الفهرس 
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Abstract
Lipoprotein(a) [Lp(a)] consists of an apolipoprotein B containing low-density lipoprotein (LDL) like a particle, covalently linked to plasminogen-like glycoprotein apo(a) (Nordestgaard et al., 2016). Lp(a) is mainly determined genetically by the LPA gene and is considered proatherogenic, proinflammatory, and potentially antifibrinolytic (Tsimikas, 2016).
Evidence from epidemiological and clinical analyses in both primary and secondary prevention populations show an independent association between Lp(a) and risk for cardiovascular disease and death (Willeit et al., 2014 and O’Donoghue et al., 2014), results that are further supported by genetic studies indicating that Lp(a) has a causal role in the development of coronary artery disease (CAD) (Waldeyer et al., 2017).
Nevertheless, despite these associations, the value of Lp(a) as a prognostic biomarker remains controversial and is incompletely defined due to the lack of standardized assays (Marcovina & Albers, 2016), the limited therapeutic options for significantly lowering lp(a), and the need of outcome data showing the benefit of lowering Lp(a) levels (Tsimikas et al., 2018).
Patients with acute coronary syndrome (ACS) are at high risk for recurrent ischemic cardiovascular events, despite high-intensity statin treatment and other secondary prevention strategies. It is uncertain whether Lp(a) is an independent risk factor for further cardiovascular events after ACS, particularly when LDL-C is controlled. In addition, Lp(a) is a positive acute-phase reactant with increased concentration for several weeks following (Honda et al., 1994 and Maeda et al., 1989).
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Therefore, the predictive value of Lp(a) after ACS may be more reliably determined after a period of clinical stabilization. If residual cardiovascular risk after ACS were associated with levels of Lp(a), the findings might suggest Lp(a) as an additional target of therapy. This possibility assumes additional relevance in light of new treatments that reduce levels of Lp(a)substantially, including PCSK9 (proprotein convertase subtilisin/Kexin type 9) antibodies8 and antisense oligonucleotide to apolipoprotein (a) (Viney et al., 2016).
Familial hypercholesterolemia (FH) has been recognized as an inherited disease with extremely elevated levels of low-density lipoprotein cholesterol (LDL-C) and thus premature coronary heart disease (CHD) (Nordestgaard et al., 2013). Patients with homozygous phenotype even could suffer cardiovascular morbidity and mortality in their childhood (Sanchez-Hernandez et al., 2016 and Cuchel et al., 2014). Despite increasing awareness of FH, it has still been underdiagnosed and undertreated worldwide, partly attributed to the complexity and disunity of the current diagnostic criteria and underutilized genetic testing (Sturm et al., 2018).
Until now, Dutch Lipid Clinic Network (DLCN) criteria, Simon Broome Register (SBR), Make Early Diagnosis-Prevent Early Death (MEDPED), criteria given by the 2015 American Heart Association scientific statement and other national diagnostic algorithms have been adopted worldwide (Gidding et aal., 2015 and Hovingh et al., 2013). However, there are several limitations in regard to their utilization in clinical practice. First, the cut-off value of LDL-C may be only applicable to specific populations. Second, a comprehensive family history of dyslipidemia and/or CHD is usually unavailable or inaccurate (Casula et
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al., 2018). Third, the discordance between different clinical diagnostic criteria and heterogeneity of phenotype and genotype often confused the physicians (Damgaad et aal., 2018), especially for those without their own diagnostic guidelines including China. Last but not least, the calculation is complex and could not promote diagnosis conveniently in primary care. With a deeper understanding of FH, more factors have been described responsible for the manifestations, among which lipoprotein (a) [Lp(a)] has received a lot of attention (Isimikas, 2016). Previous studies have demonstrated significantly higher levels of Lp(a) in patients with FH compared to non-FH and its independent role in the risk stratifications (Alonso et al., 2014). The biochemical measurement of Lp(a) may explain 5% to 20% prevalence of the suspected FH, especially for those with negative FH-causing mutations (Nenseter et al., 2011).
This cross-sectional observational analysis used data from the dal-Outcomes randomized clinical trial to determine whether Lp(a) concentration is associated with the risk of major adverse cardiovascular events following ACS (Civeira, 2004).