Original Article
Lipoprotein-Associated Phospholipase A2 as an Independent Predictor of Coronary Heart Disease
N Engl J Med 2000; 343:1148-1155October 19, 2000
- Abstract
Background
Chronic inflammation is believed to increase the risk of coronary events by making atherosclerotic plaques in coronary vessels prone to rupture. We examined blood constituents potentially affected by inflammation as predictors of risk in men with hypercholesterolemia who were enrolled in the West of Scotland Coronary Prevention Study, a trial that evaluated the value of pravastatin in the prevention of coronary events.
Methods
A total of 580 men who had had a coronary event (nonfatal myocardial infarction, death from coronary heart disease, or a revascularization procedure) were each matched for age and smoking status with 2 control subjects (total, 1160) from the same cohort who had not had a coronary event. Lipoprotein-associated phospholipase A2, C-reactive protein, and fibrinogen levels and the white-cell count were measured at base line, along with other traditional risk factors. The association of these variables with the risk of coronary events was tested in regression models and by dividing the range of values according to quintiles.
Results
Levels of C-reactive protein, the white-cell count, and fibrinogen levels were strong predictors of the risk of coronary events; the risk in the highest quintile of the study cohort for each variable was approximately twice that in the lowest quintile. However, the association of these variables with risk was markedly attenuated when age, systolic blood pressure, and lipoprotein levels were included in multivariate models. Levels of lipoprotein-associated phospholipase A2 (platelet-activating factor acetylhydrolase), the expression of which is regulated by mediators of inflammation, had a strong, positive association with risk that was not confounded by other factors. It was associated with almost a doubling of the risk in the highest quintile as compared with the lowest quintile.
Conclusions
Inflammatory markers are predictors of the risk of coronary events, but their predictive ability is attenuated by associations with other coronary risk factors. Elevated levels of lipoprotein-associated phospholipase A2 appear to be a strong risk factor for coronary heart disease, a finding that has implications for atherogenesis and the assessment of risk.
Media in This Article
Figure 1
Associations of the C-Reactive Protein Level, Lipoprotein-Associated Phospholipase A2 Level, and the White-Cell Count with the Risk of a Coronary Event.Table 1
Base-Line Characteristics of the Subjects.Article Activity
- Article
The discovery of inflammatory cells in the cap of atherosclerotic plaques led to the postulate that inflammation has a key role in the cascade of events leading to plaque rupture.1,2 Supporting this idea are recent reports that levels of plasma markers of inflammation such as C-reactive protein are elevated in those at risk for coronary heart disease.3-5 A2 phospholipases are a family of enzymes that can hydrolyze phospholipids at the sn2 position to generate lysophospholipids and fatty acids. Several recent reports link type II secretory phospholipase A2 to atherogenesis and the risk of coronary heart disease.6-8 This enzyme, found in the media of normal and diseased arteries,9 may be involved in modifying low-density lipoprotein (LDL) that is present in the artery wall.6,10
We examined the role of a distinct phospholipase, lipoprotein-associated phospholipase A2, also known as platelet-activating factor acetylhydrolase, in a small case–control study and found it to be a potential predictor of the risk of coronary heart disease.11 The expression of this enzyme is regulated by mediators of inflammation.12 It circulates bound mainly to LDL and has a structure and properties distinct from those of the 14-kd calcium-dependent type II secretory phospholipase A2.13 We evaluated its association with the risk of coronary events in a prospective study with a nested case–control design, drawing samples from the biologic bank of the West of Scotland Coronary Prevention Study.14 The enzyme, in theory, could promote atherogenesis if the products it releases from LDL phospholipids have a deleterious effect on the artery wall,15 or it could be protective if, in hydrolyzing platelet-activating factor, it reduces inflammation and the thrombotic tendency of blood.16
The West of Scotland Coronary Prevention Study demonstrated that pravastatin therapy reduced the incidence of coronary events and death from cardiac causes by about one third in men with hypercholesterolemia.14 We evaluated the extent to which levels of lipoprotein-associated phospholipase A2 and C-reactive protein, as measured by a sensitive assay in stored base-line samples, and other markers of inflammation (such as the white-cell count and fibrinogen levels) predicted the risk of a coronary event in this primary prevention study. Findings regarding white-cell counts and fibrinogen levels have been reported previously.17
Methods
Study Design and Subjects
In the West of Scotland Coronary Prevention Study, 6595 men who had LDL cholesterol levels between 174 and 232 mg per deciliter (4.5 and 6.0 mmol per liter) but who had no history of a myocardial infarction were randomly assigned to receive 40 mg of pravastatin or placebo daily.14 All subjects provided written informed consent. The study was approved by the ethics committees of the University of Glasgow and all participating health boards. The first patient was enrolled on February 1, 1989, and the study ended on May 15, 1995. The incidence of the primary end point, a composite of nonfatal myocardial infarction and death from coronary heart disease, was 31 percent lower with pravastatin treatment. Risk reductions of the same magnitude were seen for revascularization procedures (coronary-artery bypass and percutaneous transluminal coronary angioplasty). Since the same underlying atherothrombotic process is believed to give rise to myocardial infarction and the need for revascularization, in the present case–control study we used an expanded end point comprising the primary end point plus revascularization as a first event to increase the statistical power of the study. A total of 580 men had such an event and were included in the current analysis: 503 had a myocardial infarction or death from cardiac causes as a first event, and 77 underwent revascularization as a first event. We matched each patient with 2 controls (also drawn from the original cohort of 6595 men), for a total of 1160 controls, on the basis of age (using two-year age categories) and smoking status, with subjects categorized as either nonsmokers (those who had never smoked or who had quit smoking) or current smokers. At randomization, 6.2 percent of patients with an event and 2.9 percent of controls were taking aspirin.
Measurements
All major risk factors were assessed during recruitment.18 Plasma total cholesterol, triglycerides, and very-low-density lipoprotein, LDL, and high-density lipoprotein (HDL) cholesterol were measured twice during screening, and the average was used as the base-line level.18 At the third screening visit,18 hematologic variables, including the white-cell count, were determined (model STKR or S+1, Beckman Coulter, Luton, United Kingdom) and fibrinogen was assayed by heat-precipitation nephelometry.19
C-reactive protein and lipoprotein-associated phospholipase A2 were measured in aliquots of plasma collected at the third screening visit and stored at –70°C. A high-sensitivity, two-site enzyme-linked immunoassay was developed with use of a peroxidase-conjugated rabbit antihuman C-reactive protein antibody (DK2600, Dako, Glostrup, Denmark) and a polyclonal anti–C-reactive protein capture antibody. The assay was calibrated with a standard (CRM470-CAP/IFCC; lot 91/0619, Behringwerke, Marburg, Germany). The lower limit of the working range of the assay was 0.1 mg per liter. Values obtained in this study ranged from 0.1 to 45.2 mg per liter. The intraassay and interassay coefficients of variation were 1.9 percent and 6.2 percent, respectively (the assay yielded results similar to those of Ridker et al.3).
Lipoprotein-associated phospholipase A2 mass was measured with an enzyme-linked immunoassay according to previously described methods.11 Samples were captured with a monoclonal antibody against lipoprotein-associated phospholipase A2. The enzyme was identified by a second monoclonal antibody labeled with biotin and a streptavidin–alkaline phosphatase conjugate. The standard was purified lipoprotein-associated phospholipase A2. The range of detection was 0.5 to 6.0 mg per liter, and the intraassay and interassay coefficients of variation were 4.5 percent and 8.3 percent, respectively. There was no cross-reactivity with other A2 phospholipases. The results of the mass assay correlated well with levels of enzyme activity (r=0.86) when both were measured in fresh samples.11 All analyses were conducted by personnel who did not know whether the samples were from the patients with coronary events or the controls.
Statistical Analysis
The distributions of C-reactive protein and plasma triglyceride levels were markedly skewed and were therefore log-transformed. We established quintile ranges according to the values in the control subjects, and we obtained risk ratios by comparing the frequency of the end point in patients in quintiles 2 through 5 with that in the reference quintile 1. We used multivariate conditional logistic-regression models to assess the independent prognostic value of variables. Each was included as a continuous variable and in a separate analysis as a categorical variable (in which quintiles were used). We calculated relative risks and 95 percent confidence intervals. We assessed associations among variables in the 1160 control subjects with use of Spearman's rank-correlation coefficient.
We assessed differences between plasma levels of lipoprotein-associated phospholipase A2 and inflammatory markers in smokers and nonsmokers with use of a two-sample t-test. We examined the effect of smoking on the relation of C-reactive protein and lipoprotein-associated phospholipase A2 levels to risk with separate conditional logistic-regression models for smokers and nonsmokers and then in a model that included all 1740 subjects and in which these variables were introduced first as main effects; all interactions between smoking status and C-reactive protein levels and lipoprotein-associated phospholipase A2 levels were then investigated. We used a similar approach to evaluate the association of these variables with risk among 833 men in the pravastatin group and 907 men in the placebo group.
Results
The base-line characteristics of the patients and controls in the current analysis as well as of the patients in the original study group are shown in Table 1Table 1
Base-Line Characteristics of the Subjects.. As compared with the entire original study cohort, the patients who had a coronary event were older and more likely to be smokers and had higher blood pressure and LDL cholesterol levels and lower HDL cholesterol levels. A history of diabetes, hypertension, angina, and nitrate use were all predictors of coronary events in the trial itself,20 and the proportions of subjects with these characteristics differed between patients and controls in the current study (Table 1). Base-line levels of C-reactive protein, lipoprotein-associated phospholipase A2, and fibrinogen and the white-cell count, all of which are potentially perturbed in a state of chronic inflammation, were evaluated as predictors of the risk of coronary events (Table 2Table 2
Univariate Analysis of the Association between Inflammatory Markers and the Risk of a Coronary Event.). In univariate analyses, increasing levels of all four variables were associated with a significantly greater risk of the composite end point of nonfatal myocardial infarction, death from cardiac causes, or revascularization as a first event; a change of 1 SD (the standard deviations are given in Table 1) generated an increase in risk of 19 to 27 percent. A similar association was present when each component of the composite end point was analyzed separately (Table 2).C-reactive protein levels correlated significantly with both the white-cell count and fibrinogen levels, and the latter two variables also showed a strong positive interdependence (Table 3Table 3
Associations between Inflammatory Markers and Coronary Risk Factors in Control Subjects.). Other risk factors showed significant associations with C-reactive protein, including age, systolic blood pressure, plasma triglycerides, LDL cholesterol, and HDL cholesterol. Likewise, the white-cell count was associated positively with plasma triglycerides and negatively with HDL cholesterol. C-reactive protein levels, white-cell counts, and fibrinogen levels were significantly higher in smokers than in nonsmokers in the control group (Table 4Table 4
Effect of Smoking Status on Inflammatory Markers in Control Subjects.). Lipoprotein-associated phospholipase A2 exhibited a weak positive association with fibrinogen but little relation to C-reactive protein or the white-cell count. It also exhibited a positive relation with LDL cholesterol but little association with other risk factors (Table 3). Furthermore, it was not affected by smoking status (Table 4).The independence of these variables as predictors of coronary events was assessed, as shown in Table 5Table 5
Multivariate Assessment of the Effect of Inflammatory Markers on the Risk of a Coronary Event. and Figure 1Figure 1Associations of the C-Reactive Protein Level, Lipoprotein-Associated Phospholipase A2 Level, and the White-Cell Count with the Risk of a Coronary Event.. When the white-cell counts and the C-reactive protein and lipoprotein-associated phospholipase A2 levels in the patients were divided into quintiles, the risk for the highest quintile of each variable was approximately twice the risk for the lowest quintile (Figure 1). Adjustment for the presence of other inflammatory markers markedly attenuated the risk associated with the fibrinogen level (Table 5) but had a less dramatic effect on risk associated with the C-reactive protein level and the white-cell count (Table 5 and Figure 1); these two variables remained significant predictors of risk in this model. The lipoprotein-associated phospholipase A2 level remained significant in a model that included inflammatory markers, whether it was entered as a continuous variable (Table 5) or a categorical variable (Figure 1).After adjustment for age, systolic blood pressure, and lipoprotein levels, the white-cell count was no longer associated with a significant risk except in the highest quintile (more than 8100 per cubic millimeter) (Figure 1). A similar effect was seen with C-reactive protein: there was a trend toward increased risk with increasing levels of the protein when these other factors were included in the model, but again, the risk ratio was significantly increased only in the highest quintile (more than 4.59 mg per liter). Furthermore, when both traditional risk factors and other inflammatory markers were adjusted for, the risk ratio for the highest quintile of C-reactive protein was 1.49 (95 percent confidence interval, 0.95 to 2.33). C-reactive protein levels, the white-cell count, and fibrinogen levels were not significantly associated with risk when they were included as continuous variables in a model that also included age, systolic blood pressure, lipoprotein levels, and inflammatory markers (Table 5). For C-reactive protein the main confounding factor was the white-cell count (Table 5). In contrast, the association of lipoprotein-associated phospholipase A2 with risk remained significant when other factors were included (Figure 1 and Table 5).
In separate univariate models, the relative risks and 95 percent confidence intervals were estimated for smokers as compared with nonsmokers and for patients in the pravastatin group as compared with patients in the placebo group. An increase of 1 SD in the lipoprotein-associated phospholipase A2 level was associated with a relative risk of 1.32 (95 percent confidence interval, 1.00 to 1.76) among nonsmokers and a relative risk of 1.44 (95 percent confidence interval, 1.11 to 1.87) among smokers. For nonsmokers the relative risk associated with an increase of 1 SD in the C-reactive protein level was 1.19 (95 percent confidence interval, 1.03 to 1.38), and for smokers it was 1.30 (95 percent confidence interval, 1.13 to 1.50). Interaction terms included in a regression model that included all 1740 subjects in the study were not significant.
Patients who were receiving pravastatin were, of course, at lower overall risk than those receiving placebo.14 Within the pravastatin and placebo groups, an increase of 1 SD in the C-reactive protein level was associated with a relative risk of 1.39 (95 percent confidence interval, 1.17 to 1.65) and 1.17 (95 percent confidence interval, 1.01 to 1.35), respectively. Similarly, an increase of 1 SD in the lipoprotein-associated phospholipase A2 level was associated with a relative risk of 1.67 (95 percent confidence interval, 1.24 to 2.25) in the pravastatin group and of 1.17 (95 percent confidence interval, 0.90 to 1.51) in the placebo group. Again, interaction terms in a regression model that included all 1740 subjects were not significant.
Discussion
We confirmed that recognized indicators of a proinflammatory state — the C-reactive protein level, the white-cell count, and the fibrinogen level — were predictors of the risk of a coronary event in a population of middle-aged men with hypercholesterolemia. However, our principal finding was that the level of lipoprotein-associated phospholipase A2 (platelet-activating factor acetylhydrolase), an enzyme that is also regulated by mediators of inflammation,12 had a strong positive association with the risk of coronary heart disease.
When we compared the subjects in the highest quintile for C-reactive protein, white-cell count, and fibrinogen with those in the lowest quintile, the risk was approximately doubled — a finding that is in line with the results of a recent meta-analysis.21 As others have found in recent studies,22-24 we found that these markers of inflammation correlated with one another and were also related to the body-mass index, systolic blood pressure, plasma triglyceride levels, and HDL cholesterol levels. In our large, prospective study, the association of C-reactive protein levels, possibly the most sensitive of the inflammatory markers, was substantially attenuated in multivariate analyses that included these covariates and was no longer significant when the white-cell count was included in the model. Our findings indicate that an assessment of inflammatory status is important in risk stratification and that measurement of C-reactive protein is helpful in this regard, as exemplified by the findings of Ridker et al.3 The statistical independence of the association of the C-reactive protein level appears to depend on which of the other markers of inflammation are included in the models. Our cohort was not a random sample of the population, and C-reactive protein may retain its independent association with risk in other populations.
Why a marker of inflammation such as C-reactive protein should show such strong associations with other risk factors, as noted earlier22,24 and confirmed in our study, has until recently been unclear. This liver-derived protein is regulated by interleukin-6, which is produced by inflammatory cells.24 Thus, elevated C-reactive protein levels may simply reflect the presence of atherosclerotic disease and potentially unstable plaque. However, as pointed out by Ridker et al.,3 high levels of C-reactive protein can predate a coronary event by many years.
Clues as to the mechanism underlying the association of C-reactive protein with classic risk factors, such as hypertension, elevated plasma lipid levels, and insulin resistance,23,24 come from the work of Yudkin et al.25 and Mohamed-Ali et al.,26 who found that subcutaneous adipose tissue was a further source of interleukin-6 and that plasma levels of C-reactive protein, interleukin-6, and tumor necrosis factor α were all related to measures of obesity.25 Therefore, in addition to marking the presence of a proinflammatory condition, high levels of C-reactive protein (and of fibrinogen, since it too has an interleukin-6–responsive promoter24) may to some extent be yet another facet of the insulin-resistant, obese state. The same may also be true of type II secretory phospholipase A2, which also responds to cytokine stimulation.7 The plasma level of this enzyme, unlike that of lipoprotein-associated phospholipase A2, exhibits a strong association with C-reactive protein levels (r=0.53, P< 0.001).7 It has recently been suggested that C-reactive protein may not be an entirely passive marker of the atherogenic process. Reports have appeared indicating that the protein can bind to damaged LDL and trigger the activation of complement.24,27
The importance of our finding regarding lipoprotein-associated phospholipase A2 is threefold. First, it clarifies the clinical significance of this enzyme in atherosclerosis. Platelet-activating factor has potent biologic effects, including the activation of platelets and monocytes and macrophages28; thus, the hydrolysis of this phospholipid by lipoprotein-associated phospholipase A2 may be expected to lead to a decreased risk of disease. Our observation that the level of lipoprotein-associated phospholipase A2 was strongly related to the risk of a coronary event indicates that other actions of the enzyme are more pertinent to the atherosclerotic process. In this regard, it has been shown that lipoprotein-associated phospholipase A2 on LDL is solely responsible for the hydrolysis of oxidized phospholipids in the particle. Blocking the enzyme does not alter the rate of LDL oxidation, but it does inhibit the release of products with biologic activity, such as factors that promote the chemotaxis of monocytes.15 On the basis of our findings and previous findings,15,29 we propose that, owing to its properties and location on the LDL particle, lipoprotein-associated phospholipase A2 is placed to act as a key agent in the release of products of LDL oxidation into the artery wall.
Second, lipoprotein-associated phospholipase A2 appears to be a novel risk factor that is statistically independent of markers of inflammation or classic risk factors. If our findings are confirmed in other populations, then measurement of lipoprotein-associated phospholipase A2 mass will be a valuable addition to risk assessment in the future.
Third, inhibition of the activity of the enzyme has demonstrable biologic effects,15 at least in vitro. Now that its association with the risk of coronary events is clear, it can become a new therapeutic target that is separate from current lipid-lowering or antiinflammatory approaches. In this context, it is noteworthy that the increase in risk with increasing lipoprotein-associated phospholipase A2 levels was as strong in the men who received pravastatin in this study as in those who received placebo.
In conclusion, indicators of chronic inflammation were strongly associated with the risk of coronary heart disease in this nested case–control study and may be useful in risk stratification. C-reactive protein, fibrinogen, and the white-cell count are interrelated markers whose levels are influenced not only by chronic inflammation but also potentially by the presence of obesity and the insulin-resistance syndrome (as evidenced by increased blood pressure and plasma triglyceride levels and decreased HDL cholesterol levels in our patients). Lipoprotein-associated phospholipase A2 is a potential risk factor that may have a direct role in atherogenesis.
Supported by a project grant (PG 97/160) from the British Heart Foundation and by a grant from Bristol-Myers Squibb (to the study data center).
We are indebted to Ms. Shelley Wilkie for her excellent help in preparing the manuscript.
Source Information
From the Departments of Pathological Biochemistry (C.J.P., D.S.J.O., M.J.C, J.C.) and Medicine (A.R., G.D.O.L.), Glasgow Royal Infirmary, Glasgow, Scotland; the Robertson Centre for Biostatistics, Glasgow University, Glasgow, Scotland (A.D.M., I.F.); SmithKline Beecham Pharmaceuticals, Harlow, United Kingdom (C.H.M., K.E.S.); and diaDexus, Santa Clara, Calif. (M.K., F.E.W.).
Address reprint requests to Dr. Packard at the Department of Pathological Biochemistry, Glasgow Royal Infirmary University NHS Trust, 4th Fl. Queen Elizabeth Bldg., 10 Alexandra Parade, Glasgow G31 2ER, Scotland, or at chris.packard@clinmed.gla.ac.uk.
Other authors were Gillian Docherty, B.Sc., Robertson Centre, Glasgow University, Glasgow, Scotland; and John D. Burczak, Ph.D., diaDexus, Santa Clara, Calif.
Appendix
In addition to the authors, the following persons are members of the West of Scotland Coronary Prevention Study Group: J. Shepherd, S.M. Cobbe, A.R. Lorimer, P.W. Macfarlane, and J.H. McKillop, Glasgow Royal Infirmary, Glasgow, Scotland; and C.G. Isles, Dumfries and Galloway Royal Infirmary, Dumfries, Scotland.
- References
References
1
Davies MJ ,Richardson PD ,Woolf N ,Katy DR ,Mann J . Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content. Br Heart J 1993;69:377-381
CrossRef | Web of Science | Medline2
Ross R . Atherosclerosis -- an inflammatory disease. N Engl J Med 1999;340:115-126
Full Text | Web of Science | Medline3
Ridker PM ,Cushman M ,Stampfer MJ ,Tracy RP ,Hennekens CH . Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997;336:973-979[Erratum, N Engl J Med 1997;337:356.]
Full Text | Web of Science | Medline4
Kuller LH ,Tracy RP ,Shaten J ,Meilahn EN . Relationship of C-reactive protein and coronary heart disease in the MRFIT nested case-control study: Multiple Risk Factor Intervention Trial. Am J Epidemiol 1996;144:537-547
Web of Science | Medline5
Koenig W ,Sund M ,Frohlich M , et al. C-reactive protein, a sensitive marker of inflammation, predicts future risk of coronary heart disease in initially healthy middle-aged men: results from the MONICA (Monitoring Trends and Determinants in Cardiovascular Disease) Augsburg Cohort Study, 1984 to 1992. Circulation 1999;99:237-242
Web of Science | Medline6
Leitinger N ,Watson AD ,Hama SY , et al. Role of group II secretory phospholipase A2 in atherosclerosis. 2. Potential involvement of biologically active oxidized phospholipids. Arterioscler Thromb Vasc Biol 1999;19:1291-1298
CrossRef | Web of Science | Medline7
Kugiyama K ,Ota Y ,Takazoe K , et al. Circulating levels of secretory type II phospholipase A2 predict coronary events in patients with coronary artery disease. Circulation 1999;100:1280-1284
Web of Science | Medline8
Ivandic B ,Castellani LW ,Wang X-P , et al. Role of group II phospholipase A2 in atherosclerosis. 1. Increased atherogenesis and altered lipoproteins in transgenic mice expressing group IIa phospholipase A2. Arterioscler Thromb Vasc Biol 1999;19:1284-1290
CrossRef | Web of Science | Medline9
Elinder LS ,Dumitrescu A ,Larsson P ,Hedin U ,Frostegard J ,Claesson H-E . Expression of phospholipase A2 isoforms in human normal and atherosclerotic arterial wall. Arterioscler Thromb Vasc Biol 1997;17:2257-2263
CrossRef | Web of Science | Medline10
Sartipy P ,Camejo G ,Svensson L ,Hurt-Camejo E . Phospholipase A2 modification of low density lipoproteins forms small high density particles with increased affinity for proteoglycans and glycosaminoglycans. J Biol Chem 1999;274:25913-25920
CrossRef | Web of Science | Medline11
Caslake MJ ,Packard CJ ,Suckling KE ,Holmes SD ,Chamberlain P ,Macphee CH . Lipoprotein-associated phospholipase A2, platelet-activating factor acetylhydrolase: a potential new risk factor for coronary artery disease. Atherosclerosis 2000;150:413-419
CrossRef | Web of Science | Medline12
Cao Y ,Stafforini DM ,Zimmerman GA ,McIntyre TM ,Prescott SM . Expression of plasma platelet-activating factor acetylhydrolase is transcriptionally regulated by mediators of inflammation. J Biol Chem 1998;273:4012-4020
CrossRef | Web of Science | Medline13
Tew DG ,Southan C ,Rice SQJ , et al. Purification, properties, sequencing, and cloning of a lipoprotein-associated, serine-dependent phospholipase involved in the oxidative modification of low-density lipoproteins. Arterioscler Thromb Vasc Biol 1996;16:591-599
CrossRef | Web of Science | Medline14
Shepherd J ,Cobbe SM ,Ford I , et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N Engl J Med 1995;333:1301-1307
Full Text | Web of Science | Medline15
Macphee CH ,Moores KE ,Boyd HF , et al. Lipoprotein-associated phospholipase A2, platelet-activating factor acetylhydrolase, generates two bioactive products during the oxidation of low-density lipoprotein: use of a novel inhibitor. Biochem J 1999;338:479-487
CrossRef | Web of Science | Medline16
Berliner J ,Leitinger N ,Watson A ,Huber J ,Fogelman A ,Navab M . Oxidized lipids in atherogenesis: formation, destruction and action. Thromb Haemost 1997;78:195-199
Web of Science | Medline17
Lowe GDO, Rumley A, Norrie J, et al. Blood rheology, cardiovascular risk factors and cardiovascular disease in the West of Scotland Coronary Prevention Study. Thromb Haemost (in press).
18
The WOSCOPS Study Group
CrossRef | Web of Science | Medline19
Yarnell JWG ,Baker IA ,Sweetnam PM , et al. Fibrinogen, viscosity and white blood cell count are major risk factors for ischaemic heart disease: the Caerphilly and Speedwell collaborative heart disease studies. Circulation 1991;83:836-844
Web of Science | Medline20
The West of Scotland Coronary Prevention Study Group
CrossRef | Web of Science | Medline21
Danesh J ,Collins R ,Appleby P ,Peto R . Association of fibrinogen, C-reactive protein, albumin, or leukocyte count with coronary heart disease: meta-analyses of prospective studies. JAMA 1998;279:1477-1482
CrossRef | Web of Science | Medline22
Danesh J ,Muir J ,Wong YK ,Ward M ,Gallemore JR ,Pepys MB . Risk factors for coronary heart disease and acute-phase proteins: a population-based study. Eur Heart J 1999;20:954-959
CrossRef | Web of Science | Medline23
Hak AE ,Stehouwer CDA ,Bots ML , et al. Associations of C-reactive protein with measures of obesity, insulin resistance, and subclinical atherosclerosis in healthy, middle-aged women. Arterioscler Thromb Vasc Biol 1999;19:1986-1991
CrossRef | Web of Science | Medline24
Tracy RP . Inflammation markers and coronary heart disease. Curr Opin Lipidol 1999;10:435-441
CrossRef | Web of Science | Medline25
Yudkin JS ,Stehouwer CDA ,Emeis JJ ,Coppack SW . C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for cytokines originating from adipose tissue? Arterioscler Thromb Vasc Biol 1999;19:972-978
CrossRef | Web of Science | Medline26
Mohamed-Ali V ,Goodrick S ,Rawesh A , et al. Subcutaneous adipose tissue releases interleukin-6, but not tumor necrosis factor α, in vivo. J Clin Endocrinol Metab 1997;82:4196-4200
CrossRef | Web of Science | Medline27
Bhakdi S ,Torzewski M ,Klouche M ,Hemmes M . Complement and atherogenesis: binding of CRP to degraded, nonoxidized LDL enhances complement activation. Arterioscler Thromb Vasc Biol 1999;19:2348-2354
CrossRef | Web of Science | Medline28
Snyder F . Platelet-activating factor and its analogs: metabolic pathways and related intracellular processes. Biochim Biophys Acta 1995;1254:231-249[Erratum, Biochim Biophys Acta 1995;1257:297, 1259:121.]
Web of Science | Medline29
Hakkinen T ,Luoma JS ,Hiltunen MO , et al. Lipoprotein-associated phospholipase A2, platelet-activating factor acetylhydrolase, is expressed by macrophages in human and rabbit atherosclerotic lesions. Arterioscler Thromb Vasc Biol 1999;19:2909-2917
CrossRef | Web of Science | Medline
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G. Sarlon-Bartoli, A. Boudes, C. Buffat, M.A. Bartoli, M.D. Piercecchi-Marti, E. Sarlon, L. Arnaud, Y. Bennis, B. Thevenin, C. Squarcioni, F. Nicoli, F. Dignat-George, F. Sabatier, P.E. Magnan. (2011) Circulating Lipoprotein-associated Phospholipase A2 in High-grade Carotid Stenosis: A New Biomarker for Predicting Unstable Plaque. European Journal of Vascular and Endovascular Surgery
CrossRef12
Yuichiro Yamamoto, Nobuhito Hirawa, Satoshi Yamaguchi, Nariaki Ogawa, Hideyuki Takeda, Ken Shibuya, Kimiko Kawahara, Hirofumi Kojima, Yasushi Dobashi, Megumi Fujita, Kengo Azusima, Nobuko Miyazaki, Mayumi Kobayashi, Chinatsu Kobayashi, Akira Fujiwara, Jun Yuto, Sanae Saka, Keisuke Yatsu, Yoshiyuki Toya, Gen Yasuda, Toshimasa Ohnishi, Satoshi Umemura. (2011) Long-Term Efficacy and Safety of the Small-Sized β2-Microglobulin Adsorption Column for Dialysis-Related Amyloidosis. Therapeutic Apheresis and Dialysis 15:5, 466-474
CrossRef13
Lawrence K. Oliver, Nikolay Voskoboev, Don Heser, Joseph P. McConnell, Shannon Hodel-Hanson, Heidi Callanan, Allan S. Jaffe. (2011) Assessment of clinical performance without adequate analytical validation: A prescription for confusion. Clinical Biochemistry 44:14-15, 1247-1252
CrossRef14
Miao-miao Hu, Jie Zhang, Wen-yi Wang, Wen-yu Wu, Yan-ling Ma, Wei-hai Chen, Yi-ping Wang. (2011) The inhibition of lipoprotein-associated phospholipase A2 exerts beneficial effects against atherosclerosis in LDLR-deficient mice. Acta Pharmacologica Sinica 32:10, 1253-1258
CrossRef15
Damian O. McCall, Michelle C. McKinley, Rebecca Noad, Pascal P. McKeown, David R. McCance, Ian S. Young, Jayne V. Woodside. (2011) The assessment of vascular function during dietary intervention trials in human subjects. British Journal of Nutrition 106:07, 981-994
CrossRef16
Liyun Li, Liping Qi, Naqiang Lv, Qian Gao, Yanmei Cheng, Yingjie Wei, Jue Ye, Xiaowei Yan, Aimin Dang. (2011) Association between Lipoprotein-Associated Phospholipase A2 Gene Polymorphism and Coronary Artery Disease in the Chinese Han Population. Annals of Human Genetics 75:5, 605-611
CrossRef17
XiaoFei Li, Miranda C. Kramer, Chris M. van der Loos, Karel T. Koch, Onno J. de Boer, José P.S. Henriques, Jan Baan, Marije M. Vis, Jan J. Piek, Jan G.P. Tijssen, Robbert J. de Winter, Allard C. van der Wal. (2011) A pattern of disperse plaque microcalcifications identifies a subset of plaques with high inflammatory burden in patients with acute myocardial infarction. Atherosclerosis 218:1, 83-89
CrossRef18
Guo-Hua Zheng, Hai-Ying Chen, Shang-Quan Xiong, Jian-Feng Chu. (2011) Lipoprotein-associated phospholipase A2 gene V279F polymorphisms and coronary heart disease: a meta-analysis. Molecular Biology Reports 38:6, 4089-4099
CrossRef19
Alexander K. Tsai, Brian T. Steffen, Jose M. Ordovas, Robert Straka, Xia Zhou, Naomi Q. Hanson, Donna Arnett, Michael Y. Tsai. (2011) Short-term fenofibrate treatment reduces elevated plasma Lp-PLA2 mass and sVCAM-1 levels in a subcohort of hypertriglyceridemic GOLDN participants. Translational Research 158:2, 99-105
CrossRef20
Alexander Constantinides, L. Joost van Pelt, Jeroen J. J. van Leeuwen, Rindert de Vries, René A. Tio, Iwan C. C. van der Horst, Wim J. Sluiter, Robin P. F. Dullaart. (2011) Carotid intima media thickness is associated with plasma lipoprotein-associated phospholipase A2 mass in nondiabetic subjects but not in patients with type 2 diabetes. European Journal of Clinical Investigation 41:8, 820-827
CrossRef21
Byambaa Enkhmaa, Erdembileg Anuurad, Zeynep Ozturk, Wei Zhang, Thomas A. Pearson, Lars Berglund. (2011) Differential associations of serum amyloid A and pentraxin-3 with allele-specific lipoprotein(a) levels in African Americans and Caucasians. Translational Research 158:2, 92-98
CrossRef22
Chih-hung Lin, Chia-lang Fang, Saleh A Al-suwayeh, Shih-yun Yang, Jia-you Fang. (2011) In vitro and in vivo percutaneous absorption of seleno-L-methionine, an antioxidant agent, and other selenium species. Acta Pharmacologica Sinica
CrossRef23
Naveed Adoni, Ghassan Abusaid, Ken Fujise. 2011. Inflammation and Heart Diseases. .
CrossRef24
Xiang Ying Ouyang, Wen Mei Xiao, Yi Chu, Shuang Ying Zhou. (2011) Influence of periodontal intervention therapy on risk of cardiovascular disease. Periodontology 2000 56:1, 227-257
CrossRef25
Christos V. Rizos, Evangelos N. Liberopoulos, Constantinos C. Tellis, Matilda Florentin, Moses S. Elisaf, Alexandros D. Tselepis. (2011) Combining Rosuvastatin with Sartans of Different Peroxisome Proliferator-Activated Receptor-γ Activating Capacity Is Not Associated with Different Changes in Low-Density Lipoprotein Subfractions and Plasma Lipoprotein-Associated Phospholipase A 2. Metabolic Syndrome and Related Disorders 9:3, 217-223
CrossRef26
Cristiano Fava, Martina Montagnana, Gian Cesare Guidi, Olle Melander. (2011) From circulating biomarkers to genomics and imaging in the prediction of cardiovascular events in the general population. Annals of Medicine1-15
CrossRef27
Yimeng Du, Fengtao Wei, Zhaoqiang Dong, Junni Liu, Weidong Jiang, Qinghua Lu. (2011) Prognostic Value of Serum LP-PLA2 and hs-CRP in Unstable Atherosclerotic Plaques. Clinical and Experimental Hypertension 33:2, 113-116
CrossRef28
J.-C. Charniot, R. Khani-Bittar, D. Bonnefont-Rousselot. (2011) La lipoprotéine phospholipase A2 : un nouveau biomarqueur de l’inflammation vasculaire. Archives des Maladies du Coeur et des Vaisseaux - Pratique 2011:197, 27-30
CrossRef29
Mira Katan, Mitchell SV Elkind. (2011) Inflammatory and neuroendocrine biomarkers of prognosis after ischemic stroke. Expert Review of Neurotherapeutics 11:2, 225-239
CrossRef30
Taha Tahir Bekci, Mehmet Kayrak, Aysel Kiyici, Hatem Ari, Turgut Teke, Emin Maden, Hakan Akilli. (2011) The relation between Lp-PLA2 levels with periodic limb movements. Sleep and Breathing
CrossRef31
Chih-Wei Chen, Chih-Ta Lin, Ying-Lung Lin, Tin-Kwang Lin, Chin-Lon Lin. (2011) Taiwanese Female Vegetarians Have Lower Lipoprotein-Associated Phospholipase A2 Compared with Omnivores. Yonsei Medical Journal 52:1, 13
CrossRef32
K. C. Epps, R. L. Wilensky. (2011) Lp-PLA2- a novel risk factor for high-risk coronary and carotid artery disease. Journal of Internal Medicine 269:1, 94-106
CrossRef33
Keane K Lee, Stephen P Fortmann, Ann Varady, Joan M Fair, Alan S Go, Thomas Quertermous, Mark A Hlatky, Carlos Iribarren. (2011) Racial variation in lipoprotein-associated phospholipase A2 in older adults. BMC Cardiovascular Disorders 11:1, 38
CrossRef34
Carmen A. Peralta, Ronit Katz, Michael Shlipak, Ruth Dubin, Ian DeBoer, Nancy Jenny, Annette Fitzpatrick, Carol Koro, Bryan Kestenbaum, Joachim Ix, Mark Sarnak, Mary Cushman. (2011) Kidney Function Decline in the Elderly: Impact of Lipoprotein-Associated Phospholipase A<sub>2</sub>. American Journal of Nephrology 34:6, 512-518
CrossRef35
Yonghong Li, Marc S. Sabatine, Carmen H. Tong, Ian Ford, Todd G. Kirchgessner, Christopher J. Packard, Michele Robertson, Charles M. Rowland, Lance A. Bare, James Shepherd, James J. Devlin, Olga A. Iakoubova. (2011) Genetic variants in the KIF6 region and coronary event reduction from statin therapy. Human Genetics 129:1, 17-23
CrossRef36
Sheng Liu, Xiao-Bo Hu, Hong-Zhuan Li, Wei-Dong Jiang, Xin Wang, Hao Lin, Ai-Qiong Qin, Yong-Mei Wang, Tong Zhao, Zhao-Qiang Dong, Mei Zhang, Qing-Hua Lu. (2011) Association of Lipoprotein-Associated Phospholipase A2 with Characteristics of Vulnerable Coronary Atherosclerotic Plaques. Yonsei Medical Journal 52:6, 914
CrossRef37
Tatjana Rundek, Ralph L. Sacco. 2011. Prognosis after Stroke. , 219-241.
CrossRef38
Qianqian Wang, Yongchen Hao, Xingbo Mo, Laiyuan Wang, Xiangfeng Lu, Jianfeng Huang, Jie Cao, Hongfan Li, Dongfeng Gu. (2010) PLA2G7 gene polymorphisms and coronary heart disease risk: A meta-analysis. Thrombosis Research 126:6, 498-503
CrossRef39
Philip Greenland, Joseph S. Alpert, George A. Beller, Emelia J. Benjamin, Matthew J. Budoff, Zahi A. Fayad, Elyse Foster, Mark A. Hlatky, John McB. Hodgson, Frederick G. Kushner, Michael S. Lauer, Leslee J. Shaw, Sidney C. Smith, Allen J. Taylor, William S. Weintraub, Nanette K. Wenger. (2010) 2010 ACCF/AHA Guideline for Assessment of Cardiovascular Risk in Asymptomatic Adults. Journal of the American College of Cardiology 56:25, e50-e103
CrossRef40
Linda Hermus, Joop D. Lefrandt, René A. Tio, Jan-Cees Breek, Clark J. Zeebregts. (2010) Carotid plaque formation and serum biomarkers. Atherosclerosis 213:1, 21-29
CrossRef41
Keith Suckling. (2010) Phospholipase A2s: Developing drug targets for atherosclerosis. Atherosclerosis 212:2, 357-366
CrossRef42
Byambaa Enkhmaa, Erdembileg Anuurad, Wei Zhang, Thomas A. Pearson, Lars Berglund. (2010) Association of Lp-PLA2 activity with allele-specific Lp(a) levels in a bi-ethnic population. Atherosclerosis 211:2, 526-530
CrossRef43
Ryoko Mitsutake, Shin-ichiro Miura, Bo Zhang, Keijiro Saku. (2010) HDL-associated factors provide additional prognostic information for coronary artery disease as determined by multi-detector row computed tomography. International Journal of Cardiology 143:1, 72-78
CrossRef44
Rüdiger Siekmeier, Tanja B. Grammer, Hubert Scharnagl, Tatjana Stojakovic, Wolfgang König, Winfried März. (2010) Lipoprotein-assoziierte Phospholipase A 2 : ein neuer Marker für kardiovaskuläre Erkrankungen / Lipoprotein-associated phospholipase A 2 : a novel marker of cardiovascular diseases. LaboratoriumsMedizin 34:4, 217-222
CrossRef45
Vikas Singh, Pedro Martinezclark, Mario Pascual, Eric Scot Shaw, William W. OʼNeill. (2010) Cardiac biomarkers – the old and the new: a review. Coronary Artery Disease 21:4, 244-256
CrossRef46
Sonia-Athina Karabina, Sarah Gora, Rajai Atout, Ewa Ninio. (2010) Extracellular phospholipases in atherosclerosis. Biochimie 92:6, 594-600
CrossRef47
Muriel J. Caslake, Chris J. Packard, Michele Robertson, Josephine Cooney, Jeanenne J. Nelson, Ian Ford, Allan Gaw, J. Wouter Jukema, Peter W. Macfarlane, David J. Stott, James Shepherd. (2010) Lipoprotein-associated phospholipase A2, inflammatory biomarkers, and risk of cardiovascular disease in the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER). Atherosclerosis 210:1, 28-34
CrossRef48
(2010) Lipoprotein-associated phospholipase A2 and risk of coronary disease, stroke, and mortality: collaborative analysis of 32 prospective studies. The Lancet 375:9725, 1536-1544
CrossRef49
Nancy Swords Jenny, Cam Solomon, Mary Cushman, Russell P. Tracy, Jeanenne J. Nelson, Bruce M. Psaty, Curt D. Furberg. (2010) Lipoprotein-associated phospholipase A2 (Lp-PLA2) and risk of cardiovascular disease in older adults: Results from the Cardiovascular Health Study. Atherosclerosis 209:2, 528-532
CrossRef50
Jean Kyung Paik, Jey Sook Chae, Yangsoo Jang, Ji Young Kim, Oh Yoen Kim, Tae-Sook Jeong, Sang-Hyun Lee, Jong Ho Lee. (2010) Effects of V279F in the Lp-PLA2 gene on markers of oxidative stress and inflammation in Koreans. Clinica Chimica Acta 411:7-8, 486-493
CrossRef51
Eva Lonn. (2010) Lipoprotein-associated phospholipase A2: A new therapeutic target. Canadian Journal of Cardiology 26, 27A-31A
CrossRef52
W.-Y. Wang, J. Li, D. Yang, W. Xu, R.-p. Zha, Y.-p. Wang. (2010) OxLDL stimulates lipoprotein-associated phospholipase A2 expression in THP-1 monocytes via PI3K and p38 MAPK pathways. Cardiovascular Research 85:4, 845-852
CrossRef53
Lewis H Kuller. (2010) Cardiovascular disease is preventable among women. Expert Review of Cardiovascular Therapy 8:2, 175-187
CrossRef54
Kyung-Hyun Cho, Joo-Heon Hong, Ki-Teak Lee. (2010) Monoacylglycerol (MAG)-Oleic Acid Has Stronger Antioxidant, Anti-Atherosclerotic, and Protein Glycation Inhibitory Activities than MAG-Palmitic Acid. Journal of Medicinal Food 13:1, 99-107
CrossRef55
Mahir Karakas, Wolfgang Koenig. (2010) Phospholipase A 2 as a therapeutic target for atherosclerosis. Clinical Lipidology 5:1, 43-56
CrossRef56
Tsuyoshi Nozue, Ichiro Michishita, Ichiro Mizuguchi. (2010) Effects of Ezetimibe on Remnant-Like Particle Cholesterol, Lipoprotein (a), and Oxidized Low-Density Lipoprotein in Patients with Dyslipidemia. Journal of Atherosclerosis and Thrombosis 17:1, 37-44
CrossRef57
Mohamad C. N. Sinno, Mouaz Al-Mallah. (2010) Impact of Medical Therapy on Atheroma Volume Measured by Different Cardiovascular Imaging Modalities. Cardiology Research and Practice 2010, 1-13
CrossRef58
Carlos Iribarren. (2010) Lipoprotein-Associated Phospholipase A2 and C-Reactive Protein for Measurement of Inflammatory Risk: Independent or Complementary?. Current Cardiovascular Risk Reports 4:1, 57-67
CrossRef59
J. Herrmann, D. Mannheim, C. Wohlert, D. Versari, F. B. Meyer, J. P. McConnell, M. Gossl, L. O. Lerman, A. Lerman. (2009) Expression of lipoprotein-associated phospholipase A2 in carotid artery plaques predicts long-term cardiac outcome. European Heart Journal 30:23, 2930-2938
CrossRef60
Joung Hee Lee, Marguerite M. Engler. (2009) Lipoprotein-Associated Phospholipase A2: A Promising Vascular-Specific Marker for Screening Cardiovascular Risk?. Progress in Cardiovascular Nursing 24:4, 181-189
CrossRef61
Bradley Bale, Amy Doneen, Michael Wegner. (2009) The identification of occult cardiovascular disease through the use of a novel biomarker: a case report. Journal of Clinical Lipidology 3:5, 351-354
CrossRef62
Houman Khakpour, William H. Frishman. (2009) Lipoprotein-Associated Phospholipase A2. Cardiology in Review 17:5, 222-229
CrossRef63
Aruna Poduri, Madhu Khullar, Ajay Bahl, Yash Paul Sharma, Kewal K. Talwar. (2009) A Combination of Proatherogenic Single-Nucleotide Polymorphisms Is Associated with Increased Risk of Coronary Artery Disease and Myocardial Infarction in Asian Indians. DNA and Cell Biology 28:9, 451-460
CrossRef64
Marilia Brito Gomes, Roberta Arnold Cobas, Edson Nunes, Hugo Caire Castro-Faria-Neto, Maria Fátima Bevilacqua da Matta, Ricardo Neves, Eduardo Tibiriçá. (2009) Plasma PAF-acetylhydrolase activity, inflammatory markers and susceptibility of LDL to in vitro oxidation in patients with type 1 diabetes mellitus. Diabetes Research and Clinical Practice 85:1, 61-68
CrossRef65
Tao Wang, Kenji Karino, Masayuki Yamasaki, Yan Zhang, Junichi Masuda, Shuhei Yamaguchi, Kuninori Shiwaku, Toru Nabika. (2009) Effects of G994T in the Lp-PLA2 Gene on the Plasma Oxidized LDL Level and Carotid Intima-Media Thickness in Japanese: The Shimane Study. American Journal of Hypertension 22:7, 742-747
CrossRef66
Chris J Packard. (2009) Lipoprotein-associated phospholipase A2 as a biomarker of coronary heart disease and a therapeutic target. Current Opinion in Cardiology 24:4, 358-363
CrossRef67
Anna-Maria Kampoli, Dimitris Tousoulis, Charalambos Antoniades, Gerasimos Siasos, Christodoulos Stefanadis. (2009) Biomarkers of premature atherosclerosis. Trends in Molecular Medicine 15:7, 323-332
CrossRef68
Livia Lenzini, Katia Antezza, Brasilina Caroccia, Robert L. Wolfert, Radoslaw Szczech, Maurizio Cesari, Krzysztof Narkiewicz, Christopher J. Williams, Gian Paolo Rossi. (2009) A twin study of heritability of plasma lipoprotein-associated phospholipase A2 (Lp-PLA2) mass and activity. Atherosclerosis 205:1, 181-185
CrossRef69
TD Filippatos, CS Derdemezis, MS Elisaf. (2009) Effects of orlistat, alone or combined with hypolipidemic drugs, on cardiovascular risk factors. Clinical Lipidology 4:3, 331-341
CrossRef70
Kota J. Reddy, Manmeet Singh, Joey R. Bangit, Richard R. Batsell. (2009) The role of lipoprotein-associated phospholipase A2 on cardiovascular disease risk assessment and plaque rupture: a clinical review. Journal of Clinical Lipidology 3:2, 85-93
CrossRef71
Yariv Gerber, Shannon M. Dunlay, Allan S. Jaffe, Joseph P. McConnell, Susan A. Weston, Jill M. Killian, Véronique L. Roger. (2009) Plasma lipoprotein-associated phospholipase A2 levels in heart failure: Association with mortality in the community. Atherosclerosis 203:2, 593-598
CrossRef72
Muzammil Ali, Mohammad Madjid. (2009) Lipoprotein-associated phospholipase A2: a cardiovascular risk predictor and a potential therapeutic target. Future Cardiology 5:2, 159-173
CrossRef73
Liping Hou, Shufeng Chen, Hongjiang Yu, Xiangfeng Lu, Jianhong Chen, Laiyuan Wang, Jianfeng Huang, Zhongjie Fan, Dongfeng Gu. (2009) Associations of PLA2G7 gene polymorphisms with plasma lipoprotein-associated phospholipase A2 activity and coronary heart disease in a Chinese Han population: the Beijing atherosclerosis study. Human Genetics 125:1, 11-20
CrossRef74
Wolfgang Koenig, Natalie Khuseyinova. (2009) Lipoprotein-Associated and Secretory Phospholipase A2 in Cardiovascular Disease: The Epidemiological Evidence. Cardiovascular Drugs and Therapy 23:1, 85-92
CrossRef75
Maria Weinkouff Pedersen, Wolfgang Koenig, Jeppe Hagstrup Christensen, Erik Berg Schmidt. (2009) The effect of marine n-3 fatty acids in different doses on plasma concentrations of Lp-PLA2 in healthy adults. European Journal of Nutrition 48:1, 1-5
CrossRef76
Kyung-Hyun Cho, Dong-Gu Shin, Suk-Hwan Baek, Jae-Ryong Kim. (2009) Myocardial infarction patients show altered lipoprotein properties and functions when compared with stable angina pectoris patients. Experimental and Molecular Medicine 41:2, 67
CrossRef77
M. M. HOFFMANN, K. WINKLER, W. RENNER, B. R. WINKELMANN, U. SEELHORST, B. WELLNITZ, B. O. BOEHM, W. MÄRZ. (2009) Genetic variants and haplotypes of lipoprotein associated phospholipase A2 and their influence on cardiovascular disease (The Ludwigshafen Risk and Cardiovascular Health Study). Journal of Thrombosis and Haemostasis 7:1, 41-48
CrossRef78
Marilia de Brito Gomes, Roberta Arnold Cobas, Edson Nunes, Michele Nery, Hugo Caire Castro-Faria-Neto, Eduardo Tibiriçá. (2008) Serum platelet-activating factor acetylhydrolase activity: A novel potential inflammatory marker in type 1 diabetes. Prostaglandins & Other Lipid Mediators 87:1-4, 42-46
CrossRef79
Atul Tiwari. (2008) Current and emerging paradigms in the therapeutic management of atherosclerosis. Expert Opinion on Therapeutic Targets 12:12, 1523-1546
CrossRef80
J. P. Casas, T. Shah, A. D. Hingorani, J. Danesh, M. B. Pepys. (2008) C-reactive protein and coronary heart disease: a critical review. Journal of Internal Medicine 264:4, 295-314
CrossRef81
Salim S. Virani, Christie M. Ballantyne. (2008) How to identify patients with vulnerable plaques. Diabetes, Obesity and Metabolism 10:10, 824-833
CrossRef82
Nancy R Webb. (2008) Getting to the core of atherosclerosis. Nature Medicine 14:10, 1015-1016
CrossRef83
T. Tzotzas, T.D. Filippatos, A. Triantos, E. Bruckert, A.D. Tselepis, D.N. Kiortsis. (2008) Effects of a low-calorie diet associated with weight loss on lipoprotein-associated phospholipase A2 (Lp-PLA2) activity in healthy obese women. Nutrition, Metabolism and Cardiovascular Diseases 18:7, 477-482
CrossRef84
Patrik K E Magnusson, Marcus Boman, Ulf de Faire, Markus Perola, Leena Peltonen, Nancy L Pedersen. (2008) Genome-wide search for QTLs for apolipoprotein A-I level in elderly Swedish DZ twins: evidence of female-specific locus on 15q11–13. European Journal of Human Genetics 16:9, 1103-1110
CrossRef85
Margaretha Persson, Göran Berglund, Jeanenne J. Nelson, Bo Hedblad. (2008) Lp-PLA2 activity and mass are associated with increased incidence of ischemic stroke. Atherosclerosis 200:1, 191-198
CrossRef86
Barry A Franklin, Justin E Trivax, Thomas E Vanhecke. (2008) New insights in preventive cardiology and cardiac rehabilitation. Current Opinion in Cardiology 23:5, 477-486
CrossRef87
Mark A. Crandall, Marshall A. Corson. (2008) Use of biomarkers to develop treatment strategies for atherosclerosis. Current Treatment Options in Cardiovascular Medicine 10:4, 304-315
CrossRef88
Ngoc-Anh Le. (2008) Reducing oxidized lipids to prevent cardiovascular disease. Current Treatment Options in Cardiovascular Medicine 10:4, 263-272
CrossRef89
S. Tsimikas, J. Willeit, M. Knoflach, M. Mayr, G. Egger, M. Notdurfter, J. L. Witztum, C. J. Wiedermann, Q. Xu, S. Kiechl. (2008) Lipoprotein-associated phospholipase A2 activity, ferritin levels, metabolic syndrome, and 10-year cardiovascular and non-cardiovascular mortality: results from the Bruneck study. European Heart Journal 30:1, 107-115
CrossRef90
Emmanouil S. Brilakis, Amit Khera, Darren K. McGuire, Raphael See, Subhash Banerjee, Sabina A. Murphy, James A. de Lemos. (2008) Influence of race and sex on lipoprotein-associated phospholipase A2 levels: Observations from the Dallas Heart Study. Atherosclerosis 199:1, 110-115
CrossRef91
Nels Olson, Ellen S. O'Meara, Nancy S. Jenny, Aaron R. Folsom, Edwin G. Bovill, Curt D. Furberg, Susan R. Heckbert, Bruce M. Psaty, Mary Cushman. (2008) Lipoprotein‐associated phospholipase A 2 and risk of venous thrombosis in older adults. American Journal of Hematology 83:7, 524-527
CrossRef92
Martin Möckel, Oliver Danne, Reinhold Müller, Jörn O. Vollert, Christian Müller, Christian Lueders, Thomas Störk, Ulrich Frei, Wolfgang Koenig, Rainer Dietz, Allan S. Jaffe. (2008) Development of an optimized multimarker strategy for early risk assessment of patients with acute coronary syndromes. Clinica Chimica Acta 393:2, 103-109
CrossRef93
Shahar Lavi, Joerg Herrmann, Ronit Lavi, Joseph P. McConnell, Lilach O. Lerman, Amir Lerman. (2008) Role of lipoprotein-associated phospholipase A2 in atherosclerosis. Current Atherosclerosis Reports 10:3, 230-235
CrossRef94
Curt D. Furberg, Jeanenne J. Nelson, Cam Solomon, Mary Cushman, Nancy Swords Jenny, Bruce M. Psaty. (2008) Distribution and Correlates of Lipoprotein-Associated Phospholipase A2 in an Elderly Cohort: The Cardiovascular Health Study. Journal of the American Geriatrics Society 56:5, 792-799
CrossRef95
Emile R. Mohler, Christie M. Ballantyne, Michael H. Davidson, Markolf Hanefeld, Luis M. Ruilope, Joel L. Johnson, Andrew Zalewski. (2008) The Effect of Darapladib on Plasma Lipoprotein-Associated Phospholipase A2 Activity and Cardiovascular Biomarkers in Patients With Stable Coronary Heart Disease or Coronary Heart Disease Risk Equivalent. Journal of the American College of Cardiology 51:17, 1632-1641
CrossRef96
Hongtao Liu, Bo Shi, Chiang-Ching Huang, Polikseni Eksarko, Richard M. Pope. (2008) Transcriptional diversity during monocyte to macrophage differentiation. Immunology Letters 117:1, 70-80
CrossRef97
Eugenia Raichlin, Joseph P. McConnell, Jang-Ho Bae, Walter K. Kremers, Amir Lerman, Robert P. Frantz. (2008) Lipoprotein-Associated Phospholipase A2 Predicts Progression of Cardiac Allograft Vasculopathy and Increased Risk of Cardiovascular Events in Heart Transplant Patients. Transplantation 85:7, 963-968
CrossRef98
Salim S. Virani, Venkateshwar R. Polsani, Vijay Nambi. (2008) Novel markers of inflammation in atherosclerosis. Current Atherosclerosis Reports 10:2, 164-170
CrossRef99
Bonnie Ky, Anne Burke, Sotirios Tsimikas, Megan L. Wolfe, Mahlet G. Tadesse, Philippe O. Szapary, Joseph L. Witztum, Garret A. FitzGerald, Daniel J. Rader. (2008) The Influence of Pravastatin and Atorvastatin on Markers of Oxidative Stress in Hypercholesterolemic Humans. Journal of the American College of Cardiology 51:17, 1653-1662
CrossRef100
Lori B. Daniels, Gail A. Laughlin, Mark J. Sarno, Ricki Bettencourt, Robert L. Wolfert, Elizabeth Barrett-Connor. (2008) Lipoprotein-Associated Phospholipase A2 Is an Independent Predictor of Incident Coronary Heart Disease in an Apparently Healthy Older Population. Journal of the American College of Cardiology 51:9, 913-919
CrossRef101
Robert S. Rosenson. (2008) Fenofibrate reduces lipoprotein associated phospholipase A2 mass and oxidative lipids in hypertriglyceridemic subjects with the metabolic syndrome. American Heart Journal 155:3, 499.e9-499.e16
CrossRef102
Masanori Iwase, Kazuo Sonoki, Nobuhiro Sasaki, Shigehiro Ohdo, Shun Higuchi, Hiroaki Hattori, Mitsuo Iida. (2008) Lysophosphatidylcholine contents in plasma LDL in patients with type 2 diabetes mellitus: Relation with lipoprotein-associated phospholipase A2 and effects of simvastatin treatment. Atherosclerosis 196:2, 931-936
CrossRef103
Erik Berg Schmidt, Wolfgang Koenig, Natalie Khuseyinova, Jeppe Hagstrup Christensen. (2008) Lipoprotein-associated phospholipase A2 concentrations in plasma are associated with the extent of coronary artery disease and correlate to adipose tissue levels of marine n-3 fatty acids. Atherosclerosis 196:1, 420-424
CrossRef104
Olga A. Iakoubova, Carmen H. Tong, Charles M. Rowland, Todd G. Kirchgessner, Bradford A. Young, Andre R. Arellano, Dov Shiffman, Marc S. Sabatine, Hannia Campos, Christopher J. Packard, Marc A. Pfeffer, Thomas J. White, Eugene Braunwald, James Shepherd, James J. Devlin, Frank M. Sacks. (2008) Association of the Trp719Arg Polymorphism in Kinesin-Like Protein 6 With Myocardial Infarction and Coronary Heart Disease in 2 Prospective Trials. Journal of the American College of Cardiology 51:4, 435-443
CrossRef105
M. Gomez Lira, L. Provezza, C. Terranova, N. Martinelli, C. Bozzini, P. F. Pignatti. (2007) Two new highly polymorphic markers in the 3' UTR region of the PLA2G7 gene. International Journal of Immunogenetics 34:6, 465-468
CrossRef106
Clifford Rubin, Thomas D Nolin, Jonathan Himmelfarb. (2007) Are biomarkers useful for assessing cardiovascular risk in patients with chronic kidney disease?. Current Opinion in Nephrology and Hypertension 16:6, 506-511
CrossRef107
Gulnara Chapidze, Nino Dolidze, Daniel A. Enquobahrie, Simon Kapanadze, Nino Latsabidze, Michelle A. Williams. (2007) Metabolic Syndrome and C-reactive Protein among Cardiology Patients. Archives of Medical Research 38:7, 783-788
CrossRef108
Cristina Tosti Guerra, Patrizio Caini, Carlo Giannini, Francesca Giannelli, Laura Gragnani, Antonio Petrarca, Vera Solazzo, Monica Monti, Giacomo Laffi, Anna Linda Zignego. (2007) Effect of chronic hepatitis C virus infection on inflammatory lipid mediators. Digestive and Liver Disease 39, S76-S82
CrossRef109
Matthew A. Allison, Julie O. Denenberg, Jeanenne J. Nelson, Loki Natarajan, Michael H. Criqui. (2007) The association between lipoprotein-associated phospholipase A2 and cardiovascular disease and total mortality in vascular medicine patients. Journal of Vascular Surgery 46:3, 500-506
CrossRef110
M. Möckel, Reinhold Müller, Jörn O. Vollert, Christian Müller, Oilver Danne, Ragnar Gareis, Thomas Störk, Rainer Dietz, Wolfgang Koenig. (2007) Lipoprotein-associated phospholipase A2 for early risk stratification in patients with suspected acute coronary syndrome: a multi-marker approach. Clinical Research in Cardiology 96:9, 604-612
CrossRef111
John F Carlquist, Joseph B Muhlestein, Jeffrey L Anderson. (2007) Lipoprotein-associated phospholipase A 2 : a new biomarker for cardiovascular risk assessment and potential therapeutic target. Expert Review of Molecular Diagnostics 7:5, 511-517
CrossRef112
Subramaniam Pennathur, Jay W. Heinecke. (2007) Oxidative stress and endothelial dysfunction in vascular disease. Current Diabetes Reports 7:4, 257-264
CrossRef113
T.D. Filippatos, I.F. Gazi, E.N. Liberopoulos, V.G. Athyros, M.S. Elisaf, A.D. Tselepis, D.N. Kiortsis. (2007) The effect of orlistat and fenofibrate, alone or in combination, on small dense LDL and lipoprotein-associated phospholipase A2 in obese patients with metabolic syndrome. Atherosclerosis 193:2, 428-437
CrossRef114
Ghainsom D. Kom, Edzard Schwedhelm, Renke Maas, Lydia Schneider, Ralf Benndorf, Rainer H. Böger. (2007) Impact of atorvastatin treatment on platelet-activating factor acetylhydrolase and 15-F 2trans -isoprostane in hypercholesterolaemic patients. British Journal of Clinical Pharmacology 63:6, 672-679
CrossRef115
M.L. Muzzio, G. Berg, V. Zago, F. Basilio, S. Sanguinetti, G. Lopez, F. Brites, R. Wikinski, L. Schreier. (2007) Circulating small dense LDL, endothelial injuring factors and fibronectin in healthy postmenopausal women. Clinica Chimica Acta 381:2, 157-163
CrossRef116
Dimitrios S. Christidis, Evangelos N. Liberopoulos, Anna I. Kakafika, George A. Miltiadous, George L. Liamis, Barbara Kakaidi, Alexandros D. Tselepis, Marios A. Cariolou, Moses S. Elisaf. (2007) Effect of Paraoxonase 1 Polymorphisms on the Response of Lipids and Lipoprotein-associated Enzymes to Treatment with Fluvastatin. Archives of Medical Research 38:4, 403-410
CrossRef117
Vijay Nambi, Christie M. Ballantyne. (2007) Role of Biomarkers in Developing New Therapies for Vascular Disease. World Journal of Surgery 31:4, 676-681
CrossRef118
Isabella Kardys, Hok-Hay S. Oei, Albert Hofman, Matthijs Oudkerk, Jacqueline C.M. Witteman. (2007) Lipoprotein-associated phospholipase A2 and coronary calcification. Atherosclerosis 191:2, 377-383
CrossRef119
Salim S. Virani, Vijay Nambi. (2007) The role of lipoprotein-associated phospholipase A2 as a marker for atherosclerosis. Current Atherosclerosis Reports 9:2, 97-103
CrossRef120
S. M. Marcovina, F. Crea, J. Davignon, J. C. Kaski, W. Koenig, U. Landmesser, P. L. Pieri, J. Schulz-Menger, L. J. Shaw, J. Sobesky. (2007) Biochemical and bioimaging markers for risk assessment and diagnosis in major cardiovascular diseases: a road to integration of complementary diagnostic tools. Journal of Internal Medicine 261:3, 214-234
CrossRef121
Ngoc-Anh Le, Mary F. Walter. (2007) Intrinsic enzymes of high-density lipoprotein. Journal of Clinical Lipidology 1:1, 20-30
CrossRef122
Yi Shi, Ping Zhang, LiFeng Zhang, Hashim Osman, Emile R. Mohler, Colin Macphee, Andrew Zalewski, Anthony Postle, Robert L. Wilensky. (2007) Role of lipoprotein-associated phospholipase A2 in leukocyte activation and inflammatory responses. Atherosclerosis 191:1, 54-62
CrossRef123
LaDale St. Clair, Christie M. Ballantyne. (2007) Biological Surrogates for Enhancing Cardiovascular Risk Prediction in Type 2 Diabetes Mellitus. The American Journal of Cardiology 99:4, 80-88
CrossRef124
Margaretha Persson, Jan-Åke Nilsson, Jeanenne J. Nelson, Bo Hedblad, Göran Berglund. (2007) The epidemiology of Lp-PLA2: Distribution and correlation with cardiovascular risk factors in a population-based cohort. Atherosclerosis 190:2, 388-396
CrossRef125
(2007) Collaborative meta-analysis of individual participant data from observational studies of Lp-PLA2 and cardiovascular diseases. European Journal of Cardiovascular Prevention & Rehabilitation 14:1, 3-11
CrossRef126
Christie M. Ballantyne. (2007) Lipoprotein-associated phospholipase A2: Risk marker or target of therapy?. Current Cardiovascular Risk Reports 1:1, 66-71
CrossRef127
Carolina A. Garza, Victor M. Montori, Joseph P. McConnell, Virend K. Somers, Iftikhar J. Kullo, Francisco Lopez-Jimenez. (2007) Association Between Lipoprotein-Associated Phospholipase A2 and Cardiovascular Disease: A Systematic Review. Mayo Clinic Proceedings 82:2, 159-165
CrossRef128
C. A. Garza, V. M. Montori, J. P. McConnell, V. K. Somers, I. J. Kullo, F. Lopez-Jimenez. (2007) Association Between Lipoprotein-Associated Phospholipase A2 and Cardiovascular Disease: A Systematic Review. Mayo Clinic Proceedings 82:2, 159-165
CrossRef129
Keisuke Okamura, Shin-ichiro Miura, Bo Zhang, Yoshinari Uehara, Kunihiro Matsuo, Koichiro Kumagai, Keijiro Saku. (2007) Ratio of LDL- to HDL-Associated Platelet-Activating Factor Acetylhydrolase may be a Marker of Inflammation in Patients With Paroxysmal Atrial Fibrillation. Circulation Journal 71:2, 214-219
CrossRef130
P. Caini, C. Tosti Guerra, C. Giannini, F. Giannelli, L. Gragnani, A. Petrarca, V. Solazzo, M. Monti, G. Laffi, A. L. Zignego. (2007) Modifications of plasma platelet-activating factor (PAF)-acetylhydrolase/PAF system activity in patients with chronic hepatitis C virus infection. Journal of Viral Hepatitis 14:1, 22-28
CrossRef131
Shao-Yan ZHANG, Hiroshi SHIBATA, Kenji KARINO, Bin-You WANG, Shotai KOBAYASHI, Junichi MASUDA, Toru NABIKA. (2007) Comprehensive Evaluation of Genetic and Environmental Factors Influencing the Plasma Lipoprotein-Associated Phospholipase A2 Activity in a Japanese Population. Hypertension Research 30:5, 403-409
CrossRef132
Sarah D. de Ferranti, Nader Rifai. (2007) C-reactive protein: a nontraditional serum marker of cardiovascular risk. Cardiovascular Pathology 16:1, 14-21
CrossRef133
Peter T.E. Wootton, David M. Flavell, Hugh E. Montgomery, Mike World, Steve E. Humphries, Philippa J. Talmud. (2007) Lipoprotein-associated phospholipase A2 A379V variant is associated with body composition changes in response to exercise training. Nutrition, Metabolism and Cardiovascular Diseases 17:1, 24-31
CrossRef134
Scott W Brouilette, Jasbir S Moore, Alex D McMahon, John R Thompson, Ian Ford, James Shepherd, Chris J Packard, Nilesh J Samani. (2007) Telomere length, risk of coronary heart disease, and statin treatment in the West of Scotland Primary Prevention Study: a nested case-control study. The Lancet 369:9556, 107-114
CrossRef135
Mary Cushman, Barbara M. Alving. 2007. Risk Factors for Cardiovascular Disease and Arterial Thrombosis. , 371-378.
CrossRef136
Ishwarlal Jialal. (2006) Contemporary Scientific Insights. Critical Pathways in Cardiology: A Journal of Evidence-Based Medicine 5:4, 191-210
CrossRef137
P.T.E Wootton, J.W. Stephens, S.J. Hurel, H. Durand, J. Cooper, E. Ninio, S.E. Humphries, P.J. Talmud. (2006) Lp-PLA2 activity and PLA2G7 A379V genotype in patients with diabetes mellitus. Atherosclerosis 189:1, 149-156
CrossRef138
Jeffrey S Berger, John L Petersen, James E Tcheng, Harry R Phillips. (2006) Clinical implications of vulnerable plaque. Future Cardiology 2:6, 721-731
CrossRef139
Natalie Khuseyinova, Wolfgang Koenig. (2006) Biomarkers of outcome from cardiovascular disease. Current Opinion in Critical Care 12:5, 412-419
CrossRef140
John A. Farmer. 2006. Inflammatory Mediators and C-Reactive Protein. , 441-462.
CrossRef141
Mikko J Järvisalo, Markus Juonala, Olli T Raitakari. (2006) Assessment of inflammatory markers and endothelial function. Current Opinion in Clinical Nutrition and Metabolic Care 9:5, 547-552
CrossRef142
Vijay Nambi, Christie M. Ballantyne. (2006) Lipoprotein-associated phospholipase A2: Pathogenic mechanisms and clinical utility for predicting cardiovascular events. Current Atherosclerosis Reports 8:5, 374-381
CrossRef143
Achikam Grinberg, Kyung W Park. (2006) Nuclear Peroxisome Proliferator-Activated Receptors and Thiazolidinediones. International Anesthesiology Clinics 43:2, 1-21
CrossRef144
Gemma Francisco, Cristina Hernández, Rafael Simó. (2006) Serum markers of vascular inflammation in dyslipemia. Clinica Chimica Acta 369:1, 1-16
CrossRef145
Naoki Unno, Takanori Sakaguchi, Toshio Nakamura, Naoto Yamamoto, Junko Sugatani, Masao Miwa, Hiroyuki Konno. (2006) A Single Nucleotide Polymorphism in the Plasma PAF Acetylhydrolase Gene and Risk of Atherosclerosis in Japanese Patients With Peripheral Artery Occlusive Disease. Journal of Surgical Research 134:1, 36-43
CrossRef146
Fu-jun ZHANG, Mao-jun CAI, Jing-kang SHEN, Yi-ping WANG. (2006) Expression and purification of lipoprotein-associated phospholipase A2, a key enzyme involved in atherosclerosis1. Acta Pharmacologica Sinica 27:6, 679-684
CrossRef147
J.A. Gómez-Gerique. (2006) Utilidad de los marcadores de inflamación en el diagnóstico del riesgo cardiovascular. Clínica e Investigación en Arteriosclerosis 18, 56-71
CrossRef148
Bo Zhang, Ping Fan, Eiso Shimoji, Hiroyuki Itabe, Shin-ichiro Miura, Yoshinari Uehara, Akira Matsunaga, Keijiro Saku. (2006) Modulating effects of cholesterol feeding and simvastatin treatment on platelet-activating factor acetylhydrolase activity and lysophosphatidylcholine concentration. Atherosclerosis 186:2, 291-301
CrossRef149
Richard B. Lanman, Robert L. Wolfert, James K. Fleming, Allan S. Jaffe, William L. Roberts, G. Russell Warnick, Joseph P. McConnell. (2006) Lipoprotein-Associated Phospholipase A 2 : Review and Recommendation of a Clinical Cut Point for Adults. Preventive Cardiology 9:3, 138-143
CrossRef150
Mitchell S. V. Elkind. (2006) Inflammation, Atherosclerosis, and Stroke. The Neurologist 12:3, 140-148
CrossRef151
P.-Y. LIU, Y.-H. LI, H.-L. WU, T.-H. CHAO, L.-M. TSAI, L.-J. LIN, G.-Y. SHI, J.-H. CHEN. (2006) Platelet-activating factor-acetylhydrolase A379V (exon 11) gene polymorphism is an independent and functional risk factor for premature myocardial infarction. Journal of Thrombosis and Haemostasis 4:5, 1023-1028
CrossRef152
Arduino A. Mangoni. (2006) Folic acid, inflammation, and atherosclerosis: False hopes or the need for better trials?. Clinica Chimica Acta 367:1-2, 11-19
CrossRef153
James T. Wu, Lily L. Wu. (2006) Linking inflammation and atherogenesis: Soluble markers identified for the detection of risk factors and for early risk assessment. Clinica Chimica Acta 366:1-2, 74-80
CrossRef154
Sotirios Tsimikas, James T. Willerson, Paul M. Ridker. (2006) C-Reactive Protein and Other Emerging Blood Biomarkers to Optimize Risk Stratification of Vulnerable Patients. Journal of the American College of Cardiology 47:8, C19-C31
CrossRef155
Krishnankutty Sudhir. (2006) Lipoprotein-associated phospholipase A2, vascular inflammation and cardiovascular risk prediction. Vascular Health and Risk Management 2:2, 153-156
CrossRef156
Karam M. Kostner, Robert B. Fahti, Colin Case, Peter Hobson, Jil Tate, Thomas H. Marwick. (2006) Inflammation, complement activation and endothelial function in stable and unstable coronary artery disease. Clinica Chimica Acta 365:1-2, 129-134
CrossRef157
J. SOLEM, M. LEVIN, T. KARLSSON, L. GRIP, P. ALBERTSSON, O. WIKLUND. (2006) Composition of coronary plaques obtained by directional atherectomy in stable angina: its relation to serum lipids and statin treatment. Journal of Internal Medicine 259:3, 267-275
CrossRef158
Pablo Piñón, Juan Carlos Kaski. (2006) Inflamación, aterosclerosis y riesgo cardiovascular: PAPP-A, Lp-PLA2 y cistatina C. ¿Nuevas aportaciones o información redundante?. Revista Española de Cardiología 59:3, 247-258
CrossRef159
Francisco Rodríguez Esparragón, Yaridé Hernández Trujillo, Antonio Macías Reyes, Enrique Hernández Ortega, Alfonso Medina, José C. Rodríguez Pérez. (2006) Sobre los genes paraoxonasa-1 y SR-B1, y su importancia en la aterosclerosis. Revista Española de Cardiología 59:2, 154-164
CrossRef160
Marieke van Oijen, Irene M. van der Meer, Albert Hofman, Jacqueline C. M. Witteman, Peter J. Koudstaal, Monique M. B. Breteler. (2006) Lipoprotein-associated phospholipase A2 is associated with risk of dementia. Annals of Neurology 59:1, 139-144
CrossRef161
Jan K. Damås, Pål Aukrust. (2006) Systemic markers of inflammation – are they useful predictive tools in coronary artery disease?. Scandinavian Cardiovascular Journal 40:5, 262-266
CrossRef162
Pedro Xavier, Luís Belo, Jorge Beires, Irene Rebelo, José Martinez-de-Oliveira, Nuno Lunet, Henrique Barros. (2006) Serum levels of VEGF and TNF-α and their association with C-reactive protein in patients with endometriosis. Archives of Gynecology and Obstetrics 273:4, 227-231
CrossRef163
Jennifer M. Aviles, Ronnier J. Aviles. (2005) Advances in Cardiac Biomarkers. Emergency Medicine Clinics of North America 23:4, 959-975
CrossRef164
Muriel J Caslake, Chris J Packard. (2005) Lipoprotein-associated phospholipase A2 as a biomarker for coronary disease and stroke. Nature Clinical Practice Cardiovascular Medicine 2:10, 529-535
CrossRef165
Annie C. St-Pierre, Bernard Cantin, Jean Bergeron, Matteo Pirro, Gilles R. Dagenais, Jean-Pierre Després, Benoît Lamarche. (2005) Inflammatory markers and long-term risk of ischemic heart disease in men. Atherosclerosis 182:2, 315-321
CrossRef166
Natalie Khuseyinova, Armin Imhof, Dietrich Rothenbacher, Gerlinde Trischler, Silke Kuelb, Hubert Scharnagl, Winfried Maerz, Hermann Brenner, Wolfgang Koenig. (2005) Association between Lp-PLA2 and coronary artery disease: Focus on its relationship with lipoproteins and markers of inflammation and hemostasis. Atherosclerosis 182:1, 181-188
CrossRef167
Michelle A. Albert, Robert J. Glynn, Robert L. Wolfert, Paul M. Ridker. (2005) The effect of statin therapy on lipoprotein associated phospholipase A2 levels. Atherosclerosis 182:1, 193-198
CrossRef168
Colin H Macphee, Jeanenne J Nelson, Andrew Zalewski. (2005) Lipoprotein-associated phospholipase A2 as a target of therapy. Current Opinion in Lipidology 16:4, 442-446
CrossRef169
Howard S. Weintraub. (2005) Treatment of multiple-risk patients: Using combination therapy to treat beyond LDL lowering. Current Hypertension Reports 7:4, 265-270
CrossRef170
Satish M Rachapalli. (2005) Inflammatory bowel diseases and atherosclerosis: Do we need more studies?. Inflammatory Bowel Diseases 11:7, 705-705
CrossRef171
David S. Celermajer. (2005) Primary and a Half Prevention. Journal of the American College of Cardiology 45:12, 1994-1996
CrossRef172
J. FROSTEGARD. (2005) SLE, atherosclerosis and cardiovascular disease. Journal of Internal Medicine 257:6, 485-495
CrossRef173
Colin Macphee, G Martin Benson, Yi Shi, Andrew Zalewski. (2005) Lipoprotein-associated phospholipase A 2 : a novel marker of cardiovascular risk and potential therapeutic target. Expert Opinion on Investigational Drugs 14:6, 671-679
CrossRef174
Haralampos J. Milionis, Afroditi P. Tambaki, Chrisa N. Kanioglou, Moses S. Elisaf, Alexandros D. Tselepis, Agathocles Tsatsoulis. (2005) Thyroid Substitution Therapy Induces High-Density Lipoprotein–Associated Platelet-Activating Factor–Acetylhydrolase in Patients with Subclinical Hypothyroidism: A Potential Antiatherogenic Effect. Thyroid 15:5, 455-460
CrossRef175
H-J Song, I Grant, D Rotondo, I Mohede, N Sattar, S D Heys, K W J Wahle. (2005) Effect of CLA supplementation on immune function in young healthy volunteers. European Journal of Clinical Nutrition 59:4, 508-517
CrossRef176
Roland W. McCallum, Christopher A. R. Sainsbury, Angela Spiers, Anna F. Dominiczak, John R. Petrie, Naveed Sattar, John M. C. Connell. (2005) Growth hormone replacement reduces C-reactive protein and large-artery stiffness but does not alter endothelial function in patients with adult growth hormone deficiency. Clinical Endocrinology 62:4, 473-479
CrossRef177
Ewa Ninio. (2005) Phospholipid mediators in the vessel wall: involvement in atherosclerosis. Current Opinion in Clinical Nutrition and Metabolic Care 8:2, 123-131
CrossRef178
Evangelos Rizos, Afroditi P. Tambaki, Irene Gazi, Alexandros D. Tselepis, Moses Elisaf. (2005) Lipoprotein-associated PAF-acetylhydrolase activity in subjects with the metabolic syndrome. Prostaglandins, Leukotrienes and Essential Fatty Acids 72:3, 203-209
CrossRef179
E. M. Stuveling. (2005) Biochemical risk markers: a novel area for better prediction of renal risk?. Nephrology Dialysis Transplantation 20:3, 497-508
CrossRef180
Evagelos N. Liberopoulos, Stella S. Daskalopoulou, Dimitri P. Mikhailidis, Anthony S. Wierzbicki, Moses S. Elisaf. (2005) A review of the lipid-related effects of fluvastatin. Current Medical Research and Opinion 21:2, 231-243
CrossRef181
I. J. Kullo, C. M. Ballantyne. (2005) Conditional Risk Factors for Atherosclerosis. Mayo Clinic Proceedings 80:2, 219-230
CrossRef182
Ron C Hoogeveen, Christie M Ballantyne. (2005) PLAC™ test for identification of individuals at increased risk for coronary heart disease. Expert Review of Molecular Diagnostics 5:1, 9-14
CrossRef183
David Brieger, S Benedict Freedman, Leonard Kritharides, Harry Lowe. 2004. Treatment of Vulnerable Plaques. , 164-202.
CrossRef184
Pai, Jennifer K., Pischon, Tobias, Ma, Jing, Manson, JoAnn E., Hankinson, Susan E., Joshipura, Kaumudi, Curhan, Gary C., Rifai, Nader, Cannuscio, Carolyn C., Stampfer, Meir J., Rimm, Eric B., . (2004) Inflammatory Markers and the Risk of Coronary Heart Disease in Men and Women. New England Journal of Medicine 351:25, 2599-2610
Full Text185
Eugene Davidov, Clary B. Clish, Matej Oresic, Michael Meys, Wayne Stochaj, Philip Snell, Gary Lavine, Thomas R. Londo, Aram Adourian, Xiang Zhang, Mark Johnston, Nicole Morel, Edward W. Marple, Thomas N. Plasterer, Eric Neumann, Elwin Verheij, Jack T.W.E. Vogels, Louis M. Havekes, Jan Van Der Greef, Stephen Naylor. (2004) Methods for the Differential Integrative Omic Analysis of Plasma from a Transgenic Disease Animal Model. OMICS: A Journal of Integrative Biology 8:4, 267-288
CrossRef186
AJ Marian, Vijay Nambi. (2004) Biomarkers of cardiac disease. Expert Review of Molecular Diagnostics 4:6, 805-820
CrossRef187
Anthony S Wierzbicki. (2004) Lipid-lowering therapies in development. Expert Opinion on Investigational Drugs 13:11, 1405-1418
CrossRef188
A.S. Wierzbicki. (2004) Lipid-altering agents: the future. International Journal of Clinical Practice 58:11, 1063-1072
CrossRef189
Takeshi Kujiraoka, Hiroaki Hattori, Mayumi Ito, M.Nazeem Nanjee, Mitsuaki Ishihara, Makoto Nagano, Tadao Iwasaki, C.Justin Cooke, Waldemar L Olszewski, Irina P Stepanova, Tohru Egashira, Norman E Miller. (2004) Effects of intravenous apolipoprotein A-I/phosphatidylcholine discs on paraoxonase and platelet-activating factor acetylhydrolase in human plasma and tissue fluid. Atherosclerosis 176:1, 57-62
CrossRef190
Anna Cederholm, Elisabet Svenungsson, Dominique Stengel, Guo-Zhong Fei, A. Graham Pockley, Ewa Ninio, Johan Frosteg
rd. (2004) Platelet-activating factor-acetylhydrolase and other novel risk and protective factors for cardiovascular disease in systemic lupus erythematosus. Arthritis & Rheumatism 50:9, 2869-2876
CrossRef191
Daniel M Robinson, Christian Schwahn, Dietrich Alte, Ulrich John, Stephan B Felix, Henry V??lzke. (2004) Plasma fibrinogen levels are associated with a strong family history of myocardial infarction. Blood Coagulation & Fibrinolysis 15:6, 497-502
CrossRef192
Mike Mackness, Paul Durrington, Bharti Mackness. (2004) Paraoxonase 1 activity, concentration and genotype in cardiovascular disease. Current Opinion in Lipidology 15:4, 399-404
CrossRef193
David W McCarey, Iain B McInnes, Rajan Madhok, Rosie Hampson, Olga Scherbakova, Ian Ford, Hilary A Capell, Naveed Sattar. (2004) Trial of Atorvastatin in Rheumatoid Arthritis (TARA): double-blind, randomised placebo-controlled trial. The Lancet 363:9426, 2015-2021
CrossRef194
Chu-Huang Chen. (2004) Platelet-activating factor acetylhydrolase: is it good or bad for you?. Current Opinion in Lipidology 15:3, 337-341
CrossRef195
Danesh, John, Wheeler, Jeremy G., Hirschfield, Gideon M., Eda, Shinichi, Eiriksdottir, Gudny, Rumley, Ann, Lowe, Gordon D.O., Pepys, Mark B., Gudnason, Vilmundur, . (2004) C-Reactive Protein and Other Circulating Markers of Inflammation in the Prediction of Coronary Heart Disease. New England Journal of Medicine 350:14, 1387-1397
Full Text196
Eliana Reyes, Constantinos Anagnostopoulos. (2004) The prognostic value of myocardial perfusion imaging in patients with suspected or known coronary artery disease. Nuclear Medicine Communications 25:3, 217-220
CrossRef197
Doron Aronson. (2004) Inflammatory markers: linking unstable plaques to coronary event, an interventional perspective. Acute Cardiac Care 6:3-4, 110-118
CrossRef198
Clary B. Clish, Eugene Davidov, Matej Oresic, Thomas N. Plasterer, Gary Lavine, Tom Londo, Michael Meys, Philip Snell, Wayne Stochaj, Aram Adourian, Xiang Zhang, Nicole Morel, Eric Neumann, Elwin Verheij, Jack T.W.E. Vogels, Louis M. Havekes, Noubar Afeyan, Fred Regnier, Jan Van Der Greef, Stephen Naylor. (2004) Integrative Biological Analysis of the APOE*3-Leiden Transgenic Mouse. OMICS: A Journal of Integrative Biology 8:1, 3-13
CrossRef199
Michael I Mackness, Paul N Durrington, Bharti Mackness. (2004) The Role of Paraoxonase 1 Activity in Cardiovascular Disease. American Journal of Cardiovascular Drugs 4:4, 211-217
CrossRef200
Jerzy Be??towski, Gra??yna W??jcicka, Anna Jamroz. (2004) Effect of 3-hydroxy-3-methylglutarylcoenzyme A Reductase Inhibitors (Statins) on Tissue Paraoxonase 1 and Plasma Platelet Activating Factor Acetylhydrolase Activities. Journal of Cardiovascular Pharmacology 43:1, 121-127
CrossRef201
J. Skogsberg, A. D. McMahon, F. Karpe, A. Hamsten, C. J. Packard, E. Ehrenborg, . (2003) Peroxisome proliferator activated receptor delta genotype in relation to cardiovascular risk factors and risk of coronary heart disease in hypercholesterolaemic men. Journal of Internal Medicine 254:6, 597-604
CrossRef202
Anthony S Wierzbicki. (2003) New lipid-lowering agents. Expert Opinion on Emerging Drugs 8:2, 365-376
CrossRef203
Gavin J. Blake. (2003) Inflammatory biomarkers of the patient with myocardial insufficiency. Current Opinion in Critical Care 9:5, 369-374
CrossRef204
Marcello Rattazzi, Massimo Puato, Elisabetta Faggin, Barbara Bertipaglia, Alberto Zambon, Paolo Pauletto. (2003) C-reactive protein and interleukin-6 in vascular disease. Journal of Hypertension 21:10, 1787-1803
CrossRef205
Paul M. Ridker, Shari S. Bassuk, Peter P. Toth. (2003) C-reactive protein and risk of cardiovascular disease: Evidence and clinical application. Current Atherosclerosis Reports 5:5, 341-349
CrossRef206
Muriel J. Caslake, Chris J. Packard. (2003) Lipoprotein-associated phospholipase A2 (platelet-activating factor acetylhydrolase) and cardiovascular disease. Current Opinion in Lipidology 14:4, 347-352
CrossRef207
Ronald G. Craig, Julie K. Yip, Man Ki So, Robert J. Boylan, Sigmund S. Socransky, Anne D. Haffajee. (2003) Relationship of Destructive Periodontal Disease to the Acute-Phase Response. Journal of Periodontology 74:7, 1007-1016
CrossRef208
A.M. Abuzeid, E. Hawe, S.E. Humphries, Philippa J. Talmud. (2003) Association between the Ala379Val variant of the lipoprotein associated phospholipase A2 and risk of myocardial infarction in the north and south of Europe. Atherosclerosis 168:2, 283-288
CrossRef209
Anho Liem, Giny H Reynierse-Buitenwerf, Aeilko H Zwinderman, J.Wouter Jukema, Dirk J van Veldhuisen. (2003) Secondary prevention with folic acid: effects on clinical outcomes. Journal of the American College of Cardiology 41:12, 2105-2113
CrossRef210
F. Stam. (2003) Impaired renal function is associated with markers of endothelial dysfunction and increased inflammatory activity. Nephrology Dialysis Transplantation 18:5, 892-898
CrossRef211
H. Robert Superko. (2003) Sophisticated Tests for Susceptibility to Atherosclerosis:An Added Value for Heart Hospitals. The American Heart Hospital Journal 1:2, 135-140
CrossRef212
Steven E Lipshultz, Stacy D Fisher, Wyman W Lai, Tracie L Miller. (2003) Cardiovascular risk factors, monitoring, and therapy for HIV-infected patients. AIDS 17, S96-S122
CrossRef213
Josie A. Blackie, Jackie C. Bloomer, Murray J.B. Brown, Hung-Yuan Cheng, Beverley Hammond, Deirdre M.B. Hickey, Robert J. Ife, Colin A. Leach, V.Ann Lewis, Colin H. Macphee, Kevin J. Milliner, Kitty E. Moores, Ivan L. Pinto, Stephen A. Smith, Ian G. Stansfield, Steven J. Stanway, Maxine A. Taylor, Colin J. Theobald. (2003) The identification of clinical candidate SB-480848: a potent inhibitor of lipoprotein-associated phospholipase A2. Bioorganic & Medicinal Chemistry Letters 13:6, 1067-1070
CrossRef214
Ken Karasawa, Ayako Harada, Noriko Satoh, Keizo Inoue, Morio Setaka. (2003) Plasma platelet activating factor-acetylhydrolase (PAF-AH). Progress in Lipid Research 42:2, 93-114
CrossRef215
Gavin J Blake, Paul M Ridker. (2003) C-reactive protein and other inflammatory risk markers in acute coronary syndromes. Journal of the American College of Cardiology 41:4, S37-S42
CrossRef216
Polkit Sangvanich, Bharti Mackness, Simon J Gaskell, Paul Durrington, Michael Mackness. (2003) The effect of high-density lipoproteins on the formation of lipid/protein conjugates during in vitro oxidation of low-density lipoprotein. Biochemical and Biophysical Research Communications 300:2, 501-506
CrossRef217
M.A van de Ree, M.V Huisman, H.M.G Princen, A.E Meinders, C Kluft. (2003) Strong decrease of high sensitivity C-reactive protein with high-dose atorvastatin in patients with type 2 diabetes mellitus. Atherosclerosis 166:1, 129-135
CrossRef218
M. Serban, Cristina Tanaseanu, T. Kosaka, Cristina Vidulescu, Irina Stoian, Daciana S. Marta, S. Tanaseanu, Elena Moldoveanu. (2002) Significance of platelet-activating factor acetylhydrolase in patients with non-insulin-dependent (type 2) diabetes mellitus. Journal of Cellular and Molecular Medicine 6:4, 643-647
CrossRef219
Josie A. Blackie, Jackie C. Bloomer, Murray J.B. Brown, Hung-Yuan Cheng, Richard L. Elliott, Beverley Hammond, Deirdre M.B. Hickey, Robert J. Ife, Colin A. Leach, V.Ann Lewis, Colin H. Macphee, Kevin J. Milliner, Kitty E. Moores, Ivan L. Pinto, Stephen A. Smith, Ian G. Stansfield, Steven J. Stanway, Maxine A. Taylor, Colin J. Theobald, Caroline M. Whittaker. (2002) The discovery of SB-435495. Bioorganic & Medicinal Chemistry Letters 12:18, 2603-2606
CrossRef220
Makoto Hase, Masashi Tanaka, Mitsuhiro Yokota, Yoshiji Yamada. (2002) Reduction in the extent of atherosclerosis in apolipoprotein E-deficient mice induced by electroporation-mediated transfer of the human plasma platelet-activating factor acetylhydrolase gene into skeletal muscle. Prostaglandins & Other Lipid Mediators 70:1-2, 107-118
CrossRef221
James S. Zebrack, Jeffrey L. Anderson. (2002) Role of Inflammation in Cardiovascular Disease: How to Use C-Reactive Protein in Clinical Practice. Progress in Cardiovascular Nursing 17:4, 174-185
CrossRef222
Bharti Mackness, Paul N. Durrington, Michael I. Mackness. (2002) The paraoxonase gene family and coronary heart disease. Current Opinion in Lipidology 13:4, 357-362
CrossRef223
Colin H Macphee, Keith E Suckling. (2002) Lipoprotein-associated phospholipase A 2 : a target directed at the atherosclerotic plaque. Expert Opinion on Therapeutic Targets 6:3, 309-314
CrossRef224
C. Erik Hack, Hans W. M. Niessen. (2002) Cardiovascular secrets of secretory phospholipase A2. European Journal of Clinical Investigation 32:6, 381-382
CrossRef225
Charlotte A Burton, Sushma Patel, Steven Mundt, Heide Hassing, Donghui Zhang, Anne Hermanowski-Vosatka, Samuel D Wright, Yu-Sheng Chao, Patricia A Detmers, Carl P Sparrow. (2002) Deficiency in does not affect HDL levels or atherosclerosis in mice. Biochemical and Biophysical Research Communications 294:1, 88-94
CrossRef226
Helen F. Boyd, Stephen C.M. Fell, Deirdre M.B. Hickey, Robert J. Ife, Colin A. Leach, Colin H. Macphee, Kevin J. Milliner, Ivan L. Pinto, D.Anthony Rawlings, Stephen A. Smith, Ian G. Stansfield, Steven J. Stanway, Colin J. Theobald, Caroline M. Whittaker. (2002) Potent, orally active inhibitors of lipoprotein-associated phospholipase A2: 1-(biphenylmethylamidoalkyl)-pyrimidones. Bioorganic & Medicinal Chemistry Letters 12:1, 51-55
CrossRef227
David Williams, John Feely. (2002) Pharmacokinetic-Pharmacodynamic Drug Interactions with HMG-CoA Reductase Inhibitors. Clinical Pharmacokinetics 41:5, 343-370
CrossRef228
Nisha Dada, Nam W Kim, Robert L Wolfert. (2002) Lp-PLA2: an emerging biomarker of coronary heart disease. Expert Review of Molecular Diagnostics 2:1, 17-22
CrossRef229
STEVEN E. LIPSHULTZ, STACY D. FISHER, WYMAN W. LAI, TRACIE L. MILLER. (2001) Cardiovascular Monitoring and Therapy for HIV-Infected Patients. Annals of the New York Academy of Sciences 946:1, 236-273
CrossRef230
Gavin J Blake, Nisha Dada, Jonathan C Fox, JoAnn E Manson, Paul M Ridker. (2001) A prospective evaluation of lipoprotein-associated phospholipase A2 levels and the risk of future cardiovascular events in women. Journal of the American College of Cardiology 38:5, 1302-1306
CrossRef231
Marek H. Dominiczak. (2001) Risk Factors for Coronary Disease: the Time for a Paradigm Shift?. Clinical Chemistry and Laboratory Medicine 39:10, 907-919
CrossRef232
Antonio Cano, W.Marchien Van Baal. (2001) The mechanisms of thrombotic risk induced by hormone replacement therapy. Maturitas 40:1, 17-38
CrossRef233
Christie M. Ballantyne. (2001) Newer risk markers and surrogate endpoints in atherosclerosis management. Clinical Cardiology 24:S3, 13-17
CrossRef234
Jackie C. Bloomer, Helen F. Boyd, Deirdre M.B. Hickey, Robert J. Ife, Colin A. Leach, Colin H. Macphee, Kevin J. Milliner, Ivan L. Pinto, D.Anthony Rawlings, Stephen A. Smith, Ian G. Stansfield, Steven J. Stanway, Maxine A. Taylor, Colin J. Theobald, Caroline M. Whittaker. (2001) 1-(Arylpiperazinylamidoalkyl)-pyrimidones: orally active inhibitors of lipoprotein-associated phospholipase A2. Bioorganic & Medicinal Chemistry Letters 11:14, 1925-1929
CrossRef235
Craig H Selzman. (2001) Current approaches to therapy for vascular injury. Expert Opinion on Pharmacotherapy 2:5, 753-764
CrossRef236
C Macphee. (2001) Lipoprotein-associated phospholipase A2: a potential new risk factor for coronary artery disease and a therapeutic target. Current Opinion in Pharmacology 1:2, 121-125
CrossRef237
Helen F. Boyd, Beverley Hammond, Deirdre M.B. Hickey, Robert J. Ife, Colin A. Leach, V.Ann Lewis, Colin H. Macphee, Kevin J. Milliner, Ivan L. Pinto, Stephen A. Smith, Ian G. Stansfield, Colin J. Theobald, Caroline M. Whittaker. (2001) The identification of a potent, water soluble inhibitor of lipoprotein-associated phospholipase A2. Bioorganic & Medicinal Chemistry Letters 11:5, 701-704
CrossRef238
Rader, Daniel J., . (2000) Inflammatory Markers of Coronary Risk. New England Journal of Medicine 343:16, 1179-1182
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