Independent association of Lp(a) with platelet reactivity in subjects without statins or antiplatelet agents

Liu, Huixing; Fu, Di; Luo, Yonghong; Peng, Daoquan

doi:10.1038/s41598-022-21121-7

Cited by 9 publications

(2 citation statements)

References 43 publications

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“…The apolipoprotein(a) (apo(a)) domain of Lp(a) shows homology to plasminogen; hence, Lp(a) interferes with the ability of plasminogen to facilitate fibrinolysis and promote thrombi formation [ 15 , 21 ]. High serum Lp(a) levels were positively associated with platelet aggregation, which is an alternative explanation of the thrombogenic effect of Lp(a) [ 22 , 23 ]. Lp(a) accelerates coagulation by promoting tissue factor expression and inhibiting the activity of the tissue factor pathway inhibitors [ 24 , 25 , 26 ].…”

Section: Discussionmentioning

confidence: 99%

Elevated Lipoprotein(a) Levels Measured by Cardio-Ankle Vascular Index are Associated with Arterial Stiffness in Patients Undergoing Peritoneal Dialysis

Huang,

Hsu,

Lin

et al. 2023

Rev. Cardiovasc. Med.

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Background: Arterial stiffness (AS) can be used to predict future cardiovascular diseases. High lipoprotein(a) (Lp(a)) levels were independently correlated with cardiovascular (CV) morbidity and death in patients with chronic renal insufficiency. The cardio-ankle vascular index (CAVI) is a useful biomarker of arteriosclerotic disorders and has a close relationship with a variety of CV events. This study aimed to investigate the correlation between serum Lp(a) levels and AS in patients on peritoneal dialysis (PD) using the CAVI. Methods: A total of 86 adult patients who were on regular PD for at least 3 months were recruited in this study. The CAVI values were determined using the waveform device (VaSera VS-1000). A CAVI value of 9.0 on either side was defined as high. Serum Lp(a) levels were measured by an enzyme-linked immunosorbent assay. Results: Among these participants, 35 of 86 (40.7%) belonged to the high CAVI group. In contrast to those with a normal CAVI, PD recipients in the high CAVI group had higher serum levels of total cholesterol ( p = 0.003), triglycerides ( p = 0.044), C-reactive protein ( p 0.001), and Lp(a) ( p 0.001), whereas their albumin levels were significantly lower ( p = 0.026). Based on multivariable logistic regression analysis, serum Lp(a) (odds ratio [OR] 1.025, 95% confidence interval [CI] 1.010–1.040, p = 0.001), total cholesterol (OR 1.042, 95% CI 1.005–1.081, p = 0.027), and C-reactive protein (each increase 0.1 mg/dL, OR 1.217, 95% CI 1.008–1.469, p = 0.041) levels were found as the parameters that could independently predict AS in patients on PD. Further, using Spearman’s correlation analysis, both the left and right CAVIs revealed a significantly positive correlation with log-transformed Lp(a) levels ( r = 0.588, p 0.001; r = 0.639, p 0.001, respectively). Conclusions: Serum Lp(a) levels were postulated to participate in the pathogenic processes of AS in adult patients undergoing PD.

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Section: Discussionmentioning

confidence: 99%

Elevated Lipoprotein(a) Levels Measured by Cardio-Ankle Vascular Index are Associated with Arterial Stiffness in Patients Undergoing Peritoneal Dialysis

Huang,

Hsu,

Lin

et al. 2023

Rev. Cardiovasc. Med.

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“…Lp(a) is positively correlated with platelet aggregation independent of lipoprotein-associated phospholipase A2 (Lp-PLA2), which may be partly responsible for the atherothrombotic effect of Lp(a). The exact mechanisms demand further investigation [21].…”

Section: Pathogenicity Of Lp(a)mentioning

confidence: 99%

Lipoprotein(a)—60 Years Later—What Do We Know?

Pasławska,

Tomasik

2023

Cells

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Lipoprotein(a) (Lp(a)) molecule includes two protein components: apolipoprotein(a) and apoB100. The molecule is the main transporter of oxidized phospholipids (OxPL) in plasma. The concentration of this strongly atherogenic lipoprotein is predominantly regulated by the LPA gene expression. Lp(a) is regarded as a risk factor for several cardiovascular diseases. Numerous epidemiological, clinical and in vitro studies showed a strong association between increased Lp(a) and atherosclerotic cardiovascular disease (ASCVD), calcific aortic valve disease/aortic stenosis (CAVD/AS), stroke, heart failure or peripheral arterial disease (PAD). Although there are acknowledged contributions of Lp(a) to the mentioned diseases, clinicians struggle with many inconveniences such as a lack of well-established treatment lowering Lp(a), and common guidelines for diagnosing or assessing cardiovascular risk among both adult and pediatric patients. Lp(a) levels are different with regard to a particular race or ethnicity and might fluctuate during childhood. Furthermore, the lack of standardization of assays is an additional impediment. The review presents the recent knowledge on Lp(a) based on clinical and scientific research, but also highlights relevant aspects of future study directions that would approach more suitable and effective managing risk associated with increased Lp(a), as well as control the Lp(a) levels.

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On-treatment platelet reactivity through the thromboxane A2 or P2Y12 platelet receptor pathways is not affected by pelacarsen

Karwatowska‐Prokopczuk

Yang

et al. 2023

J Thromb Thrombolysis

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Independent association of Lp(a) with platelet reactivity in subjects without statins or antiplatelet agents

Cited by 9 publications

References 43 publications

Elevated Lipoprotein(a) Levels Measured by Cardio-Ankle Vascular Index are Associated with Arterial Stiffness in Patients Undergoing Peritoneal Dialysis

Elevated Lipoprotein(a) Levels Measured by Cardio-Ankle Vascular Index are Associated with Arterial Stiffness in Patients Undergoing Peritoneal Dialysis

Lipoprotein(a)—60 Years Later—What Do We Know?

On-treatment platelet reactivity through the thromboxane A2 or P2Y12 platelet receptor pathways is not affected by pelacarsen

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