Lipoprotein(a) and Pulmonary Embolism Severity-A Retrospective Data Analysis.

Paul Gressenberger,Jakob Riedl,Moritz Pechtold,Marianne Brodmann,Reinhard B Raggam,Johannes Schmid,Viktoria Muster,Thomas Gary,Katharina Gütl,Philipp Jud,Ewald Kolesnik,Florian Posch,Günther Silbernagel

doi:10.3389/fcvm.2022.808605

Paul Gressenberger, Jakob Riedl + Show 11 more

Open Access

https://doi.org/10.3389/fcvm.2022.808605

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Abstract

AimWe aimed to investigate a correlation between PE severity and Lp(a) levels.MethodsWe performed a retrospective data analysis from our medical records of PE patients admitted to the University Hospital Graz, Austria. Patients with an Lp(a) reading within a 1-year interval before and after PE diagnosis were included. In accordance with the 2019 ESC guidelines for the diagnosis and management of acute PE, severity assessment was carried out classifying patients into four groups: low risk (LR), intermediate low risk (IML), intermediate high risk (IMH) and high risk (HR). The study period of interest was between January 1, 2002 and August 1, 2020.ResultsWe analyzed 811 patients with PE, of whom 323 (40%) had low-risk PE, 343 (42%) had intermediate-low-risk PE, 64 (8%) had intermediate-high-risk PE, and 81 (10%) had high-risk PE, respectively. We did not observe an association between PE severity and Lp(a) concentrations. In detail, median Lp(a) concentrations were 17 mg/dL [25–75th percentile: 10-37] in low-risk PE patients, 16 mg/dL [10–37] in intermediate-low-risk PE patients, 15mg/dL [10–48] in intermediate-high-risk PE patients, and 13mg/dL [10–27] in high-risk PE patients, respectively (Kruskal-Wallis p = 0.658, p for linear trend = 0.358).ConclusionThe current findings suggest no correlation between PE severity and Lp(a) levels.

Highlights

Lipoprotein(a) (Lp(a)) is a genetically determined low-density lipoprotein (LDL) particle
Remains elusive whether this inhibitory effect is strong enough to play a significant role in the development of venous thrombotic events (VTE) such as pulmonary embolism (PE) [7]
In accordance with the 2019 European Society of Cardiology (ESC) guidelines [10] for the diagnosis and management of acute PE, severity assessment was carried out classifying patients into four groups: low risk (LR), intermediate low risk (IML), intermediate high risk (IMH) and high risk (HR)

Summary

Introduction

Lipoprotein(a) (Lp(a)) is a genetically determined low-density lipoprotein (LDL) particle. In the absence of acute inflammation, the Lp(a) level is stable through an individual’s lifetime, regardless of lifestyle [1]. Elevated Lp(a) levels are strongly associated with the development of atherosclerotic cardiovascular diseases (ASCVD) such as stroke, peripheral artery disease or coronary heart disease [2, 3]. A Lp(a) level over 50 mg/dL is generally considered as an additional factor that indicates a high risk of ASCVD, whereas the highest risk is strongly restricted to those with very high Lp(a)-concentrations [3]. The European Society of Cardiology (ESC) recommends measuring Lp(a) levels in selected patients at high risk of ASCVD [4]. Potential pathogenic mechanisms of Lp(a) include their propensity to oxidize after entry into the vessel wall, creating highly immunogenic and proinflammatory phospholipids, the presence of lysine binding sites that allow accumulation in the arterial wall, and similarities of Lp(a) to plasminogen, resulting in a decrease of plasmin synthesis and inhibition of fibrinolysis [5, 6]. Remains elusive whether this inhibitory effect is strong enough to play a significant role in the development of venous thrombotic events (VTE) such as pulmonary embolism (PE) [7]

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