CoChat
Sign Up
Cited by 45

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Endothelial function improvement in patients with familial hypercholesterolemia receiving PCSK-9 inhibitors on top of maximally tolerated lipid lowering therapy

Di Minno, Alessandro, Gentile, Marco, Iannuzzo, Gabriella, Calcaterra, Ilenia, Tripaldella, Maria, Porro, Benedetta, Cavalca, Viviana, Di Taranto, Maria Donata, Tremoli, Elena, Fortunato, Giuliana, Rubba, Paolo Osvaldo Federico, Di Minno, Matteo Nicola Dario·2020·Thrombosis Research
DOI 10.1016/j.thromres.2020.07.049
Open this paper in CoChat — free account

Abstract

Background Treatment with protein convertase subtilisin kexin type 9 inhibitors (PCSK-9i) reduced cholesterol levels and cardiovascular events in patients with hypercholesterolemia. We assessed changes in lipid profile, oxidation markers and endothelial function in patients with familial hypercholesterolemia (FH) after a 12-week treatment with a PCSK-9i. Methods Patients with FH starting a treatment with PCSK-9i were included. Total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), lipoprotein(a) (Lp(a)), small dense LDL (assessed by LDL score), 11-dehydro-thromboxane (11-TXB2), 8-isoprostaglandin-2alpha (8-iso-PGF2α), flow-mediated dilation (FMD) and reactive hyperaemia index (RHI) were evaluated before starting PCSK-9i treatment and after a 12-week treatment. Results Twenty-five subjects were enrolled (52% males, mean age 51.5 years). At the 12-week assessment, we observed a 38% median reduction in TC, 52% in LDL-C, 7% in Lp(a) and 46% in LDL score. In parallel, 11-TXB2 and 8-iso-PGF2α showed a reduction of 18% and 17%, respectively. FMD changed from 4.78% ± 2.27 at baseline to 10.6% ± 5.89 at 12 weeks (p Conclusions Small dense LDL reduction (assessed by LDL score) is related to changes in oxidation markers and endothelial function in patients with FH treated with PCSK-9i.

Overview

Integrity signals

Registry

Crossref · 10.1016/j.thromres.2020.07.049

Cites

4 of 4 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Show all 4 references

Research works printed but not linked: 55

  1. M. Authors/Task Force, E.S.C.C.f.P. Guidelines, E.S.C.N.C. Societies, 2019, ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk, Atherosclerosis, 290, 140
  2. Daiber, 2017, Targeting vascular (endothelial) dysfunction, Br. J. Pharmacol., 174, 1591, 10.1111/bph.13517 · DOI · Paper page
  3. Corretti, 2002, Guidelines for the ultrasound assessment of endothelial-dependent flow-mediated vasodilation of the brachial artery: a report of the International Brachial Artery Reactivity Task Force, J. Am. Coll. Cardiol., 39, 257, 10.1016/S0735-1097(01)01746-6 · DOI
  4. Ras, 2013, Flow-mediated dilation and cardiovascular risk prediction: a systematic review with meta-analysis, Int. J. Cardiol., 168, 344, 10.1016/j.ijcard.2012.09.047 · DOI
  5. Cavieres, 2014, Vascular hypercontractility and endothelial dysfunction before development of atherosclerosis in moderate dyslipidemia: role for nitric oxide and interleukin-6, Am J Cardiovasc Dis, 4, 114
  6. Nicholls, 2010, Meta-analysis of comparative efficacy of increasing dose of atorvastatin versus Rosuvastatin versus simvastatin on lowering levels of atherogenic lipids (from VOYAGER), Am. J. Cardiol., 105, 69, 10.1016/j.amjcard.2009.08.651 · DOI
  7. Sundboll, 2019, Cardiovascular event rates and trajectories of LDL-cholesterol levels and lipid-lowering therapy in patients with atherosclerotic cardiovascular disease: a population-based cohort study, Thromb. Res., 183, 124, 10.1016/j.thromres.2019.09.034 · DOI
  8. Giugliano, 2017, Clinical efficacy and safety of achieving very low LDL-cholesterol concentrations with the PCSK9 inhibitor evolocumab: a prespecified secondary analysis of the FOURIER trial, Lancet, 390, 1962, 10.1016/S0140-6736(17)32290-0 · DOI · Paper page
  9. Maulucci, 2018, Improved endothelial function after short-term therapy with evolocumab, J Clin Lipidol, 12, 669, 10.1016/j.jacl.2018.02.004 · DOI
  10. Hirayama, 2012, Small dense LDL: an emerging risk factor for cardiovascular disease, Clin. Chim. Acta, 414, 215, 10.1016/j.cca.2012.09.010 · DOI
  11. St-Pierre, 2005, Low-density lipoprotein subfractions and the long-term risk of ischemic heart disease in men: 13-year follow-up data from the Quebec Cardiovascular Study, Arterioscler. Thromb. Vasc. Biol., 25, 553, 10.1161/01.ATV.0000154144.73236.f4 · DOI · Paper page
  12. Di Minno, 2020, Changes in carotid stiffness in patients with familial hypercholesterolemia treated with Evolocumab (R): a prospective cohort study, Nutr. Metab. Cardiovasc. Dis., 30, 996, 10.1016/j.numecd.2020.02.018 · DOI
  13. Paneni, 2017, The aging cardiovascular system: understanding it at the cellular and clinical levels, J. Am. Coll. Cardiol., 69, 1952, 10.1016/j.jacc.2017.01.064 · DOI · Paper page
  14. Walker, 2015, Greater impairments in cerebral artery compared with skeletal muscle feed artery endothelial function in a mouse model of increased large artery stiffness, J. Physiol., 593, 1931, 10.1113/jphysiol.2014.285338 · DOI
  15. Pirillo, 2017, Spectrum of mutations in Italian patients with familial hypercholesterolemia: new results from the LIPIGEN study, Atheroscler Suppl, 29, 17, 10.1016/j.atherosclerosissup.2017.07.002 · DOI
  16. Stitziel, 2015, Exome sequencing in suspected monogenic dyslipidemias, Circ. Cardiovasc. Genet., 8, 343, 10.1161/CIRCGENETICS.114.000776 · DOI
  17. Di Taranto, 2015, Association of USF1 and APOA5 polymorphisms with familial combined hyperlipidemia in an Italian population, Mol. Cell. Probes, 29, 19, 10.1016/j.mcp.2014.10.002 · DOI
  18. Staiano, 2013, Investigation of single nucleotide polymorphisms associated to familial combined hyperlipidemia with random forests, Neural Nets and Surroundings, 169, 10.1007/978-3-642-35467-0_18 · DOI
  19. Di Minno, 2011, Abnormally high prevalence of major components of the metabolic syndrome in subjects with early-onset idiopathic venous thromboembolism, Thromb. Res., 127, 193, 10.1016/j.thromres.2010.12.005 · DOI
  20. Casula, 2018, Evaluation of the performance of Dutch lipid clinic network score in an Italian FH population: the LIPIGEN study, Atherosclerosis, 277, 413, 10.1016/j.atherosclerosis.2018.08.013 · DOI
  21. Di Taranto, 2017, Identification and in vitro characterization of two new PCSK9 gain of function variants found in patients with familial hypercholesterolemia, Sci. Rep., 7, 10.1038/s41598-017-15543-x · DOI
  22. Gentile, 2016, Association between Lp (a) and atherosclerosis in menopausal women without metabolic syndrome, Biomark. Med, 10, 397, 10.2217/bmm.16.4 · DOI
  23. Marz, 1993, Determination of lipoprotein(a): evaluation of three methods, Eur. J. Clin. Chem. Clin. Biochem., 31, 295
  24. Hoefner, 2001, Development of a rapid, quantitative method for LDL subfractionation with use of the Quantimetrix Lipoprint LDL System, Clin. Chem., 47, 266, 10.1093/clinchem/47.2.266 · DOI
  25. Gentile, 2013, Association between small dense LDL and early atherosclerosis in a sample of menopausal women, Clin. Chim. Acta, 426, 1, 10.1016/j.cca.2013.08.010 · DOI
  26. Di Minno, 2012, Urinary excretion of iPF(2alpha)-III predicts the risk of future thrombotic events. A 10-year follow-up, Thromb. Res., 129, 208, 10.1016/j.thromres.2011.10.006 · DOI
  27. Di Minno, 2011, Genotype-independent in vivo oxidative stress following a methionine loading test: maximal platelet activation in subjects with early-onset thrombosis, Thromb. Res., 128, e43, 10.1016/j.thromres.2011.05.017 · DOI
  28. Bonetti, 2004, Noninvasive identification of patients with early coronary atherosclerosis by assessment of digital reactive hyperemia, J. Am. Coll. Cardiol., 44, 2137, 10.1016/j.jacc.2004.08.062 · DOI
  29. McKenney, 2015, Understanding PCSK9 and anti-PCSK9 therapies, J Clin Lipidol, 9, 170, 10.1016/j.jacl.2015.01.001 · DOI
  30. Raal, 2016, PCSK9 inhibition-mediated reduction in Lp(a) with evolocumab: an analysis of 10 clinical trials and the LDL receptor’s role, J. Lipid Res., 57, 1086, 10.1194/jlr.P065334 · DOI
  31. Burgess, 2018, C. European prospective investigation into, C. nutrition-cardiovascular disease, association of LPA variants with risk of coronary disease and the implications for lipoprotein(a)-lowering therapies: a Mendelian randomization analysis, JAMA Cardiol., 3, 619, 10.1001/jamacardio.2018.1470 · DOI · Paper page
  32. Emerging Risk Factors, 2009, Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality, JAMA, 302, 412, 10.1001/jama.2009.1063 · DOI · Paper page
  33. Romagnuolo, 2018, Apolipoprotein(a) inhibits the conversion of Glu-plasminogen to Lys-plasminogen on the surface of vascular endothelial and smooth muscle cells, Thromb. Res., 169, 1, 10.1016/j.thromres.2018.07.002 · DOI
  34. Marston, 2020, The effect of PCSK9 (Proprotein convertase Subtilisin/Kexin type 9) inhibition on the risk of venous thromboembolism, Circulation, 141, 1600, 10.1161/CIRCULATIONAHA.120.046397 · DOI
  35. Heitzer, 2001, Endothelial dysfunction, oxidative stress, and risk of cardiovascular events in patients with coronary artery disease, Circulation, 104, 2673, 10.1161/hc4601.099485 · DOI · Paper page
  36. Casino, 1993, The role of nitric oxide in endothelium-dependent vasodilation of hypercholesterolemic patients, Circulation, 88, 2541, 10.1161/01.CIR.88.6.2541 · DOI
  37. Mihos, 2014, Cardiovascular effects of statins, beyond lipid-lowering properties, Pharmacol. Res., 88, 12, 10.1016/j.phrs.2014.02.009 · DOI
  38. Tesfamariam, 2006, The effects of HMG-CoA reductase inhibitors on endothelial function, Am. J. Cardiovasc. Drugs, 6, 115, 10.2165/00129784-200606020-00005 · DOI
  39. Brunetti, 2007, Improvement in endothelium dysfunction in diabetics treated with statins: a randomized comparison of atorvastatin 20 mg versus rosuvastatin 10 mg, J. Interv. Cardiol., 20, 481, 10.1111/j.1540-8183.2007.00293.x · DOI
  40. Gong, 2014, Long-term atorvastatin improves age-related endothelial dysfunction by ameliorating oxidative stress and normalizing eNOS/iNOS imbalance in rat aorta, Exp. Gerontol., 52, 9, 10.1016/j.exger.2014.01.015 · DOI
  41. Vlachopoulos, 2007, Protective effect of atorvastatin on acute systemic inflammation-induced endothelial dysfunction in hypercholesterolaemic subjects, Eur. Heart J., 28, 2102, 10.1093/eurheartj/ehm247 · DOI
  42. Grammer, 2015, Low-density lipoprotein particle diameter and mortality: the Ludwigshafen Risk and Cardiovascular Health Study, Eur. Heart J., 36, 31, 10.1093/eurheartj/ehu055 · DOI
  43. Pontrelli, 2002, Atorvastatin treatment beneficially alters the lipoprotein profile and increases low-density lipoprotein particle diameter in patients with combined dyslipidemia and impaired fasting glucose/type 2 diabetes, Metabolism, 51, 334, 10.1053/meta.2002.30510 · DOI
  44. Skyrme-Jones, 2000, Endothelial vasodilator function is related to low-density lipoprotein particle size and low-density lipoprotein vitamin E content in type 1 diabetes, J. Am. Coll. Cardiol., 35, 292, 10.1016/S0735-1097(99)00547-1 · DOI
  45. Galeano, 1998, Small dense low density lipoprotein has increased affinity for LDL receptor-independent cell surface binding sites: a potential mechanism for increased atherogenicity, J. Lipid Res., 39, 1263, 10.1016/S0022-2275(20)32551-7 · DOI
  46. Ricci, 2018, PCSK9 induces a pro-inflammatory response in macrophages, Sci. Rep., 8, 10.1038/s41598-018-20425-x · DOI
  47. Bernelot Moens, 2017, PCSK9 monoclonal antibodies reverse the pro-inflammatory profile of monocytes in familial hypercholesterolaemia, Eur. Heart J., 38, 1584, 10.1093/eurheartj/ehx002 · DOI
  48. Dubuc, 2004, Statins upregulate PCSK9, the gene encoding the proprotein convertase neural apoptosis-regulated convertase-1 implicated in familial hypercholesterolemia, Arterioscler. Thromb. Vasc. Biol., 24, 1454, 10.1161/01.ATV.0000134621.14315.43 · DOI · Paper page
  49. Veglia, 2014, Potentially spurious correlations between arterial size, flow-mediated dilation, and shear rate, Hypertension, 64, 1328, 10.1161/HYPERTENSIONAHA.114.03608 · DOI
  50. Donald, 2006, Non-invasive assessment of endothelial function: which technique?, J. Am. Coll. Cardiol., 48, 1846, 10.1016/j.jacc.2006.07.039 · DOI
  51. Neunteufl, 1997, Systemic endothelial dysfunction is related to the extent and severity of coronary artery disease, Atherosclerosis, 129, 111, 10.1016/S0021-9150(96)06018-2 · DOI
  52. Chan, 2003, The prognostic importance of endothelial dysfunction and carotid atheroma burden in patients with coronary artery disease, J. Am. Coll. Cardiol., 42, 1037, 10.1016/S0735-1097(03)00927-6 · DOI
  53. Sorensen, 2019, Statin treatment, oxidative stress and inflammation in a Danish population, Redox Biol., 21, 10.1016/j.redox.2018.101088 · DOI
  54. Ye, 2012, Effect of high-dose statin versus low-dose statin plus ezetimibe on endothelial function: a meta-analysis of randomized trials, J. Cardiovasc. Pharmacol. Ther., 17, 357, 10.1177/1074248412449384 · DOI
  55. Phadnis, 2019, Sample size calculation for small sample single-arm trials for time-to-event data: Logrank test with normal approximation or test statistic based on exact chi-square distribution?, Contemp Clin Trials Commun, 15, 10.1016/j.conctc.2019.100360 · DOI

Cited by

Sorted by citations

Metadata

Authors
Di Minno, A., Gentile, M., Iannuzzo, G., Calcaterra, I., Tripaldella, M., Porro, B., Cavalca, V., Di Taranto, M. D., Tremoli, E., Fortunato, G., Rubba, P. O. F., & Di Minno, M. N. D.
ORCID
Venue
Thrombosis Research
Publisher
Elsevier BV
Published
2020-10
Volume
194
Pages
229-236
ISSN
0049-3848
DOI
10.1016/j.thromres.2020.07.049
Cited by
45
References
4
Language
en
Licence

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review