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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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 |
format | Article |
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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.</description><identifier>ISSN: 1523-3804</identifier><identifier>EISSN: 1534-6242</identifier><identifier>DOI: 10.1007/s11883-020-00867-3</identifier><identifier>PMID: 32710255</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject><![CDATA[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]]></subject><ispartof>Current atherosclerosis reports, 2020-07, Vol.22 (9), p.48-48, Article 48</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>59</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000551930800001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c446t-6438e83eb540649d4ad0e189485940788ac02d169a53c430129fe9456be5bcb43</citedby><cites>FETCH-LOGICAL-c446t-6438e83eb540649d4ad0e189485940788ac02d169a53c430129fe9456be5bcb43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11883-020-00867-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11883-020-00867-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,315,781,785,886,27929,27930,28253,41493,42562,51324</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32710255$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><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><title>Lipoprotein(a) and Its Potential Association with Thrombosis and Inflammation in COVID-19: a Testable Hypothesis</title><title>Current atherosclerosis reports</title><addtitle>Curr Atheroscler Rep</addtitle><addtitle>CURR ATHEROSCLER REP</addtitle><addtitle>Curr Atheroscler Rep</addtitle><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.</description><subject>Acute-Phase Proteins - analysis</subject><subject>Acute-Phase Proteins - genetics</subject><subject>Angiology</subject><subject>Anticoagulants - therapeutic use</subject><subject>Apolipoprotein E4 - genetics</subject><subject>Atherosclerosis - etiology</subject><subject>Betacoronavirus</subject><subject>Biomarkers - blood</subject><subject>Biomedical Research</subject><subject>Blood Component Removal</subject><subject>Cardiology</subject><subject>Cardiovascular System & Cardiology</subject><subject>Coronavirus Infections - blood</subject><subject>Coronavirus Infections - complications</subject><subject>Coronavirus Infections - epidemiology</subject><subject>COVID-19</subject><subject>Genotype</subject><subject>Hot Topics in Atherosclerosis (A Gotto</subject><subject>Hot Topics in Atherosclerosis (A Gotto, Section Editor)</subject><subject>Humans</subject><subject>Inflammation - etiology</subject><subject>Inflammation - prevention & control</subject><subject>Interleukin-6 - antagonists & inhibitors</subject><subject>Interleukin-6 - blood</subject><subject>Life Sciences & Biomedicine</subject><subject>Lipoprotein(a) - blood</subject><subject>Lipoprotein(a) - genetics</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Pandemics</subject><subject>Peripheral Vascular Disease</subject><subject>Pneumonia, Viral - blood</subject><subject>Pneumonia, Viral - complications</subject><subject>Pneumonia, Viral - epidemiology</subject><subject>Race Factors</subject><subject>Racial Groups - genetics</subject><subject>Risk Factors</subject><subject>SARS-CoV-2</subject><subject>Science & Technology</subject><subject>Section Editor</subject><subject>Severity of Illness Index</subject><subject>Thrombosis - etiology</subject><subject>Thrombosis - prevention & control</subject><subject>Topical Collection on Hot Topics in Atherosclerosis</subject><issn>1523-3804</issn><issn>1534-6242</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>AOWDO</sourceid><sourceid>EIF</sourceid><recordid>eNqNkUtv1DAURiMEoqXwB1ggL4tQ4PqVOCyQqvDoSCOVxcDWchyn4yqxg-1Q9d_jacoINoiVLft81_f6FMVLDG8xQP0uYiwELYFACSCquqSPilPMKSsrwsjjw57QkgpgJ8WzGG8gk6LCT4sTSmoMhPPTYt7a2c_BJ2PduXqNlOvRJkX0NZ-4ZNWILmL02qpkvUO3Nu3Rbh_81Plo40q7YVTTtALWofbq--ZjiZv3SKGdiUl1o0GXd7NPe5Mzz4sngxqjefGwnhXfPn_atZfl9urLpr3YlpqxKpUVo8IIajrOoGJNz1QPBouGCd4wqIVQGkiPq0ZxqhkFTJrBNIxXneGd7hg9Kz6sdeelm0yv8zRBjXIOdlLhTnpl5d83zu7ltf8payoww1UucP5QIPgfSx5ETjZqM47KGb9Emb-4Jg3DzQElK6qDjzGY4fgMBnlQJVdVMguQ96okzaFXfzZ4jPx2k4E3K3BrOj9EbY3T5ogBAOe4oSDyDnCmxf_TrU33vlq_uJSjdI3GjLtrE-SNX4LLdv7V_y96Gr_a</recordid><startdate>20200725</startdate><enddate>20200725</enddate><creator>Moriarty, Patrick M.</creator><creator>Gorby, Lauryn K.</creator><creator>Stroes, Erik S.</creator><creator>Kastelein, John P.</creator><creator>Davidson, Michael</creator><creator>Tsimikas, Sotirios</creator><general>Springer US</general><general>Current Medicine Group</general><scope>AOWDO</scope><scope>BLEPL</scope><scope>DTL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200725</creationdate><title>Lipoprotein(a) and Its Potential Association with Thrombosis and Inflammation in COVID-19: a Testable Hypothesis</title><author>Moriarty, Patrick M. ; Gorby, Lauryn K. ; Stroes, Erik S. ; Kastelein, John P. ; Davidson, Michael ; Tsimikas, Sotirios</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c446t-6438e83eb540649d4ad0e189485940788ac02d169a53c430129fe9456be5bcb43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Acute-Phase Proteins - analysis</topic><topic>Acute-Phase Proteins - genetics</topic><topic>Angiology</topic><topic>Anticoagulants - therapeutic use</topic><topic>Apolipoprotein E4 - genetics</topic><topic>Atherosclerosis - etiology</topic><topic>Betacoronavirus</topic><topic>Biomarkers - blood</topic><topic>Biomedical Research</topic><topic>Blood Component Removal</topic><topic>Cardiology</topic><topic>Cardiovascular System & Cardiology</topic><topic>Coronavirus Infections - blood</topic><topic>Coronavirus Infections - complications</topic><topic>Coronavirus Infections - epidemiology</topic><topic>COVID-19</topic><topic>Genotype</topic><topic>Hot Topics in Atherosclerosis (A Gotto</topic><topic>Hot Topics in Atherosclerosis (A Gotto, Section Editor)</topic><topic>Humans</topic><topic>Inflammation - etiology</topic><topic>Inflammation - prevention & control</topic><topic>Interleukin-6 - antagonists & inhibitors</topic><topic>Interleukin-6 - blood</topic><topic>Life Sciences & Biomedicine</topic><topic>Lipoprotein(a) - blood</topic><topic>Lipoprotein(a) - genetics</topic><topic>Medicine</topic><topic>Medicine & 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 & Technology</topic><topic>Section Editor</topic><topic>Severity of Illness Index</topic><topic>Thrombosis - etiology</topic><topic>Thrombosis - prevention & 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 > 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.</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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