2021
DOI: 10.1016/j.acvd.2021.10.009
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Lipoprotein(a): Pathophysiology, measurement, indication and treatment in cardiovascular disease. A consensus statement from the Nouvelle Société Francophone d’Athérosclérose (NSFA)

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Cited by 14 publications
(4 citation statements)
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“…Furthermore, apo(a) protein is encoded by the LPA gene in the long arm of chromosome 6 within region 6q2.6-2.7, so it is a conserved protein (26) with steady production rate that is only affected by liver diseases (27) and not by statin therapy (28) . In support of these assumptions, Deconinck et al (29) The reported concomitant elevations of Lp(a) and t-PA levels could be attributed to the homology of the LPA gene with the human plasminogen gene (30) and the presence of a domain of inactive serineprotease, whose amino acid sequence in Apo(a) coincides with that of plasminogen in 94%, but serine replaced arginine in the activation site equivalent to that of plasminogen, thus hinders the conversion of Lp(a) into active protease by t-PA responsible for activation (31) . These structural similarities between Lp(a) and plasminogen lead to the interference with the fibrinolytic cascade despite the increased levels of t-PA and account for the atherogenic mechanism of Lp(a) (32,30) .…”
Section: Roc Curve Analysis Defined High Levels Ofmentioning
confidence: 93%
“…Furthermore, apo(a) protein is encoded by the LPA gene in the long arm of chromosome 6 within region 6q2.6-2.7, so it is a conserved protein (26) with steady production rate that is only affected by liver diseases (27) and not by statin therapy (28) . In support of these assumptions, Deconinck et al (29) The reported concomitant elevations of Lp(a) and t-PA levels could be attributed to the homology of the LPA gene with the human plasminogen gene (30) and the presence of a domain of inactive serineprotease, whose amino acid sequence in Apo(a) coincides with that of plasminogen in 94%, but serine replaced arginine in the activation site equivalent to that of plasminogen, thus hinders the conversion of Lp(a) into active protease by t-PA responsible for activation (31) . These structural similarities between Lp(a) and plasminogen lead to the interference with the fibrinolytic cascade despite the increased levels of t-PA and account for the atherogenic mechanism of Lp(a) (32,30) .…”
Section: Roc Curve Analysis Defined High Levels Ofmentioning
confidence: 93%
“…The EAS expert panel recommends more intensive CV risk management in those with high Lp(a) concentrations and a high baseline risk [ 66 ]. It is recommended that Lp(a) levels are measured at least once in individuals with diabetes to personalise the CV risk estimation [ 66 , 67 ]. To date, there is no effective and recommended therapy targeting Lp(a).…”
Section: Therapies Mainly Targeting Lipoprotein (A)mentioning
confidence: 99%
“…Several lines of evidence suggest that large absolute reductions in Lp(a) concentrations of ~100 mg/dL are needed to achieve meaningful reductions in ASCVD risk [ 7 , 112 , 113 ]. Therefore, only those drugs that are specifically designed for the purpose of Lp(a)-lowering could be expected to have beneficial effects on ASCVD outcomes.…”
Section: Lp(a)-lowering Therapiesmentioning
confidence: 99%