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  • 1
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    Abstract 3132: Paraoxonase-1 Activity Is not Independently Related with the Risk of Future Coronary Artery Disease
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Circulation Vol. 118, No. suppl_18 ( 2008-10-28)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. suppl_18 ( 2008-10-28)
    Kurzfassung: Background Paraoxonase-1 (PON1) is a potent antioxidant enzyme bound to high-density lipoprotein (HDL). Its activity, but not its concentration, is controlled by the PON1 Q192R polymorphism. PON1 is considered to protect against atherogenesis, but it is unclear whether this relation is independent of its carrier, HDL. Objective To evaluate the predictive value of PON1 for coronary artery disease (CAD) we assessed PON1 activity and genotype (Q192R polymorphism) in a large cohort. Methods and results We performed a case-control study nested in the prospective EPIC-Norfolk cohort. Cases (n = 1138) were apparently healthy men and women aged 45–79 years who developed fatal or nonfatal CAD during a mean follow-up of 6 years. Controls (n=2237) were matched by age and sex. Serum PON1 activity was lower in cases vs. controls (59.9 ± 44.6 U/L vs. 63.4 ± 46.7 U/L, p=0.020) and correlated with HDL cholesterol (r= 0.16, p 〈 0.0001). Whereas the PON1 Q192R polymorphism strongly controlled PON1 activity (QQ: 27 ± 9, QR: 87 ± 27 and RR 152 ± 44 U/L), it was not related to the risk of future CAD (Odds Ratio [OR] per R allele 0.98 [0.84–1.15] , p=0.84). Using conditional logistic regression, quartiles of PON1 activity showed a modest inverse relation with CAD risk (OR for the highest vs. the lowest quartile 0.77 [0.63– 0.95], p=0.013; p for trend over quartiles 0.064). PON1 activity adjusted for Q192R genotype - a proxy for PON1 concentration -correlated better with HDL cholesterol (r=0.29, p 〈 0.0001) and strongly predicted CAD risk (OR for the highest versus the lowest quartile 0.72 (0.58 – 0.91), p for trend over quartiles = 0.005). However, this relation was abolished after adjustment for HDL related parameters (HDL particle number, HDL cholesterol, HDL size and apolipoprotein A-I; OR for highest vs. lowest quartile 0.87 [0.66 –1.16], p for trend over quartiles = 0.13). Conclusion In the largest prospective study to date, we show that PON1 activity inversely relates to CAD risk, but not independently of HDL, presumably due to its close association with the HDL particle. Since the Q192R polymorphism profoundly affects lifelong PON1 activity, our inability to demonstrate a relation between the Q192R polymorphism and CAD risk suggests that PON1 activity is not a causal factor in atherogenesis.
    Materialart: Online-Ressource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.118.suppl_18.S_1099
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2008
    ZDB Id: 1466401-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
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    Abstract 11043: Clinical Safety Outcomes in Relation to Lipoprotein(a) Concentration: Insights from the FOURIER Trial
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Vol. 144, No. Suppl_1 ( 2021-11-16)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 144, No. Suppl_1 ( 2021-11-16)
    Kurzfassung: Background: Lipoprotein(a) is believed to play a causal role in atherogenesis. Drugs are in development that directly target Lp(a) and lower levels by 〉 75%. Thus, the safety of low Lp(a) levels is of importance. Methods: FOURIER randomized 27,564 patients w/ stable ASCVD to evolocumab (EVO) vs placebo on background statin (median f/up 2.2 y); EVO lowered Lp(a) levels by 27%. The relationships between Lp(a) levels, change in Lp(a) and 5 safety outcomes of interest based on prior reports (diabetes [DM], serious bleeding, hemorrhagic stroke, neurocognitive events, malignancy) were examined. Analyses were conducted in the overall population and by treatment arm. Multivariable models included age, sex, race, region, clinical predictors, high-intensity statin, ezetimibe, baseline hs-CRP, “Lp(a)-corrected” LDL-C, and treatment arm. Results: Lp(a) was assessed in 25,083 participants at baseline (median 37nM, range 5-1451) and 25,686 at week 12. There was no association between baseline or achieved Lp(a) levels and risk of serious bleeding, hemorrhagic stroke, neurocognitive events, or malignancy, even in the 3271 patients with Lp(a) levels ≤6nM. There was an inverse association between baseline Lp(a) levels and prevalent or incident DM [OR 1.09, 95%CI 1.07-1.12, for every 50nM lower Lp(a) below 250nM]. However, absolute change in Lp(a) with EVO was not associated with subsequent DM risk (HR 1.03, 0.91-1.16, per 50nM) and EVO did not increase the risk of DM irrespective of baseline Lp(a) (P int=0.97), even in participants in the top decile of baseline Lp(a) (HR 0.91, 0.51-1.62) in whom EVO reduced Lp(a) by 63nM. Conclusion: Lp(a) concentration and changes in Lp(a) were not associated with serious bleeding, hemorrhagic stroke, neurocognitive events, or malignancy. Levels were inversely correlated with having DM, but Lp(a) lowering over a median of 2.2 years with EVO did not further increase the risk. These findings provide new insights for ongoing trials of Lp(a)-lowering drugs.
    Materialart: Online-Ressource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.144.suppl_1.11043
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2021
    ZDB Id: 1466401-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
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    Mycophenolate mofetil but not atorvastatin attenuates atherosclerosis in lupus-prone LDLr −/− mice
    BMJ ; 2012
    In:  Annals of the Rheumatic Diseases Vol. 71, No. 3 ( 2012-03), p. 408-414
    Details
    In: Annals of the Rheumatic Diseases, BMJ, Vol. 71, No. 3 ( 2012-03), p. 408-414
    Kurzfassung: Recent clinical and preclinical studies have demonstrated that systemic lupus erythematosus (SLE) is associated with an increased risk for cardiovascular disease (CVD). However, unlike in the general population, little is known regarding the efficacy of atheroprotective interventions in patients with SLE. The current study aims to determine the benefit of lymphocyte inhibition on reducing the atherosclerotic burden in SLE-susceptible LDLr-deficient mice. Methods Female LDLr −/− mice were lethally irradiated and reconstituted with bone marrow from C57Bl/6 mice (LDLr.B6) or the SLE-susceptible B6. Sle1.2.3 mice (LDLr. Sle ). At 16 weeks post transplant, mice were treated with atorvastatin (10 mg/kg), mycophenolate mofetil (MMF; 40 mg/kg), or both (MMF-A) for 8 weeks, after which the extent of atherosclerosis and the presence of SLE were assessed. Results Following 8 weeks of treatment, we observed that atorvastatin-mediated reduction in cholesterol levels attenuated atherogenesis in LDLr.B6 mice but failed to significantly reduce atherosclerotic lesion size in LDLr. Sle mice, in spite of a significant reduction in serum cholesterol levels. Treatment with MMF and MMF-A attenuated atherogenesis in LDLr.B6 and LDLr. Sle mice. In addition, MMF-containing regimens inhibited recruitment of CD4+ T cells to atherosclerotic lesions in LDLr.Sle mice. In these mice, MMF also reduced the proportion of activated splenic T cells, as well as interleukin 10 secretion by T cells. With regard to lupus activity, MMF had no overt effect on anti-double-stranded DNA (dsDNA) antibody titres or kidney function and pathology. Conclusions The current study demonstrates that reduction of cholesterol levels alone is not atheroprotective in lupus-mediated atherogenesis. This is the first study to demonstrate that MMF reduces the atherosclerotic burden in a model of lupus-accelerated atherosclerosis. Our results suggest that MMF treatment may prove beneficial in preventing CVD in patients with SLE.
    Materialart: Online-Ressource
    ISSN: 0003-4967 , 1468-2060
    URL: Article
    DOI: 10.1136/annrheumdis-2011-200071
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: BMJ
    Publikationsdatum: 2012
    ZDB Id: 1481557-6
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
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    Abstract 3151: Inflammatory Markers and Risk of Coronary Heart Disease in Relation to the Apob/Apoa-i Ratio in Healthy Men and Women; The Epic-Norfolk Population Study
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Circulation Vol. 118, No. suppl_18 ( 2008-10-28)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. suppl_18 ( 2008-10-28)
    Kurzfassung: Studies have shown that individuals with an elevated apoB/apoA-I ratio are at increased risk for CHD. Presence of higher levels of inflammatory markers is also associated with increased CHD risk. The respective contributions of the apoB/apoA-I ratio and inflammatory markers to CHD risk are unknown. The apoB/apoA-I ratio and the plasma concentrations of an extensive panel of inflammatory markers including CRP, adiponectin, fibrinogen, myeloperoxidase, secretory phospholipase A2 (sPLA2) as well as lipoprotein-associated phospholipase A2 (Lp-PLA2) activity were measured in a prospective case-control study of 844 cases and 1762 matched controls (1651 men and 955 women) aged between 45–79 years who participated to the EPIC-Norfolk prospective population study. In both sexes, compared to participants in bottom apoB/apoA-I ratio tertile, participants in the top tertile had the highest levels of CRP (4.4 [3.7–5.0] vs. 2.8 [2.4 –3.2] mg/dL, p 〈 0.001 in men and 4.1 [3.4 – 4.8] vs. 3.1 [2.6 –3.6] mg/dL, p=0.03 in women), fibrinogen (3.2 [3.1–3.2] vs. 2.9 [2.8 –2.9] g/L, p 〈 0.001 in men and 3.2 [3.1–3.2] vs. 3.0 [2.9 –3.1] g/L, p 〈 0.001 in women) and the highest Lp-PLA2 activity (60.7 [59.3– 62.1] vs. 47.3 [46.0 – 48.6] nmol/min/mL, p 〈 0.001 in men and 55.6 [53.8 –57.4] vs. 41.5 [40.2– 42.8] nmol/min/mL, p 〈 0.001 in women) and the lowest adiponectin levels (7.9 [7.6 – 8.3] vs. 10.2 [9.7–10.6] μg/mL, p 〈 0.001 in men and 11.3 [12.7–13.5] vs. 15.5 [14.6 –16.1] μg/mL, p 〈 0.001). Myeloperoxidase and sPLA2 levels did not differ in apoB/apoA-I ratio tertiles. Compared to men in the bottom apoB/apoA-I ratio tertile and only 0 or 1 inflammatory markers in the top tertile (bottom for adiponectin), men in the top apoB/apoA-I ratio tertile had odds ratio (OR) for future CHD of 1.7 [95%CI 1.1–2.5], whereas those with 4, 5 or 6 inflammatory markers in the top tertile had an OR of 2.1 [1.4 –3.1] for future CHD. Among women, these OR for future CHD were of 1.7 [1.05–2.9] and 2.2 [1.2–3.9] . Men and women with an elevated apoB/apoA-I ratio also exhibited increased levels of inflammatory markers. The presence of additional elevated levels of multiple inflammatory markers was associated with an elevated CHD risk independent of higher levels of apoB/apoA-I ratio.
    Materialart: Online-Ressource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.118.suppl_18.S_1104
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2008
    ZDB Id: 1466401-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
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    Very low LDL-cholesterol concentrations achieved: which target is next?
    Elsevier BV ; 2017
    In:  The Lancet Vol. 390, No. 10106 ( 2017-10), p. 1930-1931
    Details
    In: The Lancet, Elsevier BV, Vol. 390, No. 10106 ( 2017-10), p. 1930-1931
    Materialart: Online-Ressource
    ISSN: 0140-6736
    URL: Article
    DOI: 10.1016/S0140-6736(17)32292-4
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Elsevier BV
    Publikationsdatum: 2017
    ZDB Id: 2067452-1
    ZDB Id: 3306-6
    ZDB Id: 1476593-7
    SSG: 5,21
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
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    Antisense oligonucleotides targeting apolipoprotein(a) in people with raised lipoprotein(a): two randomised, double-blind, placebo-controlled, dose-ranging trials
    Elsevier BV ; 2016
    In:  The Lancet Vol. 388, No. 10057 ( 2016-11), p. 2239-2253
    Details
    In: The Lancet, Elsevier BV, Vol. 388, No. 10057 ( 2016-11), p. 2239-2253
    Materialart: Online-Ressource
    ISSN: 0140-6736
    URL: Article
    DOI: 10.1016/S0140-6736(16)31009-1
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Elsevier BV
    Publikationsdatum: 2016
    ZDB Id: 2067452-1
    ZDB Id: 3306-6
    ZDB Id: 1476593-7
    SSG: 5,21
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
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    Abstract 12066: The Long-Term Safety and Efficacy of Evinacumab in Patients With Homozygous Familial Hypercholesterolemia
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Vol. 144, No. Suppl_1 ( 2021-11-16)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 144, No. Suppl_1 ( 2021-11-16)
    Kurzfassung: Background: Homozygous familial hypercholesterolemia (HoFH) is a rare genetic lipid disorder characterized by marked elevations in LDL-C and premature atherosclerotic cardiovascular disease (ASCVD). EU guidelines recommend LDL-C treatment goals of 〈 55 mg/dL and 〈 70 mg/dL for pts with HoFH with and without ASCVD, respectively. Evinacumab (EVIN; an angiopoietin-like 3 inhibitor) significantly reduced LDL-C and was generally well tolerated in pts with HoFH during the 24-week double-blind treatment period (DBTP) of a pivotal Phase 3 study (NCT03399786). Methods: This post-hoc analysis assessed the long-term effect of EVIN on LDL-C goal attainment in pts with HoFH who participated in the subsequent 24-week open-label treatment period (OLTP) of the pivotal Phase 3 study. All pts received intravenous EVIN 15 mg/kg every 4 weeks. Efficacy by background lipid lowering medication (LLM) subgroups and the effect of EVIN on eligibility for apheresis were also assessed. Results: In total, 65 pts entered the OLTP and 64 pts (98.5%) received OL EVIN. Overall, 50.0% achieved LDL-C 〈 100mg/dL, 31.7% achieved LDL-C 〈 70 mg/dL and 23.3% achieved LDL-C 〈 55 mg/dL at Week 48 (end of OLTP) (Figure 1). For the subgroup with ASCVD (n=36), 50.0%, 37.5% and 31.3% achieved LDL-C 〈 100 mg/dL, 〈 70 mg/dL and 〈 55 mg/dL, respectively. Overall, 43.1%, 24.6% and 38.5% of pts qualified for apheresis at baseline and did not qualify for apheresis at Week 48 (using new US, US and EU criteria); no patient discontinued apheresis. EVIN markedly reduced LDL-C, irrespective of background LLM. Overall, treatment-emergent adverse events (TEAEs) occurred in 47 pts (73.4%) during the OLTP. Serious AEs (all unrelated to EVIN) were reported by 7 pts (10.9%), none led to death or EVIN discontinuation. Conclusions: EVIN enabled 31.7% of all pts to achieve LDL-C 〈 70 mg/dL and 31.3% of those with ASCVD to achieve LDL-C 〈 55 mg/dL. EVIN markedly reduced the proportion of pts qualifying for apheresis.
    Materialart: Online-Ressource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.144.suppl_1.12066
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2021
    ZDB Id: 1466401-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 8
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    Abstract 1924: Carriers of Loss-of-Function Mutations in ABCA1 Display Pancreatic Beta Cell Dysfunction
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Circulation Vol. 118, No. suppl_18 ( 2008-10-28)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. suppl_18 ( 2008-10-28)
    Kurzfassung: Background The ATP Binding Cassette transporter A1 (ABCA1) transports free cholesterol to nascent high-density lipoproteins (HDL) and maintains plasma HDL levels. In mice, ABCA1 is essential in regulating intracellular cholesterol homeostasis and insulin secretion in the β cell. The role of ABCA1 in human glucose metabolism is unclear. Objective and methods To assess the effects of ABCA1 dysfunction on glucose homeostasis in humans , we matched heterozygous carriers of disruptive mutations in ABCA1 and non-carriers for age, gender and BMI and performed oral glucose tolerance tests (OGTT; 9 vs. 8 respectively) and hyperglycemic clamping experiments (6 vs. 6). Results Carriers had lower HDL-C levels than non-carriers (0.58 ± 0.3 vs. 1.46 ± 0.4 mmol/L, p=0.001) but LDL-C did not differ (3.4 ± 1.0 vs. 2.8 ± 0.8 mmol/L, p=0.21). Fasting plasma glucose was not different (5.2 ± 1.5 vs. 5.0 ± 0.4 mmol/L). Glucose curves after OGTT were significantly higher in carriers than in non-carriers (genotype * time interaction, p=0.005; plasma glucose at t=60 min 9.0 ± 3.0 mmol/L vs. 6.0 ± 1.4 mmol/L respectively, p=0.02). During hyperglycemic clamps, carriers showed a lower first phase insulin and C-peptide response than non-carriers (genotype * time interaction, p 〈 0.05 and p 〈 0.01 respectively; insulin at t=5 min 164±118 vs. 352 ±141 pmol/L, p 〈 0.05; C-peptide at t=5 min 1033 ± 628 vs. 1942 ± 723 pmol/L, p 〈 0.05) but no difference in insulin sensitivity index (0.0216 ± 0.012 mg kg −1 . min −1 . pM −1 for carriers and 0.0197 ± 0.005 mg kg −1 . min −1 . pM −1 for non-carriers; p=0.73). Disposition index - a measure of β cell function, adjusted for insulin sensitivity - was lower in carriers than in non-carriers (1037 ± 610 vs. 2718 ± 1524; p 〈 0.05). Non-carriers responded to an arginine stimulus with an increase in C-peptide levels (from 3558 ± 1240 pM to 6817 ± 1665 pM; p 〈 0.005), whereas in carriers this increase did not reach statistical significance (from 3727 ± 1843 pM to 5480 ± 1757 pM; p=0.12). Conclusion Carriers of loss-of-function mutations in ABCA1 show impaired insulin secretion without insulin resistance, resulting in glucose intolerance. Our data confirm previous studies in mice and provide evidence for a role of ABCA1 in β cell dysfunction and the pathophysiology of diabetes mellitus in man.
    Materialart: Online-Ressource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.118.suppl_18.S_406
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2008
    ZDB Id: 1466401-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 9
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    Abstract 5507: Toll Like Receptor 4 Activation Elicits Pro-atherogenic Gene Activation In Monocytes In Humans
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Circulation Vol. 118, No. suppl_18 ( 2008-10-28)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. suppl_18 ( 2008-10-28)
    Kurzfassung: Introduction: Inflammatory activation of both circulating blood cells as well as vessel wall cells is a hallmark of atherogenesis. Agonists of the Toll-like receptor 4 pathway, present on white blood cells as well as endothelial cells, have been associated with a pro-atherogenic state. Recently, standardized inflammatory challenge models using lipopolysaccharide (LPS) have been suggested to mimick these atherogenic changes. However, similarity between circulating pathways and ’vessel wall’ pathways need further validation. Therefore, we evaluated the effects of in vivo LPS challenge on circulating monocytes in humans. Methods: A bolus of Escherichia coli endotoxin (LPS 1 ng/kg bodyweight) or NaCl was infused intravenously in healthy male volunteers (n=13). Blood was drawn at 0, 1 and 4 hours after the challenge. The monocytes (CD14+ cells) were isolated using positive MACS selection. Subsequently, mRNA sample extraction using RnaseBee was performed. cDNA was prepared, amplified, labeled and then hybridized onto spotted oligonucleotide microarrays before scanning. Data were analyzed using R-project version 2.2.0. Validation Taqman took place. Results: Following LPS challenge, CD14+ count dropped by 48% in the first hour due to margination of monocytes, followed by normalization at 4 hours. Purity of CD14+ fraction approximated 90%. LPS was associated with upregulation of a series of pro-atherogenic genes (BID, DIPA, FRA-1, HSP27, HSP70, ILRN, MIP-1a, MIP1b, S100A9, SLA1, TIMPS, TLR2), immune system related genes (CLP1, DF, CD45-AP, HLA-DPB1, BATF, C3AR1, CD14) as well as a series of unrelated genes. No genes were differentially expressed during saline control experiments. RT-PCR confirmed upregulation of CD14, SLA1, BATF, C3AR1, MIP-B, TLR-2, VCAN and ILRN. Conclusion: TLR4 activation following LPS challenge is associated with potent activation of monocytic pathways involved in chemotaxis and immune activation. These activation patterns bear great resemblance to those reported in atherogenic vessel wall. It is tempting to speculate that circulating cells (’vulnerable blood’) can be used as a surrogate to detect high-risk vessel wall lesions (vulnerable patient).
    Materialart: Online-Ressource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.118.suppl_18.S_563-b
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2008
    ZDB Id: 1466401-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 10
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    A sense of excitement for a specific Lp(a)-lowering therapy
    Elsevier BV ; 2015
    In:  The Lancet Vol. 386, No. 10002 ( 2015-10), p. 1427-1429
    Details
    In: The Lancet, Elsevier BV, Vol. 386, No. 10002 ( 2015-10), p. 1427-1429
    Materialart: Online-Ressource
    ISSN: 0140-6736
    URL: Article
    DOI: 10.1016/S0140-6736(15)60638-9
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Elsevier BV
    Publikationsdatum: 2015
    ZDB Id: 2067452-1
    ZDB Id: 3306-6
    ZDB Id: 1476593-7
    SSG: 5,21
    Standort Signatur Einschränkungen Verfügbarkeit
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