Journals / The Anatolian Journal of Cardiology / 2020 / Cilt: 23 - Sayı: 2

Increased cardiovascular risk associated with hyperlipoproteinemia (a) and the challenges of current and future therapeutic possibilities

Pages
60–69
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

The aim ofthis review was to present some of the most important accessible scientific data, as well as dilemmas related to the currently and potentiallyin the near future more widely available therapeutic options for the management of hyperlipoproteinemia (a). (Anatol J Cardiol 2020; 23: 60-9)

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Population, genetic, and clinical studies demonstrated a causative and continuous, from other plasma lipoproteins independent relationship betweenelevated plasma lipoprotein (a) [Lp(a)] concentration and the development of cardiovascular disease (CVD), mainly those related to atheroscleroticCVD, and calcific aortic stenosis.
📊
Key Findings & Data:Its prevalence in the general population is estimated to be in the range of 10%–35% inaccordance with the most commonly used threshold levels (>30 or >50 mg/dL).
💡
Conclusion & Impact:The aim ofthis review was to present some of the most important accessible scientific data, as well as dilemmas related to the currently and potentiallyin the near future more widely available therapeutic options for the management of hyperlipoproteinemia (a). (Anatol J Cardiol 2020; 23: 60-9)
🔬Design:Review & Systematic Survey
📍Scope:2020 Verileri
⚙️Variables:Domain Parameters

Özet

Population, genetic, and clinical studies demonstrated a causative and continuous, from other plasma lipoproteins independent relationship betweenelevated plasma lipoprotein (a) [Lp(a)] concentration and the development of cardiovascular disease (CVD), mainly those related to atheroscleroticCVD, and calcific aortic stenosis. Currently, a strong international consensus is still lacking regarding the single value which wouldbe commonly used to define hyperlipoproteinemia (a). Its prevalence in the general population is estimated to be in the range of 10%–35% inaccordance with the most commonly used threshold levels (>30 or >50 mg/dL). Since elevated Lp(a) can be of special importance in patients withsome genetic disorders, as well as in individuals with otherwise controlled major risk factors, the identification and establishment of the propertherapeutic interventions that would lower Lp(a) levels and lead to CVD risk reduction could be very important. The majority of the classical lipidloweringagents (statins, ezetimibe, and fibrates), as well as nutraceuticals (CoQ10 and garlic), appear to have no significant effect on its plasmalevels, whereas for the drugs with the demonstrated Lp(a)-lowering effects (aspirin, niacin, and estrogens), their clinical efficacy in reducing cardiovascular(CV) events has not been unequivocally proven yet. Both Lp(a) apheresis and proprotein convertase subtilisin/kexin type 9 inhibitorscan reduce the plasma Lp(a) by approximately 20%–30% on average, in parallel with much larger reduction of low-density lipoprotein cholesterol(up to 70%), what puts us in a difficulty to conclude about the true contribution of lowered Lp(a) to the reduction of CV events. The most recentadvancement in the field is the introduction of the novel apolipoprotein (a) [apo(a)] antisense oligonucleotide therapy targeting apo(a), which hasalready proven itself as being very effective in decreasing plasma Lp(a) (by even >90%), but should be further tested in clinical trials. The aim ofthis review was to present some of the most important accessible scientific data, as well as dilemmas related to the currently and potentiallyin the near future more widely available therapeutic options for the management of hyperlipoproteinemia (a). (Anatol J Cardiol 2020; 23: 60-9)

🔖

Cite This Article

FRAS, Z. (2020). Increased cardiovascular risk associated with hyperlipoproteinemia (a) and the challenges of current and future therapeutic possibilities. The Anatolian Journal of Cardiology, Cilt: 23 - Sayı: 2, 60–69. https://ajindex.com/articles/365681

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (12)

  1. Rawther T, Tabet F. Biology, pathophysiology and current therapies that affect lipoprotein (a) levels. J Mol Cell Cardiol 2019; 131: 1-11
  2. Tsimikas S. A Test in Context: Lipoprotein(a): Diagnosis, Prognosis, Controversies, and Emerging Therapies. J Am Coll Cardiol 2017; 69: 692-711
  3. Clarke R, Peden JF, Hopewell JC, Kyriakou T, Goel A, Heath SC, et al.; PROCARDIS Consortium. Genetic variants associated with Lp(a) lipoprotein level and coronary disease. N Engl J Med 2009; 361: 2518–28
  4. Kamstrup PR, Tybjaerg-Hansen A, Steffensen R, Nordestgaard BG. Genetically elevated lipoprotein(a) and increased risk of myocardial infarction. JAMA 2009; 301: 2331–9
  5. Haque NS, Zhang X, French DL, Li J, Poon M, Fallon JT, et al. CC chemokine I-309 is the principal monocyte chemoattractant induced by apolipoprotein(a) in human vascular endothelial cells. Circulation 2000; 102: 786-92
  6. Muramatsu Y, Minami Y, Kato A, Katsura A, Sato T, Kakizaki R, et al. Lipoprotein (a) level is associated with plaque vulnerability in patients with coronary artery disease: An optical coherence tomography study. Int J Cardiol Heart Vasc 2019; 24: 100382
  7. Nestel PJ, Barnes EH, Tonkin AM, Simes J, Fournier M, White HD, et al. Plasma lipoprotein(a) concentration predicts future coronary and cardiovascular events in patients with stable coronary heart disease. Arterioscler Thromb Vasc Biol 2013; 33: 2902-8
  8. Emerging Risk Factors Collaboration, Erqou S, Kaptoge S, Perry PL, Di Angelantonio E, Thompson A, et al. Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA 2009; 302: 412–23
  9. Nordestgaard BG, Chapman MJ, Ray K, Borén J, Andreotti F, Watts GF, et al.; European Atherosclerosis Society Consensus Panel. Lipoprotein(a) as a cardiovascular risk factor: current status. Eur Heart J 2010; 31: 2844–53
  10. Forbes CA, Quek RG, Deshpande S, Worthy G, Wolff R, Stirk L, et al. The relationship between Lp(a) and CVD outcomes: a systematic review. Lipids Health Dis 2016; 15: 95
  11. Kouvari M, Panagiotakos DB, Chrysohoou C, Georgousopoulou EN, Yannakoulia M, Tousoulis D, et al. Lipoprotein (a) and 10-year Cardiovascular Disease Incidence in Apparently Healthy Individuals: A Sex-based Sensitivity Analysis from ATTICA Cohort Study. Angiology 2019; 70: 819-29
  12. Erqou S, Thompson A, Di Angelantonio E, Saleheen D, Kaptoge S, Marcovina S, et al. Apolipoprotein(a) isoforms and the risk of vascular disease: systematic review of 40 stu