Value of repeated measurements of lipoprotein (a) to assess cardiovascular risk: a retrospective study

Deconinck, Axelle; Morra, Sofia; Glassée, Nina; Borne, Philippe van de

doi:10.1080/00015385.2022.2031377

Cited by 4 publications

(1 citation statement)

References 17 publications

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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: 85%

Estimation of serum levels of Lipoprotein(a) might help to resolve the dilemma of differentiation between Unstable Angina and Non-ST-elevation Myocardial Infarction

Elian

Mohammed

Marei

2023

Benha Medical Journal

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Objectives: Evaluation of the performance of estimated serum levels of lipoprotein(a) [Lp(a)] and tissue plasminogen activator (t-PA) in the discrimination between patients presenting by cardiac events. Patients & Methods: 314 patients presenting with a clinical picture suggestive of an acute cardiac event (ACE) underwent clinical and laboratory workup according to the 2017 ESC Guidelines for the management of acute myocardial infarction (AMI). Blood samples were obtained for ELISA estimation of serum Lp(a) and plasma t-PA levels. Results: Clinically, 247 patients had angina, 166 stable angina (SA), 81 unstable angina (UA), 67 patients had AMI, 44 had non-ST-elevation MI (NSTEMI) and 23 patients had STEMI. Serum levels of Lp(a)were significantly higher in total patients' samples especially UA and MI patients compared to control samples, but were lower in those with compared to patients' samples. Further, Lp(a) levels were significantly higher in MI than UA patients' samples. Estimated t-PA levels were significantly higher in patients' than control samples, but were significantly higher in MI than angina patients' samples. Statistical analyses defined high estimated levels of Lp(a), t-PA, total cholesterol, and obesity as the significant differentiating variables between SA and UA patients and defined high levels of LP(a), t-PA, and obesity, and age as the significant predictors for NSTEMI. Conclusion: Elevated serum levels of Lp(a) might differentiate between UA patients and SA and NSTEMI with high specificity.

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