Association of lipoprotein(a) levels with recurrent events in patients with coronary artery disease

Abstract

ObjectiveWhether lipoprotein(a) (Lp(a)) is a predictor for recurrent cardiovascular events (RCVEs) in patients with coronary artery disease (CAD) has not been established. This study, hence, aimed to examine the potential impact of Lp(a) on RCVEs in a real-world, large cohort of patients with the first cardiovascular event (CVE).MethodsIn this multicentre, prospective study, 7562 patients with angiography-diagnosed CAD who had experienced a first CVE were consecutively enrolled. Lp(a) concentrations of all subjects were measured at admission and the participants were categorised according to Lp(a) tertiles. All patients were followed-up for the occurrence of RCVEs including cardiovascular death, non-fatal myocardial infarction and stroke.ResultsDuring a mean follow-up of 61.45±19.57 months, 680 (9.0%) RCVEs occurred. The results showed that events group had significantly higher Lp(a) levels than non-events group (20.58 vs 14.95 mg/dL, p<0.001). Kaplan-Meier analysis indicated that Lp(a) tertile 2 (p=0.001) and tertile 3 (p<0.001) groups had significantly lower cumulative event-free survival rates compared with tertile 1 group. Moreover, multivariate Cox regression analysis further revealed that Lp(a) was independently associated with RCVEs risk (HR: 2.01, 95% CI: 1.44 to 2.80, p<0.001). Moreover, adding Lp(a) to the SMART risk score model led to a slight but significant improvement in C-statistic (∆C-statistic: 0.018 (95% CI: 0.011 to 0.034), p=0.002), net reclassification (6.8%, 95% CI: 0.5% to 10.9%, p=0.040) and integrated discrimination (0.3%, 95% CI: 0.1% to 0.7%, p<0.001).ConclusionsCirculating Lp(a) concentration was indeed a useful predictor for the risk of RCVEs in real-world treated patients with CAD, providing additional information concerning the future clinical application of Lp(a).

Lipoprotein(a) and Cardiovascular Outcomes in Patients with Previous Myocardial Infarction: A Prospective Cohort Study

“…Among the 3864 patients with prior MI, 3078 (79.7%) patients were men, and the mean age of the population was 61.7±16.1 years. In the overall population, plasma Lp(a) concentration had a skewed distribution with a tail toward the highest levels, which was consistent with previous studies 20 (as shown in Supplementary Figure S2). Compared to those free of events, those with CVEs were older, more likely to be female, with higher levels of FPG, HbA1c and hsCRP.…”

“…Moreover, new compounds like proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors and antisense oligonucleotide (ASO) targeting hepatic apo(a) are recently reported to reduce circulating Lp(a) levels remarkably, suggesting that the need for a precise characterization of the Lp(a)-associated CV risk is of increasing importance [14][15][16] . To date, Lp(a) has been suggested as a risk predictor in some special populations, such as acute coronary syndrome, stable or premature coronary artery disease (CAD), diabetes mellitus (DM), familial hypercholesterolemia (FH) or postmenopausal women [17][18][19][20][21] . Whether Lp(a) poses additional risk in patients with prior MI is still unclear and the existing studies with small sample size or short-term follow-up did not achieve consistent evidence [22][23][24][25][26][27] .…”

“…LDL-C was corrected for Lp(a)derived cholesterol (LDL-Ccorr), which was calculated as LDL- 28 The Lp(a) quantification was assessed using an immunoturbidimetry method [LASAY Lp(a) auto; SHIMA laboratories] and presented in mg/dL with a normal value of < 30 mg/dL as previously described. 19,20 Although this method was not apo(a) isoform-independent, an Lp(a) protein-validated standard was used to calibrate the examination, along with linking the results to the World Health Organization/International Federation of Clinical Chemistry and Laboratory Medicine International Reference Reagent. The intra-and interassay coefficients of variation were <10%.…”

“…[14][15][16] To date, Lp(a) has been suggested as a risk predictor in some special populations, such as patients with acute coronary syndrome, stable or premature coronary artery disease (CAD), diabetes mellitus (DM), familial hypercholesterolemia (FH), or postmenopausal women. [17][18][19][20][21] Whether Lp(a) poses additional risk in patients with prior MI is still unclear and the existing studies with a small sample size or short-term follow-up did not achieve consistent evidence. [22][23][24][25][26][27] Based on the situation that data regarding the prognostic importance of Lp(a) in post-MI patients are limited and new therapies are in development, 12 the present study aimed to evaluate the association between Lp(a) and long-term outcomes in patients with prior MI, which may help to provide additional information concerning the future clinical application of Lp(a).…”

Assessment of endogenous fibrinolysis in clinical practice using novel tests: ready for clinical roll-out?

“…High Lp(a) level has been identified as an independent risk factor of cardiovascular disease with causal links to atherosclerosis. Among patients with known coronary artery disease, it also predicts worse long-term outcomes in terms of allcause death, cardiovascular death, non-fatal myocardial infarction, stroke and in-stent restenosis [48,49].…”