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10.1007/s11883-020-00867-3 http://scihub22266oqcxt.onion/10.1007/s11883-020-00867-3 C7381416!7381416 !32710255     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32710255 &cmd=llinks): Failed to open stream: HTTP request failed! 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Lipoprotein(a) and Its Potential Association with Thrombosis and Inflammation in COVID-19: a Testable Hypothesis |pdf=|usr=}}{{32710255 }} gab.com Text Lipoprotein(a) and Its Potential Association with Thrombosis and Inflammation in COVID-19: a Testable Hypothesis JO: Curr Atheroscler Rep http://www.kidney.de/pget.php?&tw=1&pmid=32710255 #FOAvip 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. 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. Twit Text FOAVip Lipoprotein(a) and Its Potential Association with Thrombosis and Inflammation in COVID-19: a Testable Hypothesis ????Curr Atheroscler Rep http://www.kidney.de/pget.php?&tw=1&pmid=32710255 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32710255 #FOAvip English Wikipedia <ref>{{Cite pmid|32710255 }}</ref> Lipoprotein(a) and Its Potential Association with Thrombosis and Inflammation in COVID-19: a Testable Hypothesis #MMPMID32710255 Moriarty PM ; Gorby LK ; Stroes ES ; Kastelein JP ; Davidson M ; Tsimikas S Curr Atheroscler Rep 2020[Jul]; 22 (9 ): 48 PMID32710255 show ga 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. 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. |Acute-Phase Proteins/analysis/genetics [MESH] |Anticoagulants/therapeutic use [MESH] |Apolipoprotein E4/genetics [MESH] |Atherosclerosis/etiology [MESH] |Betacoronavirus [MESH] |Biomarkers/blood [MESH] |Biomedical Research [MESH] |Blood Component Removal [MESH] |COVID-19 [MESH] |Coronavirus Infections/*blood/*complications/epidemiology [MESH] |Genotype [MESH] |Humans [MESH] |Inflammation/*etiology/prevention & control [MESH] |Interleukin-6/antagonists & inhibitors/blood [MESH] |Lipoprotein(a)/*blood/genetics [MESH] |Pandemics [MESH] |Pneumonia, Viral/*blood/*complications/epidemiology [MESH] |Race Factors [MESH] |Racial Groups/genetics [MESH] |Risk Factors [MESH] |SARS-CoV-2 [MESH] |Severity of Illness Index [MESH]Lipoprotein(a) and Its Potential Association with Thrombosis and Infla(epmc).pdf DeepDyve Pubget Overpricing