Lipoprotein(a)—an interdisciplinary challenge

Julius, Ulrich; Tselmin, Sergey; Schatz, Ulrike; Fischer, Sabine; Bornstein, Stefan R.

doi:10.1007/s11789-019-00098-0

Cited by 3 publications

(2 citation statements)

References 38 publications

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“…While the use of PCSK9 inhibitors has led to a mean fairly modest reduction in Lp(a) levels (20–25%), there is no currently accepted indication for the use of these biosynthetic compounds to treat hyperlipoproteinemia(a) [ 154 ]. However, in combination with LA, the use of PCSK9 inhibitors decreases the need for apheresis, as most patients with HeHF and other forms of hypercholesterolemia respond very well to this therapy.…”

Section: Future Perspectives and Conclusionmentioning

confidence: 99%

Lipoprotein(a) Lowering—From Lipoprotein Apheresis to Antisense Oligonucleotide Approach

Greco

Sirtori

Corsini

et al. 2020

JCM

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It is well-known that elevated lipoprotein(a)—Lp(a)—levels are associated with a higher risk of cardiovascular (CV) mortality and all-cause mortality, although a standard pharmacotherapeutic approach is still undefined for patients with high CV risk dependent on hyperlipoproteinemia(a). Combined with high Lp(a) levels, familial hypercholesterolemia (FH) leads to a greater CVD risk. In suspected FH patients, the proportion of cases explained by a rise of Lp(a) levels ranges between 5% and 20%. In the absence of a specific pharmacological approach able to lower Lp(a) to the extent required to achieve CV benefits, the most effective strategy today is lipoprotein apheresis (LA). Although limited, a clear effect on Lp(a) is exerted by PCSK9 antagonists, with apparently different mechanisms when given with statins (raised catabolism) or as monotherapy (reduced production). In the era of RNA-based therapies, a new dawn is represented by the use of antisense oligonucleotides APO(a)Lrx, able to reduce Lp(a) from 35% to over 80%, with generally modest injection site reactions. The improved knowledge of Lp(a) atherogenicity and possible prevention will be of benefit for patients with residual CV risk remaining after the most effective available lipid-lowering agents.

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Section: Future Perspectives and Conclusionmentioning

confidence: 99%

Lipoprotein(a) Lowering—From Lipoprotein Apheresis to Antisense Oligonucleotide Approach

Greco

Sirtori

Corsini

et al. 2020

JCM

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“…As menores isoformas de apo (a) levam menos tempo de serem sintetizadas pelos hepatócitos e portanto, as concentrações de Lp(a) são inversamente proporcionais às isoformas (60,64,65).…”

Section: Lipoproteína(a)unclassified

Relação entre a lipoproteína (a) e a aterosclerose carotídea subclínica em indivíduos assintomáticos

França

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A Deus, por ter-me concedido vida e todas as condições necessárias nessa jornada.À orientadora professora Drª Eliana Cotta de Faria, pela oportunidade, ensinamentos de vida e confiança recebida.À minha coorientadora Drª Vanessa Helena de Souza Zago, pelo amparo e avultada cooperação no meu desenvolvimento acadêmico.À Coordenação de Aperfeiçoamento de Pessoal de Nível Superior -Brasil (CAPES) -Código de Financiamento 001 pelo apoio e financiamento que possibilitou a realização dessa dissertação.

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Relationship between Lipoprotein(a) and cardiovascular risk factors—data from 4602 participants of the ELITE study

Schrader¹,

Shakoor²,

Schmidt³

et al. 2021

Rev. Cardiovasc. Med.

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Lipoprotein(a) (Lp(a)) is becoming increasingly important as an independent risk factor for cardiovascular disease. Since no effective therapy currently exists other than lipid apheresis, the recommendation remains to optimally adjust all other cardiovascular risk factors (CVRF). In a Northwest German population study, the frequency of elevated Lp(a) levels and all other CVRF was investigated. The aim was to investigate whether individuals with elevated Lp(a) levels were also more likely to have other CVRFs. To date, 4602 individuals have been enrolled in the study, and blood pressure, weight, lipids, diabetes, medications, and pre-existing conditions were recorded in addition to Lp(a). In addition, questionnaires assessed physical activity, psychological stress, depression, and brain dysfunction. All participants received detailed individual recommendation about their CVRF and its treatment. In the further follow-up of 5 years, it will be examined how persons with elevated Lp(a) implemented these recommendations in comparison with participants without elevated Lp(a). The first group Lp(a) <75 nmol/L consisted of 3550 (80.2%), the Lp(a) 75–120 nmol/L group of 341 (7.4%) and the Lp(a) >120 nmol/L of 538 (11.7%). 81.6% of all participants had one or more CVRF. Age, sex, and prevalence of hypertension, diabetes, smoking, obesity, and exercise did not differ among the 3 groups. As expected, LDL-Cholesterol was significantly elevated in the Lp(a) >120 nmol/L group despite significantly more frequent use of statins. Significantly more often hypertensive patients were found in the Lp(a) >120 nmol/L group who were inadequately controlled by medication and significantly less often persons without further CVRF. No differences existed in the frequency of psychological stress, depression, and mild cognitive impairment. CVRF occur with comparable frequency in individuals with elevated Lp(a) levels. However, individuals with Lp(a) above 120 nmol/L were more likely to have poorly controlled blood pressure, elevated LDL-C, and less likely to have no other risk factors. This underlines that in case of Lp(a) elevation all further CVRF should be intensively adjusted, especially in case of strongly elevated values >120 nmol/L. However, these recommendations have not been adequately implemented in clinical care in this population to date.

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Lipoprotein(a)—an interdisciplinary challenge

Cited by 3 publications

References 38 publications

Lipoprotein(a) Lowering—From Lipoprotein Apheresis to Antisense Oligonucleotide Approach

Lipoprotein(a) Lowering—From Lipoprotein Apheresis to Antisense Oligonucleotide Approach

Relação entre a lipoproteína (a) e a aterosclerose carotídea subclínica em indivíduos assintomáticos

Relationship between Lipoprotein(a) and cardiovascular risk factors—data from 4602 participants of the ELITE study

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