Abstract
Robust associations between lipoprotein(a) [Lp(a)] and CVD outcomes among general populations have been published in previous studies. However, associations in high risk primary prevention and secondary prevention populations are less well defined. In order to investigate this further, a systematic review was performed including prospective studies, which assessed the relationship between Lp(a) and CVD outcomes using multivariable analyses. Additional information was gathered on Lp(a) assays, multivariable modelling and population characteristics.Literature searches from inception up to December 2015 retrieved 2850 records. From these 60 studies were included. Across 39 primary prevention studies in the general population (hazard ratios ranged from 1.16 to 2.97) and seven high risk primary prevention studies (hazard ratios ranged from 1.01 to 3.7), there was evidence of a statistically significant relationship between increased Lp(a) and an increased risk of future CVD. Results in 14 studies of secondary prevention populations were also suggestive of a modest statistically significant relationship (hazard ratios ranged from 0.75 to 3.7).Therefore current evidence would suggest that increased Lp(a) levels are associated with modest increases in the risk of future CVD events in both general and higher risk populations. However, further studies are required to confirm these findings.Electronic supplementary materialThe online version of this article (doi:10.1186/s12944-016-0258-8) contains supplementary material, which is available to authorized users.
Highlights
Cardiovascular disease (CVD) is a leading cause of death and disability [1, 2]
Lp(a) comparison type: Categorical Two effect sizes reported, both were statistically significant showing a positive association between Lp(a) and non-fatal myocardial infarction (MI) or coronary death (CD) (< 30 mg/dl vs. ≥ 30 mg/dl: hazard ratios (HRs) 2.98, 95 % confidence interval (CI): 1.76 to 5.03) and first ever major CVD event (< 30 mg/dl vs. ≥ 30 mg/dl: HR 3.47, 95 % CI: 2.48 to 4.85) These results show that Lp(a) concentration is independently associated with three-fold increase in risk of major adverse cardiovascular events within 15 years after coronary artery bypass grafting (CABG)
Five out of eight effect sizes were statistically significant and all were positive association. These ranged from: Lp(a) tertile 1 vs. Lp(a) tertile 3 (> 1.83 mg/dl): HR 1.9, 95 % CI: 1 to 3.5 To Lp(a) tertile 1 vs. Lp(a) tertile 2 (cutpoint 1.83 mg/dl: HR 3.7, 95 % CI: 1.4 to 10.1 Three out of eight analyses were not significant (NS) The results showed that high levels of Lp(a) were independently associated with a higher 1-year risk of major adverse cardiac events (MACE), Lp(a) comparison type: Categorical One effect size reported for the comparison of controls vs. cases
Summary
Cardiovascular disease (CVD) is a leading cause of death and disability [1, 2]. Elevated levels of low-density lipoprotein cholesterol (LDL-C) are a major contributor to atherosclerosis leading to subsequent CVD events. Numerous clinical trials of lipid lowering drugs have found that reducing LDL-C levels substantially reduces the risk of CVD [3,4,5] suggesting a strong direct relationship between plasma LDL-C levels and CVD outcomes [6, 7]. Still have residual CVD risk and suffer from CVD events despite significant LDL-C lowering. In addition to LDL-C, other risk factors are likely to influence residual cardiovascular risk. Lipoprotein(a) [Lp(a)], has been proposed to be independently associated with CVD [8]
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