Abstract

The role of lipoprotein-A [Lp (a)] as a risk factor for stroke is less well documented than for coronary heart disease. Hence, we conducted a systematic review and meta-analysis for the published observational studies in order to investigate the association of Lp (a) levels with the risk of stroke and its subtypes. In our meta-analysis, 41 studies involving 7874 ischemic stroke (IS) patients and 32,138 controls; 13 studies for the IS subtypes based on TOAST classification and 7 studies with 871 Intracerebral hemorrhage (ICH) cases and 2865 control subjects were included. A significant association between increased levels of Lp (a) and risk of IS as compared to control subjects was observed (standardized mean difference (SMD) 0.76; 95% confidence interval (CIs) 0.53–0.99). Lp (a) levels were also found to be significantly associated with the risk of large artery atherosclerosis (LAA) subtype of IS (SMD 0.68; 95% CI 0.01–1.34) as well as significantly associated with the risk of ICH (SMD 0.65; 95% CI 0.13–1.17) as compared to controls. Increased Lp (a) levels could be considered as a predictive marker for identifying individuals who are at risk of developing IS, LAA and ICH.

Highlights

  • The role of lipoprotein-A [Lp (a)] as a risk factor for stroke is less well documented than for coronary heart disease

  • The LPA gene regulates the variation in Lp (a) plasma concentrations genetically, ranging from 36% in the P­ ROCARDIS8 consortium to 70–90% in genome-wide association studies, with larger apo(a) isoforms related with lower values of Lp (a)[9,10]

  • 98 articles were found and on further exclusion, a total of 56 full text articles were reviewed for eligibility and 45 studies were included in the systematic review and meta-analysis

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Summary

Introduction

The role of lipoprotein-A [Lp (a)] as a risk factor for stroke is less well documented than for coronary heart disease. We conducted a systematic review and meta-analysis for the published observational studies in order to investigate the association of Lp (a) levels with the risk of stroke and its subtypes. Population-based cohort studies on stroke have produced mixed results, with some research associating raised Lp (a) levels to a higher incidence of I­ S16–19, while others have found no l­ink[20,21,22]. This could be due to a lack of discrimination across incidence stroke ­subtypes[22], as well as ethnic or other disparities in cohort composition. A growing number of epidemiological studies have found a link between dyslipidemia

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