Lipoprotein(a): An underestimated inflammatory mastermind

Dzobo, Kim E.; Kraaijenhof, Jordan M; Stroes, Erik S.G.; Nurmohamed, Nick S.; Kroon, Jeffrey

doi:10.1016/j.atherosclerosis.2022.04.004

Cited by 44 publications

(28 citation statements)

References 77 publications

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“…Again, this rise in Lp(a) level in HD patients versus controls was limited to large apo (a) isoform group only (14 versus 8 mg/dL) and was associated with heightened inflammation [ 127 ]. More details on the association of Lp(a) with inflammation are provided by Dzobo et al of this Lp(a) review series [ 128 ].…”

Section: Pathologies That Modify Lp(a) Concentrationsmentioning

confidence: 99%

Non-genetic influences on lipoprotein(a) concentrations

Enkhmaa

Berglund

2022

Atherosclerosis

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Section: Pathologies That Modify Lp(a) Concentrationsmentioning

confidence: 99%

Non-genetic influences on lipoprotein(a) concentrations

Enkhmaa

Berglund

2022

Atherosclerosis

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“…A limitation of this study, however, was a lack of detailed clinical information associated with dyslipidemia, together with factors that might affect the significance of serum lipoprotein(a) levels, such as: familial history of dyslipidemia and lipoprotein(a); other risk factors and conditions including inflammation; other relevant laboratory findings; and medications with lipid lowering effects [ 6 , 17 , 19 , 30 ]. Retrospective observations, which showed that a higher proportion of girls underwent the lipoprotein(a) test than boys, may also limit the generalizability of this study.…”

Section: Discussionmentioning

confidence: 99%

Lipoprotein(a) in the Korean Pediatric Population Visiting Local Clinics and Hospitals

Choi

Lee

2022

Nutrients

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In this paper we investigate serum lipoprotein(a), an independent risk factor for cardiovascular disease in the Korean pediatric population. Visiting local clinics and hospitals, 600 lipoprotein(a) tests were performed on 416 Korean children and adolescents (124 boys and 292 girls), with a median age of 11.1 years (interquartile range, IQR, 9.8–13.9). The median lipoprotein(a) level was 21.5 nmol/L (IQR, 8.2–51.7). Among the 416 patients, the 90th percentile value of the initial lipoprotein(a) measurement was 107.8 nmol/L. The proportion of patients with lipoprotein(a) ≥ 100 nmol/L was 11.3%. The lipoprotein(a) level and the proportion of patients with lipoprotein(a) ≥ 100 nmol/L were not significantly different among sex, or age group. Among the 416 patients, 122 (29.3%, 21 boys and 101 girls) underwent at least two follow-up lipoprotein(a) measurements. The median follow-up period was 6.7 months (IQR, 5.5–11.8). The median lipoprotein(a) level across the 122 patients was 25 nmol/L (IQR 10.0–72.0). Among those patients, seven (5.7%) experienced an increase in serum lipoprotein(a) to ≥100 nmol/L during follow-up measurements. Further studies are needed in the Korean pediatric population in order to clarify the clinical significance of this change long-term.

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“…The main difference between the study of Marques et al and our study is that we have included patients after an acute cardiovascular event. However, their study also does not include data on the concentration of Lp(a), which is an important factor involved in inflammatory events in the process of atherosclerosis [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

Gene Expression Profiling of Markers of Inflammation, Angiogenesis, Coagulation and Fibrinolysis in Patients with Coronary Artery Disease with Very High Lipoprotein(a) Levels Treated with PCSK9 Inhibitors

Hrovat

Likozar

Zupan

et al. 2022

JCDD

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Besides lipids, inflammation, angiogenesis, coagulation and fibrinolysis play very important roles in coronary artery disease (CAD). We measured gene expression of the inflammatory markers interleukin (IL)-1β (IL1B) and interferon (IFN)-γ (IFNG), vascular endothelial growth factor-A (VEGF-A) (VEGFA), and coagulation and fibrinolysis markers tissue factor (TF) (F3) and plasminogen activator inhibitor-1 (PAI-1) (SERPINE) in healthy controls and CAD patients with high lipoprotein(a) (Lp(a)). The aim of our study was to identify, first, if there is a difference in these markers between controls and patients; secondly, if these markers are associated with lipids; and third, what the influence of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors is on these markers. We included 124 subjects, 27 controls and 97 patients with CAD (30 in placebo and 67 in the PCSK9 group). Blood samples were collected for lipid and gene measurement. The results showed higher expression of IL1B (p < 0.0001), VEGFA (p < 0.0001), and F3 (p = 0.018) in controls in comparison with patients. Significant correlations were observed between IL1B and lipids. Treatment with PCSK9 inhibitors increased VEGFA (p < 0.0001) and F3 (p = 0.001), and decreased SERPINE (p = 0.043). The results of our study underpin the importance of IL-1β, VEGF-A and TF in CAD as well as the effect of PCSK9 treatment on these markers.

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Lipoprotein(a): An underestimated inflammatory mastermind

Cited by 44 publications

References 77 publications

Non-genetic influences on lipoprotein(a) concentrations

Non-genetic influences on lipoprotein(a) concentrations

Lipoprotein(a) in the Korean Pediatric Population Visiting Local Clinics and Hospitals

Gene Expression Profiling of Markers of Inflammation, Angiogenesis, Coagulation and Fibrinolysis in Patients with Coronary Artery Disease with Very High Lipoprotein(a) Levels Treated with PCSK9 Inhibitors

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