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September 5, 2020Advances in Therapy11 citationsOpen Access

Relation of High Lipoprotein (a) Concentrations to Platelet Reactivity in Individuals with and Without Coronary Artery Disease

RSRocío SalsosoTDTalia Falcão DalçóquioRFRemo H.M. Furtado

Key Result

High lipoprotein (a) concentrations (≥50 mg/dL) were not associated with higher ADP-induced platelet reactivity compared to lower concentrations in individuals with or without coronary artery disease.

Study Design

Type

Cross-Sectional (n=396)

Multicenter

No

Structured PICO

Does high Lp(a) concentration increase platelet reactivity in individuals with and without CAD?

P
Population
396 stable individuals (326 with CAD, 70 without CAD), median age 66, 67.2% male. Key inclusion: Stable CAD defined as previous MI and/or at least 50% coronary obstruction confirmed by coronary angiography and on non-enteric coated aspirin once daily for at least 1 month prior to enrollment; or absence of obstructive CAD confirmed by multi-detector coronary computed tomography angiography (CTA), and not taking any antithrombotic therapy prior to enrollment.
I
Intervention
High Lipoprotein (a) [Lp(a)] concentrations (≥ 50 mg/dL)
C
Comparator
Low Lipoprotein (a) [Lp(a)] concentrations (< 50 mg/dL)
O
Outcome
Association between Lp(a) and adenosine diphosphate (ADP)-induced platelet reactivity using the VerifyNow P2Y12 assaysurrogate

High Lp(a) concentrations (≥ 50 mg/dL) are not associated with increased platelet reactivity in stable individuals with or without coronary artery disease.

Main Result

Effect estimate: OR 1.00 (95% CI 0.99-1.01)

Absolute Event Rate: 249.4% vs 243.1%

p-value: p=0.590

Limitations

  • Individuals with CAD were treated with aspirin, which could attenuate Lp(a)-mediated platelet reactivity.
  • Did not assess the effect of apo(a) on platelet reactivity.
  • Unable to measure Lp(a) by isoform-independent assay.
  • Potential for type 2 error despite being the largest study to date.
  • CAD population was from a single center and included only individuals taking aspirin as the sole antiplatelet agent.

Abstract

INTRODUCTION: Lipoprotein (a) Lp(a) is a risk factor for coronary artery disease (CAD). To the best of our knowledge, this is the first study addressing the relationship between Lp(a) and platelet reactivity in primary and secondary prevention. METHODS: assay. Platelet reactivity was also induced by arachidonic acid and collagen-epinephrine (C-EPI) and assessed by Multiplate™, platelet function analyzer™ 100 (PFA-100), and light transmission aggregometry (LTA) assays. Secondary objectives included the assessment of the primary endpoint in individuals with or without CAD. RESULTS: Overall, 294 (74.2%) individuals had Lp(a) 0.05). Finally, multivariable analysis did not show a significant association between ADP-induced platelet reactivity and Lp(a) ≥ 50 mg/dL adjusted OR = 1.00 [(95% CI 0.99-1.01), P = 0.590. CONCLUSION: In individuals with or without CAD, Lp(a) ≥ 50 mg/dL was not associated with higher platelet reactivity.

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Cite This Study

Salsoso et al. (2020) conducted a cross-sectional in Coronary Artery Disease (n=396). Lipoprotein (a) ≥ 50 mg/dL vs. Lipoprotein (a) < 50 mg/dL was evaluated on ADP-induced platelet reactivity (VerifyNow P2Y12 assay) (OR 1.00, 95% CI 0.99-1.01, p=0.590). High lipoprotein (a) concentrations (≥50 mg/dL) were not associated with higher ADP-induced platelet reactivity compared to lower concentrations in individuals with or without coronary artery disease.

synapsesocial.com/papers/6a1c94d55a44e3b4a7c3daa6https://doi.org/10.1007/s12325-020-01483-y
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