scholarly journals Lipoprotein(a) concentration is associated with plasma arachidonic acid in subjects with familial hypercholesterolaemia

2019 ◽  
Vol 122 (07) ◽  
pp. 790-799
Author(s):  
Ingunn Narverud ◽  
Martin P. Bogsrud ◽  
Linn K. L. Øyri ◽  
Stine M. Ulven ◽  
Kjetil Retterstøl ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Plasma Levels ◽  
Familial Hypercholesterolaemia ◽  
Daily Intake ◽  
Lifestyle Changes ◽  
Dietary Fatty Acids ◽  
Lipoprotein A ◽  
Multivariable Analyses ◽  
Flame Ionisation Detector ◽  
Genetically Determined

AbstractElevated lipoprotein(a) (Lp(a)) is associated with CVD and is mainly genetically determined. Studies suggest a role of dietary fatty acids (FA) in the regulation of Lp(a); however, no studies have investigated the association between plasma Lp(a) concentration and n-6 FA. We aimed to investigate whether plasma Lp(a) concentration was associated with dietary n-6 FA intake and plasma levels of arachidonic acid (AA) in subjects with familial hypercholesterolaemia (FH). We included FH subjects with (n 68) and without (n 77) elevated Lp(a) defined as ≥75 nmol/l and healthy subjects (n 14). Total FA profile was analysed by GC–flame ionisation detector analysis, and the daily intake of macronutrients (including the sum of n-6 FA: 18 : 2n-6, 20 : 2n-6, 20 : 3n-6 and 20 : 4n-6) were computed from completed FFQ. FH subjects with elevated Lp(a) had higher plasma levels of AA compared with FH subjects without elevated Lp(a) (P = 0·03). Furthermore, both FH subjects with and without elevated Lp(a) had higher plasma levels of AA compared with controls (P < 0·001). The multivariable analyses showed associations between dietary n-6 FA intake and plasma levels of AA (P = 0·02) and between plasma levels of Lp(a) and AA (P = 0·006). Our data suggest a novel link between plasma Lp(a) concentration, dietary n-6 FA and plasma AA concentration, which may explain the small diet-induced increase in Lp(a) levels associated with lifestyle changes. Although the increase may not be clinically relevant, this association may be mechanistically interesting in understanding more of the role and regulation of Lp(a).

Plasma Levels of Lipoprotein(a) Are Elevated in Patients with the Antiphospholipid Antibody Syndrome

1994 ◽  
Vol 71 (04) ◽  
pp. 424-427 ◽  
Author(s):  
Masahide Yamazaki ◽  
Hidesaku Asakura ◽  
Hiroshi Jokaji ◽  
Masanori Saito ◽  
Chika Uotani ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Active Form ◽  
Plasminogen Activator Inhibitor ◽  
Arterial System ◽  
Control Group ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Lipoprotein A ◽  
Soluble Thrombomodulin ◽  
Relationship Of

SummaryThe mechanisms underlying clinical abnormalities associated with the antiphospholipid antibody syndrome (APAS) have not been elucidated. We measured plasma levels of lipoprotein(a) [Lp(a)], the active form of plasminogen activator inhibitor (active PAI), thrombin-antithrombin III complex (TAT) and soluble thrombomodulin (TM), to investigate the relationship of these factors to thrombotic events in APAS. Mean plasma levels of Lp(a), TAT, active PAI and TM were all significantly higher in patients with aPL than in a control group of subjects. Plasma levels of Lp(a) and active PAI were significantly higher in patients with aPL and arterial thromboses than in patients with aPL but only venous thromboses. There was a significant correlation between plasma levels of Lp(a) and active PAI in patients with aPL. These findings suggest that patients with aPL are in hypercoagulable state. High levels of Lp(a) in plasma may impair the fibrinolytic system resulting in thromboses, especially in the arterial system.

The d-Enantiomer Form of Indobufen Totally Accounts for the Anti-Cyclooxygenase and Antiplatelet Activity Ex Vivo and for the Increase in Bleeding Time by Indobufen in Man

1992 ◽  
Vol 67 (02) ◽  
pp. 258-263 ◽  
Author(s):  
Raffaele De Caterina ◽  
Rosa Sicari ◽  
An Yan ◽  
Walter Bernini ◽  
Daniela Giannessi ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Plasma Levels ◽  
Bleeding Time ◽  
Ex Vivo ◽  
Random Sequence ◽  
Antiplatelet Agent ◽  
Antiplatelet Drug ◽  
Double Blind

SummaryIndobufen is an antiplatelet drug able to inhibit thromboxane production and cyclooxygenase-dependent platelet aggregation by a reversible inhibition of cyclooxygenase. Indobufen exists in two enantiomeric forms, of which only d-indobufen is active in vitro in inhibiting cyclooxygenase. In order to verify that also inhibition of platelet function is totally accounted for by d-indobufen, ten patients with proven coronary artery disease (8 male, 2 female, age, mean ± S.D., 58.7 ± 7.5 years) were given, in random sequence, both 100 mg d-indobufen and 200 mg dl-indobufen as single administrations in a double-blind crossover design study with a washout period between treatments of 72 h. In all patients thromboxane (TX) B2 generation after spontaneous clotting (at 0, 1, 2, 4, 6, 8, 12, 24 h), drug plasma levels (at the same times), platelet aggregation in response to ADP, adrenaline, arachidonic acid, collagen, PAF, and bleeding time (at 0, 2, 12 h) were evaluated after each treatment. Both treatments determined peak inhibition of TXB2 production at 2 h from administration, with no statistical difference between the two treatments (97 ±3% for both treatments). At 12 h inhibition was 87 ± 6% for d-indobufen and 88 ± 6% for dl-indobufen (p = NS). Inhibition of TXB2 production correlated significantly with plasma levels of the drugs. Maximum inhibitory effect on aggregation was seen in response to collagen 1.5 pg/ml (63 ± 44% for d-indobufen and 81 ± 22% for dl-indobufen) and arachidonic acid 0.5-2 mM (78 ± 34% for d-indobufen and 88 ± 24% for dl-indobufen) at 2 h after each administration. An effect of both treatments on platelet aggregation after 12 h was present only for adrenaline 2 μM (55 ± 41% for d-indobufen and 37 ± 54% for dl-indobufen), collagen 1.5 pg/ml (69 ± 30% for d-indobufen and 51 ± 61% for dl-indobufen), arachidonic acid 0.5-2 mM (56 ± 48% for d-indobufen and 35 ± 49% for dl-indobufen). The extent of inhibition of TX production and the extent of residual platelet aggregation were never significantly different between treatments. Bleeding time prolongation was similar in the two treatment groups without showing a pronounced and long lasting effect (from 7.0 ± 2.0 min to 10.0 ± 3.0 min at 2 h and 8.0 ± 2.0 min at 12 h for d-indobufen; from 6.0 ±1.0 min to 8.5 ± 2.0 min at 2 h and 8.0 ± 1.0 min at 12 h for dl-indobufen). These results demonstrate that the biological activity of dl-indobufen as an antiplatelet agent in vivo is totally accounted for by d-indobufen.

Lipoprotein (a) Evolution: Possible Benefits and Harm. Genetic and Non-Genetic Factors Influencing its Plasma Levels

2017 ◽  
Vol 24 (10) ◽  
pp. 969-978 ◽  
Author(s):  
Peggy M. Kostakou ◽  
George Hatzigeorgiou ◽  
Vana Kolovou ◽  
Sophie Mavrogeni ◽  
Genovefa D. Kolovou
Keyword(s):  
Plasma Levels ◽  
Genetic Factors ◽  
Lipoprotein A ◽  
Factors Influencing

scholarly journals Lipoprotein(a): A Genetically Determined, Causal, and Prevalent Risk Factor for Atherosclerotic Cardiovascular Disease: A Scientific Statement From the American Heart Association

2021 ◽  
Author(s):  
Gissette Reyes-Soffer ◽  
Henry N. Ginsberg ◽  
Lars Berglund ◽  
P. Barton Duell ◽  
Sean P. Heffron ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Risk Factor ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Density Lipoprotein ◽  
Major Protein ◽  
Atherosclerotic Cardiovascular Disease ◽  
Lipoprotein A ◽  
Scientific Statement ◽  
Genetically Determined

High levels of lipoprotein(a) [Lp(a)], an apoB100-containing lipoprotein, are an independent and causal risk factor for atherosclerotic cardiovascular diseases through mechanisms associated with increased atherogenesis, inflammation, and thrombosis. Lp(a) is predominantly a monogenic cardiovascular risk determinant, with ≈70% to ≥90% of interindividual heterogeneity in levels being genetically determined. The 2 major protein components of Lp(a) particles are apoB100 and apolipoprotein(a). Lp(a) remains a risk factor for cardiovascular disease development even in the setting of effective reduction of plasma low-density lipoprotein cholesterol and apoB100. Despite its demonstrated contribution to atherosclerotic cardiovascular disease burden, we presently lack standardization and harmonization of assays, universal guidelines for diagnosing and providing risk assessment, and targeted treatments to lower Lp(a). There is a clinical need to understand the genetic and biological basis for variation in Lp(a) levels and its relationship to disease in different ancestry groups. This scientific statement capitalizes on the expertise of a diverse basic science and clinical workgroup to highlight the history, biology, pathophysiology, and emerging clinical evidence in the Lp(a) field. Herein, we address key knowledge gaps and future directions required to mitigate the atherosclerotic cardiovascular disease risk attributable to elevated Lp(a) levels.

Mipomersen treatment decreases lipoprotein (a) plasma levels by increasing its fractional clearance from plasma

2017 ◽  
Vol 263 ◽  
pp. e27
Author(s):  
Gissette Reyes-Soffer ◽  
Marianna Pavlyha ◽  
Colleen Ngai ◽  
Tiffany Thomas ◽  
Stephen Hollearn ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Lipoprotein A ◽  
Fractional Clearance

scholarly journals Lipoprotein(a) and familial hypercholesterolaemia

2016 ◽  
Vol 4 (9) ◽  
pp. 730 ◽  
Author(s):  
Leopoldo Pérez de Isla ◽  
Adriana Saltijeral Cerezo ◽  
Rodrigo Alonso ◽  
Pedro Mata
Keyword(s):  
Familial Hypercholesterolaemia ◽  
Lipoprotein A

Lipoprotein(a) Levels at Birth and in Early Childhood - The COMPARE Study

2021 ◽  
Author(s):  
Nina Strandkjær ◽  
Malene Kongsgaard Hansen ◽  
Sofie Taageby Nielsen ◽  
Ruth Frikke-Schmidt ◽  
Anne Tybjærg-Hansen ◽  
...  
Keyword(s):  
Cord Blood ◽  
Early Life ◽  
Adult Population ◽  
Venous Blood ◽  
Blood Levels ◽  
Predictive Values ◽  
Lipoprotein A ◽  
Genetically Determined ◽  
Compare Study

Abstract Background and objective High lipoprotein(a) is a genetically determined causal risk factor for cardiovascular disease and 20% of the adult population has high levels (i.e. >42 mg/dL, >88 nmol/L). We investigated whether early life lipoprotein(a) levels measured in cord blood may serve as a proxy for neonatal venous blood levels, whether lipoprotein(a) birth levels (i.e. cord or venous) predict levels later in life, and whether early life and parental levels correlate. Methods The COMPARE study is a prospective cohort study of newborns (N=450) from Copenhagen, Denmark including blood sampling of parents. Plasma lipoprotein(a) was measured in cord blood (N=402), neonatal venous blood (N=356), and at 2 (N=320) and 15 months follow-up (N=148) of infants, and in parents (N=705). Results Mean lipoprotein(a) levels were 2.2(95%CI:1.9-2.5), 2.4(2.0-2.7), 4.1(3.4-4.9), and 14.6(11.4-17.9) mg/dL in cord, neonatal venous, and 2- and 15-months venous samples, respectively. Lipoprotein(a) levels in cord blood correlated strongly with neonatal venous blood levels (R2=0.95, p<0.001) and neonatal levels correlated moderately with 2- and 15-months levels (R2=0.68 and 0.67, both p<0.001). Birth levels ≥90th percentile predicted lipoprotein(a) >42 mg/dL at 15 months with positive predictive values of 89% and 85% for neonatal venous and cord blood. Neonatal and infant levels correlated weakly with parental levels, most pronounced at 15 months (R2=0.22, p<0.001). Conclusions Lipoprotein(a) levels are low in early life, cord blood may serve as a proxy for neonatal venous blood, and birth levels ≥90th percentile can identify newborns at risk of developing high levels.

Effect of bariatric surgery on plasma levels of oxidised phospholipids, biomarkers of oxidised LDL and lipoprotein(a)

2020 ◽  
Author(s):  
Jan Hoong Ho ◽  
Safwaan Adam ◽  
Yifen Liu ◽  
Shazli Azmi ◽  
Shaishav Dhage ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Plasma Levels ◽  
Oxidised Ldl ◽  
Lipoprotein A

P6272The relationship between plasma levels of lipoprotein(a) [Lp(a)], PCSK9 and their complex in hypercholesterolemic patients depends on the apolipoprotein(a) phenotype

2018 ◽  
Vol 39 (suppl_1) ◽  
Author(s):  
E A Klesareva ◽  
O I Afanasieva ◽  
O A Razova ◽  
E A Utkina ◽  
M I Afanasieva ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Lipoprotein A ◽  
Apolipoprotein A

The unique lipoprotein(a): properties and immunochemical measurement

1990 ◽  
Vol 36 (12) ◽  
pp. 2019-2026 ◽  
Author(s):  
J J Albers ◽  
S M Marcovina ◽  
M S Lodge
Keyword(s):  
Rapid Development ◽  
Structural Complexity ◽  
Structural Domains ◽  
Lipoprotein A ◽  
Apolipoprotein A ◽  
High Amino Acid ◽  
Multiple Copies ◽  
High Concentrations ◽  
Size Heterogeneity ◽  
Genetically Determined

Abstract Lipoprotein (a) [Lp(a)] represents a class of lipoprotein particles defined by the presence of apolipoprotein(a), a unique glycoprotein linked by a disulfide bond to apolipoprotein B-100 to form a single macromolecule. Apolipoprotein(a) is formed by three different structural domains having high amino acid sequence homology with plasminogen. One of the domains, called kringle 4, is present in multiple copies, the number of which varies and is genetically determined. This accounts for the size heterogeneity of apolipoprotein(a) and thus of Lp(a). Because high concentrations of Lp(a) are associated with atherosclerotic cardiovascular and cerebrovascular disease and may inhibit fibrinolysis, interest in measuring Lp(a) has increased considerably, leading to a rapid development of commercially available immunoassays for the measurement of Lp(a) in human plasma. However, the immunochemical measurement of Lp(a) has several peculiar problems in addition to those encountered by the measurements of other apolipoproteins. The major problems that need to be carefully evaluated are (a) the structural complexity and heterogeneity of Lp(a), (b) the homology of apolipoprotein(a) with plasminogen, (c) the lack of standardization of the methods, and (d) the lack of a common means of expressing the Lp(a) values.

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