Lipoprotein(a) and Its Potential Association with Thrombosis and Inflammation in COVID-19: a Testable Hypothesis

Purpose of Review The COVID-19 pandemic has infected over > 11 million as of today people worldwide and is associated with significant cardiovascular manifestations, particularly in subjects with preexisting comorbidities and cardiovascular risk factors. Recently, a predisposition for arterial an...

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Veröffentlicht in:Current atherosclerosis reports 2020-07, Vol.22 (9), p.48-48, Article 48
Hauptverfasser: Moriarty, Patrick M., Gorby, Lauryn K., Stroes, Erik S., Kastelein, John P., Davidson, Michael, Tsimikas, Sotirios
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container_end_page 48
container_issue 9
container_start_page 48
container_title Current atherosclerosis reports
container_volume 22
creator Moriarty, Patrick M.
Gorby, Lauryn K.
Stroes, Erik S.
Kastelein, John P.
Davidson, Michael
Tsimikas, Sotirios
description Purpose of Review The COVID-19 pandemic has infected over > 11 million as of today people worldwide and is associated with significant cardiovascular manifestations, particularly in subjects with preexisting comorbidities and cardiovascular risk factors. Recently, a predisposition for arterial and venous thromboses has been reported in COVID-19 infection. We hypothesize that besides conventional risk factors, subjects with elevated lipoprotein(a) (Lp(a)) may have a particularly high risk of developing cardiovascular complications. Recent Findings The Lp(a) molecule has the propensity for inhibiting endogenous fibrinolysis through its apolipoprotein(a) component and for enhancing proinflammatory effects such as through its content of oxidized phospholipids. The LPA gene contains an interleukin-6 (IL-6) response element that may induce an acute phase–type increase in Lp(a) levels following a cytokine storm from COVID-19. Summary Thus, subjects with either baseline elevated Lp(a) or those who have an increase following COVID-19 infection, or both, may be at very high risk of developing thromboses. Elevated Lp(a) may also lead to acute destabilization of preexisting but quiescent atherosclerotic plaques, which might induce acute myocardial infarction and stroke. Ongoing studies with IL-6 antagonists may be informative in understanding this relationship, and registries are being initiated to measure Lp(a) in subjects infected with COVID-19. If indeed an association is suggestive of being causal, consideration can be given to systematic testing of Lp(a) and prophylactic systemic anticoagulation in infected inpatients. Therapeutic lipid apheresis and pharmacotherapy for the reduction of Lp(a) levels may minimize thrombogenic potential and proinflammatory effects. We propose studies to test the hypothesis that Lp(a) may contribute to cardiovascular complications of COVID-19.
doi_str_mv 10.1007/s11883-020-00867-3
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Recently, a predisposition for arterial and venous thromboses has been reported in COVID-19 infection. We hypothesize that besides conventional risk factors, subjects with elevated lipoprotein(a) (Lp(a)) may have a particularly high risk of developing cardiovascular complications. Recent Findings The Lp(a) molecule has the propensity for inhibiting endogenous fibrinolysis through its apolipoprotein(a) component and for enhancing proinflammatory effects such as through its content of oxidized phospholipids. The LPA gene contains an interleukin-6 (IL-6) response element that may induce an acute phase–type increase in Lp(a) levels following a cytokine storm from COVID-19. Summary Thus, subjects with either baseline elevated Lp(a) or those who have an increase following COVID-19 infection, or both, may be at very high risk of developing thromboses. Elevated Lp(a) may also lead to acute destabilization of preexisting but quiescent atherosclerotic plaques, which might induce acute myocardial infarction and stroke. Ongoing studies with IL-6 antagonists may be informative in understanding this relationship, and registries are being initiated to measure Lp(a) in subjects infected with COVID-19. If indeed an association is suggestive of being causal, consideration can be given to systematic testing of Lp(a) and prophylactic systemic anticoagulation in infected inpatients. Therapeutic lipid apheresis and pharmacotherapy for the reduction of Lp(a) levels may minimize thrombogenic potential and proinflammatory effects. 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Elevated Lp(a) may also lead to acute destabilization of preexisting but quiescent atherosclerotic plaques, which might induce acute myocardial infarction and stroke. Ongoing studies with IL-6 antagonists may be informative in understanding this relationship, and registries are being initiated to measure Lp(a) in subjects infected with COVID-19. If indeed an association is suggestive of being causal, consideration can be given to systematic testing of Lp(a) and prophylactic systemic anticoagulation in infected inpatients. Therapeutic lipid apheresis and pharmacotherapy for the reduction of Lp(a) levels may minimize thrombogenic potential and proinflammatory effects. 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control</topic><topic>Interleukin-6 - antagonists &amp; inhibitors</topic><topic>Interleukin-6 - blood</topic><topic>Life Sciences &amp; Biomedicine</topic><topic>Lipoprotein(a) - blood</topic><topic>Lipoprotein(a) - genetics</topic><topic>Medicine</topic><topic>Medicine &amp; Public Health</topic><topic>Pandemics</topic><topic>Peripheral Vascular Disease</topic><topic>Pneumonia, Viral - blood</topic><topic>Pneumonia, Viral - complications</topic><topic>Pneumonia, Viral - epidemiology</topic><topic>Race Factors</topic><topic>Racial Groups - genetics</topic><topic>Risk Factors</topic><topic>SARS-CoV-2</topic><topic>Science &amp; Technology</topic><topic>Section Editor</topic><topic>Severity of Illness Index</topic><topic>Thrombosis - etiology</topic><topic>Thrombosis - prevention &amp; control</topic><topic>Topical Collection on Hot Topics in Atherosclerosis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moriarty, Patrick M.</creatorcontrib><creatorcontrib>Gorby, Lauryn K.</creatorcontrib><creatorcontrib>Stroes, Erik S.</creatorcontrib><creatorcontrib>Kastelein, John P.</creatorcontrib><creatorcontrib>Davidson, Michael</creatorcontrib><creatorcontrib>Tsimikas, Sotirios</creatorcontrib><collection>Web of Science - Science Citation Index Expanded - 2020</collection><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Current atherosclerosis reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moriarty, Patrick M.</au><au>Gorby, Lauryn K.</au><au>Stroes, Erik S.</au><au>Kastelein, John P.</au><au>Davidson, Michael</au><au>Tsimikas, Sotirios</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lipoprotein(a) and Its Potential Association with Thrombosis and Inflammation in COVID-19: a Testable Hypothesis</atitle><jtitle>Current atherosclerosis reports</jtitle><stitle>Curr Atheroscler Rep</stitle><stitle>CURR ATHEROSCLER REP</stitle><addtitle>Curr Atheroscler Rep</addtitle><date>2020-07-25</date><risdate>2020</risdate><volume>22</volume><issue>9</issue><spage>48</spage><epage>48</epage><pages>48-48</pages><artnum>48</artnum><issn>1523-3804</issn><eissn>1534-6242</eissn><abstract>Purpose of Review The COVID-19 pandemic has infected over &gt; 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Recently, a predisposition for arterial and venous thromboses has been reported in COVID-19 infection. We hypothesize that besides conventional risk factors, subjects with elevated lipoprotein(a) (Lp(a)) may have a particularly high risk of developing cardiovascular complications. Recent Findings The Lp(a) molecule has the propensity for inhibiting endogenous fibrinolysis through its apolipoprotein(a) component and for enhancing proinflammatory effects such as through its content of oxidized phospholipids. The LPA gene contains an interleukin-6 (IL-6) response element that may induce an acute phase–type increase in Lp(a) levels following a cytokine storm from COVID-19. Summary Thus, subjects with either baseline elevated Lp(a) or those who have an increase following COVID-19 infection, or both, may be at very high risk of developing thromboses. Elevated Lp(a) may also lead to acute destabilization of preexisting but quiescent atherosclerotic plaques, which might induce acute myocardial infarction and stroke. Ongoing studies with IL-6 antagonists may be informative in understanding this relationship, and registries are being initiated to measure Lp(a) in subjects infected with COVID-19. If indeed an association is suggestive of being causal, consideration can be given to systematic testing of Lp(a) and prophylactic systemic anticoagulation in infected inpatients. Therapeutic lipid apheresis and pharmacotherapy for the reduction of Lp(a) levels may minimize thrombogenic potential and proinflammatory effects. We propose studies to test the hypothesis that Lp(a) may contribute to cardiovascular complications of COVID-19.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>32710255</pmid><doi>10.1007/s11883-020-00867-3</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
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subjects Acute-Phase Proteins - analysis
Acute-Phase Proteins - genetics
Angiology
Anticoagulants - therapeutic use
Apolipoprotein E4 - genetics
Atherosclerosis - etiology
Betacoronavirus
Biomarkers - blood
Biomedical Research
Blood Component Removal
Cardiology
Cardiovascular System & Cardiology
Coronavirus Infections - blood
Coronavirus Infections - complications
Coronavirus Infections - epidemiology
COVID-19
Genotype
Hot Topics in Atherosclerosis (A Gotto
Hot Topics in Atherosclerosis (A Gotto, Section Editor)
Humans
Inflammation - etiology
Inflammation - prevention & control
Interleukin-6 - antagonists & inhibitors
Interleukin-6 - blood
Life Sciences & Biomedicine
Lipoprotein(a) - blood
Lipoprotein(a) - genetics
Medicine
Medicine & Public Health
Pandemics
Peripheral Vascular Disease
Pneumonia, Viral - blood
Pneumonia, Viral - complications
Pneumonia, Viral - epidemiology
Race Factors
Racial Groups - genetics
Risk Factors
SARS-CoV-2
Science & Technology
Section Editor
Severity of Illness Index
Thrombosis - etiology
Thrombosis - prevention & control
Topical Collection on Hot Topics in Atherosclerosis
title Lipoprotein(a) and Its Potential Association with Thrombosis and Inflammation in COVID-19: a Testable Hypothesis
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