackgroundFew data exist that correlate lesion-related risk factors such as conventional cardiovascular risks or lipoprotein-associated phospholipase A2 (Lp-PLA2) with tissue types within atherosclerotic plaques in patients with single-vessel and intermediate coronary lesions.MethodsOne hundred and ninety-two patients with single-vessel and intermediate coronary lesions were enrolled in a cross-sectional study and divided into two groups: stable angina pectoris (SAP) and acute coronary syndrome (ACS) groups. Data regarding clinical characteristics and Lp-PLA2 mass were collected. Using iMAP-IVUS, lumen areas were manually traced to determine the minimum lumen area (MLA) at 1-mm intervals in diseased segments. At the minimum lumen lesion, areas of different types of atherosclerotic tissue [i.e., areas of fibrous plaque tissue (FP), fibro-fatty tissue (FF), dense calcium (DC) and necrotic core (NC)], vascular external elastic membrane (EEMCSA) and plaque and media (P&MCSA) were calculated using the built-in iMap algorithm. Plaque burden was computed as P&MCSA divided by EEMCSA.ResultsIn a univariate analysis, glycosylated hemoglobin A1C (GHbA1C), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), hypertension, Lp-PLA2 and a history of taking statins predicted the degree of FP and NC area, as well as plaque burden, but were not significant predictors of FF or DC area. In a multivariate analysis, Lp-PLA2 and HbA1c remained independent predictors of plaque burden, FP and NC area. However, the results of the regression analyses were not identical when the SAP and ACS groups were analyzed separately. Lp-PLA2, diabetes and NC area were significant predictors of acute coronary lesions, and the predictive value of Lp-PLA2 was confirmed by the finding of a high area-under-the-curve in a ROC analysis (0.837, 95% CI:0.778-0.895, P = 0.000), as well as by the reasonable sensitivity and specificity of cut-off values.ConclusionsGHbA1C and Lp-PLA2 were strong independent predictors of plaque burden and FP and NC area at the minimum lumen lesion in patients with single-vessel and intermediate coronary lesions. Furthermore, Lp-PLA2 has a certain predictive value for acute coronary lesions.

Synergistic Effect of Lipoprotein-Associated Phospholipase A2 with Classical Risk Factors on Coronary Heart Disease: A Multi-Ethnic Study in China

Aims: We evaluated the synergistic effect of lipoprotein-associated phospholipase A2 (Lp-PLA2) in association with classical risk factors in predicting coronary heart disease (CHD) and demonstrated the diagnostic value of Lp-PLA2 for predicting coronary stenotic lesions in subjects with CHD. Methods: Blood samples were acquired from 911 consecutive adult subjects (662 males and 249 females) from 11 ethnic groups. Lp-PLA2 plasma levels were detected using a commercially available turbidimetric immunoassay (TIA). CHD in patients was confirmed using coronary angiography, and the severity of coronary atherosclerosis was assessed using the Gensini scoring system. Results: A binary logistic regression was performed to analyse the relationships between Lp-PLA2 and other risk factors. A multivariate logistic regression analysis revealed that Lp-PLA2 levels were significantly associated with CHD (OR, 1.882; 95% CI, 1.369-2.587, p=0.000).The area under the receiver operating characteristic curve for Lp-PLA2 was 0.589 (95%CI, 0.549-0.629, p=0.000).The synergism between Lp-PLA2 and other risk factors was also investigated. The proportion of CHD attributable to the interaction between Lp-PLA2 and age was as high as 64%. Conclusions: Lp-PLA2 levels in human plasma were positively associated with the severity of CHD, and there was a clear positive interaction between Lp-PLA2 and classical risk factors in predicting CHD.

Lipoprotein-associated phospholipase A2 is associated with postpartum hypertension in women with history of preeclampsia.

Both hypertension and preeclampsia (PE) are considered as inflammatory diseases. Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an inflammatory marker associated with lipid metabolism. We aimed to study the correlation and predictive value of Lp-PLA2 in postpartum hypertension after PE. A group of 160 PE patients (PE group) and a separate group of 160 normal pregnant women (control group) were recruited from January 2010 to October 2011. The average age in the PE group was 28.4 ± 4.5 years and the average gestational age was 34.7 ± 1.1 weeks. The average age in the control group was 27.8 ± 4.5 years and the average gestational age was 35.5 ± 1.2 weeks. General information (including age, gestational age, parity, history of metabolic disease, family history of high blood pressure, height, body weight before childbirth, and blood pressure) and blood samples were collected for measuring Lp-PLA2 and lipid parameters. From February to April in 2013, 153 cases in the PE group and 132 in the control group were re-called. We assessed their postpartum health, pregnancy, height, weight, and blood pressure. Serum mass of Lp-PLA2 in the PE group (210.67 ± 17.98 ng/mL) was significantly higher compared with that in the control group (174.72 ± 30.26 ng/mL) (P < 0.01). The pro-gestation BMI, systolic blood pressure (SBP), diastolic blood pressure, total cholesterol, triglyceride, and low-density lipoprotein-cholesterol (LDL-C) were also significantly higher. Correlation analysis showed that the level of Lp-PLA2 and SBP (r = 0.31), LDL-C (r = 0.37) were positively correlated. The incidence of postpartum hypertension in the PE group was higher than that in the normal control group. Logistic regression analysis showed that prenatal Lp-PLA2 mass was an independent risk factor for PE postpartum hypertension (OR 1.134,95 % CI 1.086-1.185). ROC curve analysis showed that the sensitivity of predicting postpartum hypertension was 73.2% and the specific degree was 86.6%, with Lp-PLA2 level of 217.75 ng/mL for boundary value. The onset of postpartum hypertension in PE patients may contribute to vascular inflammation, which is associated with antepartum lipid metabolism.

C-reactive protein and lipoprotein-associated phospholipase A2 in smokers and nonsmokers of the Ludwigshafen Risk and Cardiovascular Health study.

Measurement of high sensitivity CRP (hsCRP) and lipoprotein-associated phospholipase A2 (LpPLA2) provides information on systemic inflammation and stability of atherosclerotic plaques. Data analyzing the effect of smoking on these parameters are sparse. The aim of our study was the analysis of these parameters in active smokers and never-smokers. The study included 777 smokers and 1,178 never-smokers, of whom 221 and 302 died during a follow-up, respectively. The values of LpPLA2 and hsCRP were significantly higher in smokers than in never-smokers. Mortality was highest in smokers and never-smokers with elevation of both biomarkers. Multivariate adjusted hazard ratios for patients in the highest tertile of both hsCRP and LpPLA2 compared with patients in the lowest tertile of both markers were 1.85 (1.04-3.28) in never-smokers and 1.94 (1.10-3.45) in smokers. Our data confirmed the predictive value of hsCRP and LpPLA2. However, there were a relevant number of patients with an increase of only one of these parameters. Therefore, beside other risk factors for cardiovascular disease, both parameters should be determined at least in high risk patients.

Utility of Lipoprotein-Associated Phospholipase A2 for Prediction of 30-day Major Adverse Coronary Event in Patients with the First Anterior ST-Segment Elevation Myocardial Infarction Treated by Primary Percutaneous Coronary Intervention

Lipoprotein-associated phospholipase A2 (Lp-PLA2) has been suggested as an inflammatory marker of cardiovascular risk. The predictive value of Lp-PLA2 in ST-segment elevation myocardial infarction (STEMI) treated by primary percutaneous coronary intervention (PCI) has not been established. The aim of this study was to determine whether plasma Lp-PLA2 is a predictor of a major adverse cardiac event (MACE) in patients with the first anterior STEMI treated by primary PCI. This study consisted of 100 consecutive patients with first anterior STEMI who underwent primary PCI within 6 hours of the symptom onset. Plasma Lp-PLA2 level was measured on admission using a turbidimetric immunoassay (diaDexus, Inc., USA). The Receiver Operating Characteristic analysis was performed to identify the most useful Lp-PLA2 cut-off level for the prediction of MACE. The patients were divided into two groups according to the cut-off Lp-PLA2 level: high Lp-PLA2 group (> or = 463 ng/mL, n = 33) and low Lp-PLA2 group (< 463 ng/mL, n = 67). MACE was defined as cardiac death, non-fatal reinfarction, and target vessel revascularization. Patients in the high Lp-PLA2 group had significantly higher total-, LDL-cholesterol, apolipoprotein B levels, and significantly lower estimated glomerular filtration rates compared with the low Lp-PLA2 group. The incidence of 30-day mortality was 18.2% (6/33) in high Lp-PLA2 group, while in the low Lp-PLA2 group no patient died (p < 0.001). The 30-day MACE occurred in 24.2% of the high Lp-PLA2 group and 3% of the low Lp-PLA2 group (p = 0.001). Multiple logistic regression analysis identified the plasma Lp-PLA2 level as an independent predictor of MACE (OR 1.011, 95%CI 1.001 - 1.013, p = 0.037). In patients with first anterior STEMI treated by primary PCI, the plasma Lp-PLA2 level is an independent predictor of 30-day MACE.

108 Long term pronostic role of lipoprotein-associated phospholipase A2 levels in patients with acute heart failure without acute coronary syndrome

Vascular inflammation increased in HFand produced pro-inflammatory cytokines, activation of complement and adhesion molecules that sustain inflammatory state. Lipoprotein-associated phospholipase A2 (Lp-PLA2) hydrolyze phospholipids and is a marker of inflammation that plays a critical role in atherogenesis and endothelial dysfunction. In this study, we evaluated (1) predictive value of Lp-PLA2 in patients with de novo cardiogenic shock (CS) without acute coronary syndrome (ACS), (2) evolution of this biomarker when cardiac function improved upon cardiac treatment during a 30 ± 3 month follow-up. Inclusion criteria for patients: CS defined by systolic BP<90 mmHg with peripheral hypoperfusion. Exclusion criteria: pace makers or other shock etiologies. All patients had cardiac (echocardiography, coronarography) and biological evaluations (troponin; NT-proBNP; Lp-PLA2 with turbidimetric immunoassay). 22 consecutive patients with CS (95% men, 57.5 ± 10.7y, LVEF 25.1 ± 7.5%, proBNP 8540 ng/L) were included: 7 ischemic CM, 15 dilated CM [12 idiopathic, 2 toxic and 1 myocarditis]. Cardiovascular risks: diabetes (n = 11), HBP (n = 7), tabacco (n = 9), dyslipidemia (n = 8). At 30 months, HF symptoms decreased in 6 patients and 3 normalized their LVEF. Mortality was 23% (due to cardiac complications) and morbidity 48% (iterative hospitalizations for HF and/or arrhythmia). Lp-PLA2 were elevated in CS (226 ± 77 μg/L), when referred to our controls (156.4 ± 45.0 μg/L, p = 0.005). Upon admission, Lp-PLA2 was more elevated in ICM than DCM group (266 ± 74 and 203 ± 72 μg/L, p = 0.08). In ICM, Lp-PLA2 levels significantly decreased when inotrope treatment was withdrawn (208 ± 63 vs 266 ± 74; p < 0.03) without significant difference with DCM group. Using multivariate regression Lp-PLA2 appears to be an independent prognostic factor for the major cardiac events (death, HF, rehospitalization, arrhythmias) (total r = 0.76; p = 0.005) with a a predictive rule-out of 254 μg/L 1) Lp-PLA2 concentrations were elevated in population with CS and more elevated in ICM group than DCM group; 2) Lp-PLA2 might be a good predictive factor for major cardiac events. Lp-PLA2 levels decreased significantly upon inotrope.

Lipoprotein-associated phospholipase A2 activity, ferritin levels, metabolic syndrome, and 10-year cardiovascular and non-cardiovascular mortality: results from the Bruneck study

To identify factors that influence plasma levels and assess the prognostic value of lipoprotein-associated phospholipase A2 (Lp-PLA2) activity in a prospective, population-based survey of the epidemiology and pathogenesis of atherosclerosis. The Bruneck study is a prospective, population-based survey initiated in 1990. Lp-PLA2 activity and baseline variables for the current analysis were measured in 765 subjects aged 45-84 years in 1995. Incident cardiovascular disease (CVD) (cardiovascular death, myocardial infarction, stroke, and transient ischaemic attack) and rates of non-CVD mortality were assessed between 1995 and 2005. Subjects with incident CVD had higher levels of Lp-PLA2 activity (884 +/- 196 vs. 771 +/- 192 micromol/min/L, P < 0.001). Increased Lp-PLA2 activity was significantly related to incident CVD [age- and sex-adjusted hazard ratio (95%CI) 2.9 (1.6-5.5); third vs. first tertile group; P < 0.001] and with vascular mortality but not with non-CVD mortality. Lp-PLA2 activity was enhanced in subjects with the metabolic syndrome and showed highly significant positive associations with LDL-C, apoB-100, ferritin, and HOMA-IR, and inverse associations with HDL-C and anti-oxidant levels. Increased Lp-PLA2 activity is associated with metabolic syndrome and incident fatal and non-fatal CVD, but not with non-CVD mortality. Furthermore, Lp-PLA2 activity is strongly influenced by ferritin levels, LDL-C, and apoB-100 supporting its integral role in lipid peroxidation. Clinical utility of Lp-PLA2 activity for prediction of cardiovascular risk has to be explored in future studies.