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Lipoprotein(a) and SARS-CoV-2 infections: susceptibility to infections, ischemic heart disease and thromboembolic events.

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TLDR
In this article, the authors evaluated whether SARS-CoV-2 infections modify the risk of high lipoprotein(a) concentrations for IHD or thromboembolic events during the first 8.5 months follow-up of the pandemic.
Abstract
Background Comorbidities including ischemic heart disease (IHD) worsen outcomes after SARS-CoV-2 infections. High lipoprotein(a) [Lp(a)] concentrations are a strong risk factor for IHD and possibly for thromboembolic events. We therefore evaluated whether SARS-CoV-2 infections modify the risk of high Lp(a) concentrations for IHD or thromboembolic events during the first 8.5 months follow-up of the pandemic. Method Cohort study using data from the UK Biobank during the SARS-CoV-2 pandemic. Baseline Lp(a) was compared between SARS-CoV-2 positive patients and the population controls. UK Biobank received ethical approval from the North West Multi-Centre Research Ethics Committee (REC reference: 11/NW/0382). All participants gave written informed consent before enrolment in the study, which was conducted in accordance with the principles of the Declaration of Helsinki. Results SARS-CoV-2 positive patients had Lp(a) concentrations similar to the population controls. The risk for IHD increased with higher Lp(a) concentrations in both, the population controls (n = 435,104) and SARS-CoV-2 positive patients (n = 6,937). The causality of the findings was supported by a genetic risk score for Lp(a). A SARS-CoV-2 infection modified the association with a steeper increase in risk for infected patients (interaction P-value = 0.03). Although SARS-CoV-2 positive patients had a 5-times higher frequency of thromboembolic events compared to the population controls (1.53% vs. 0.31%), the risk was not influenced by Lp(a). Conclusions SARS-CoV-2 infections enforce the association between high Lp(a) and IHD but the risk for thromboembolic events is not influenced by Lp(a). This article is protected by copyright. All rights reserved.

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Prognostic parameters of in-hospital mortality in COVID-19 patients-An Italian experience.

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Lipoprotein(a), venous thromboembolism and COVID-19: A pilot study

- 01 Jan 2022 - 
TL;DR: In this article , the authors investigated whether Lp(a) elevation may contribute to the pro-thrombotic state hallmarking COVID-19 patients, which is mainly driven by interleukin (IL)-6.
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Beyond fibrinolysis: The confounding role of Lp(a) in thrombosis.

Michael B. Boffa
- 01 May 2022 - 
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Post-acute Sequelae of SARS-CoV-2 Infection: A Neglected Public Health Issue

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Journal ArticleDOI

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TL;DR: In this small series, vascular angiogenesis distinguished the pulmonary pathobiology of Covid-19 from that of equally severe influenza virus infection.
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Lipoprotein(a): resurrected by genetics.

TL;DR: It has been established in a proof of principle study that lowering of very high Lp(a) by apheresis in high‐risk patients with already maximally reduced low‐density lipoprotein cholesterol levels can dramatically reduce major coronary events.
Journal ArticleDOI

Lipoprotein (a) as a cause of cardiovascular disease: insights from epidemiology, genetics, and biology

TL;DR: Human epidemiologic and genetic evidence using the Mendelian randomization approach in large-scale studies now strongly supports that elevated lipoprotein (a) [Lp(a)] is a causal risk factor for cardiovascular disease, that is, for myocardial infarction, atherosclerotic stenosis, and aortic valve stenosis.
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Registry of Arterial and Venous Thromboembolic Complications in Patients With COVID-19.

TL;DR: Major arterial or venous thromboembolism, major cardiovascular adverse events, and symptomatic venousThromboEmbolism occurred with high frequency in patients with COVID-19, especially in the intensive care setting, despite a high utilization rate of thromboprophylaxis.