Serum serial number .txt10/26/2022 16 Current guidelines in the US, Canada and Europe define 1.29 mmol/l (50 mg/dl) as a risk-enhancing factor. 2 A genome-wide association study also showed a steep increase in risk at >0.78 mmol/l and an added risk at >1.22 mmol/l. The Copenhagen City Heart Study (n=7,524) found that Lp(a) >0.78 mmol/l is associated with an increased risk of MI in a dose-dependent manner, with an adjusted HR of 1.2 (95% CI ) for Lp(a) 0.13–0.75 mmol/l (5–29 mg/dl), 1.6 (95% CI ) for Lp(a) 0.78–1.97 mmol/l (30–76 mg/dl), 1.9 (95% CI ) for Lp(a) 1.99–3.03 mmol/l (77–117 mg/dl), and 2.6 (95% CI ) for Lp(a) >3.03 mmol/l (117 mg/dl) versus for Lp(a) 0.62 mmol/l, and curvilinearly increased according to the increase in Lp(a) and became significant at around 1.24 mmol/l. Several practical cut-offs for Lp(a), including 0.78 mmol/l (30 mg/dl) and 1.29 mmol/l (50 mg/dl) for the risk stratification of coronary artery disease (CAD) and ischaemic stroke, have been proposed. 11,12 The median Lp(a) level in the general Asian population is 0.21–0.36 mmol/l, which is lower than that in black (1.01 mmol/l), Hispanic (0.49 mmol/l) and Arab (0.39 mmol/l) populations. There are ethnic differences in median Lp(a) level between countries caused by the difference in the prevalence of LPA single nucleotide polymorphisms and Apo(a) isoforms. 10 Patients with established cardiovascular disease had higher levels of Lp(a) ( Figure 2). 3 Plasma concentration is determined primarily by the LPA gene locus, without significant acquired or environmental influences. The distribution of plasma Lp(a) level is skewed and ranges widely between individuals, with no sex differences. In this review, we summarise the clinical impact of elevated Lp(a), the evaluation of Lp(a) in daily practice, and the potential therapeutic approaches for high Lp(a) ( Figure 1). 5–8 Approximately 20–30% of people have elevated Lp(a), so more clinical attention is required. However, several therapies, including proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, inclisiran and antisense oligonucleotides, have been reported to reduce the plasma level. 2 The level of Lp(a) is established during childhood and is mostly consistent throughout the lifetime because it is regulated primarily by the LPA gene locus. The independent association between elevated Lp(a) and an increased risk of cardiovascular events has been demonstrated, therefore the role of residual risk in patients with statin-based conventional therapy has been emphasised. 1–4 The increased risk is often explained by the enhanced progression of atherosclerosis in the arterial system through the proatherogenic and anti-fibrinolytic nature of Lp(a) in combination with other factors, including age, sex, ethnicity, comorbidities and LDL cholesterol level. An increased risk of cardiovascular disease, including acute coronary syndrome, ischaemic stroke and aortic stenosis, in patients with high plasma Lp(a) has been demonstrated in clinical studies, genome-wide association studies and Mendelian randomisation studies. The lipoprotein(a) (Lp(a)) molecule consists of an apolipoprotein (Apo) B-containing LDL-like segment and a plasminogen-like glycoprotein Apo(a) segment.
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