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Relationship Between Lipoprotein (a) [Lp(a)] and Cognition in Different Ischemic Stroke Subtypes.

ABSTRACT: Background and Purpose: Although elevated serum lipoprotein (a) [Lp(a)] is considered to be a risk factor of ischemic stroke, the relationship between Lp(a) and cognitive impairment after stroke remains unclear. This study investigated the association between serum Lp(a) and cognitive function after acute ischemic stroke (AIS) or transient ischemic attack (TIA). Methods: The study included 1,017 patients diagnosed with AIS or TIA from the cognition subgroup of the Third China National Stroke Registry (CNSR3). Montreal Cognitive Assessment (MoCA) at 2 weeks or discharge, 3 months, and 1 year was evaluated. The primary outcome was cognitive impairment at 1 year, defined as MoCA ≤ 22. The secondary outcome was cognition improvement at 1 year compared with 2 weeks. The association between Lp(a) levels and cognitive function was analyzed. Results: Among the 1,017 patients included, 326 (32.1%) had cognitive impairment at 1 year. Patients with MoCA ≤ 22 at 1 year were older, received less education, and had higher baseline NIHSS, higher proportion of ischemic stroke history, large artery atherosclerosis (LAA) subtype, and multiple infarctions (P < 0.05 for all). Patients with highest Lp(a) quartile had slightly higher percentage of cognitive impairment at 1 year but without statistical difference. In subgroup analysis of LAA subtype, the patients with highest Lp(a) quartile had higher percentage of cognitive impairment at 1 year (adjusted OR:2.63; 95% CI: 1.05-6.61, P < 0.05). What is more, the patients with highest Lp(a) quartile in LAA subtype had lower percentage of cognition improvement at 1 year. However, similar results were not found in small artery occlusion (SAO) subtype. Conclusion: Higher Lp(a) level was associated with cognitive impairment and less improvement of cognition in patients after AIS or TIA with large-artery atherosclerosis subtype.

SUBMITTER: Li J

PROVIDER: S-EPMC8677830 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundPrevious epidemiological and other studies have shown an association between ischemic stroke (IS) and frozen shoulder (FS). However, the causal relationship between them remains unclear. Therefore, the present study aimed to investigate the causal relationship between IS and FS using a two-sample Mendelian randomization method.MethodsOur research was divided into two stages: discovery and replication. The data were extracted from publicly available genome-wide association studies (GWAS). We selected a large sample of IS (n = 440, 328) and its subtypes (large-artery atherosclerotic stroke (LAS), cardioembolic stroke (CES), and stroke caused by small-vessel disease (SVS) and lacunar stroke (n = 254, 959) as exposure data. Additionally, we selected a large sample of FS as outcome data (n = 451, 099). Inverse variance weighting (IVW) was applied as the primary analysis method. The weighted median, MR-Egger, simple model, and weighted model were used as complementary analysis methods to assess causal effects. Moreover, heterogeneity was analyzed using Cochran's Q-test with IVW and MR-Egger. The MR-Egger intercept and MR-PRESSO analysis methods were used for pleiotropy testing. The stability of the results was also assessed using a leave-one-out analysis.ResultsIn the discovery stage, the IVW approach revealed an odds ratio (OR) of 1.207 with a 95% confidence interval (CI) of 1.027-1.417 and a P-value of 0.022. This suggests a causal association between IS levels and an increased risk of FS. In the subtype studies of IS, the findings were negative. However, during the replication stage, a significant causal link was found between selected lacunar strokes and FS with an OR of 1.252, a 95% CI of 1.105-1.419, and a P-value of 0.0004. All studies had no pleiotropy or heterogeneity, and the findings were robust.ConclusionsOur study confirmed the causal relationship between any IS level and increased risk of FS. Furthermore, the same results were obtained in the replication stage with lacunar stroke as an exposure factor. However, there was no direct causal relationship between the subtypes of IS and FS. Our study provides theoretical support for shoulder care for patients with IS.

Project description:BackgroundTo examine the association between lipoprotein(a) (Lp(a)) levels, LPA (rs10455872 and rs3798220) and IL1F9 (rs13415097) single nucleotide polymorphisms (SNPs) with coronary artery calcification (CAC), an important predictor for coronary artery disease (CAD).MethodsWe used data from 3799 (mean age ± SD: 59.0 ± 7.7 years, 47.1% men) Heinz Nixdorf Recall study participants. We applied linear regression models to explore the relation between the log-transformed Lp(a) levels and LPA and IL1F9 SNPs with loge (CAC + 1). The association between the SNPs and log-transformed Lp(a) levels was further assessed using linear regression. The models were adjusted for age and sex (Model 1) and additionally for Lp(a) levels (Model 2).ResultsWe observed a statistically significant association between log-transformed Lp(a) levels and CAC (Model 1: beta per log-unit increase in Lp(a) levels = 0.11; 95% confidence interval [95% CI] [0.04; 0.18], p = 0.002). Furthermore, the LPA SNP rs10455872 showed a statistically significant association with CAC (Model 1: beta per allele = 0.37 [0.14; 0.61], p = 0.002). The association between rs10455872 and CAC was attenuated after adjustment for Lp(a) levels (Model 2: beta per allele = 0.26 [- 0.01; 0.53], p = 0.06). Both LPA SNPs also showed a statistically significant association with Lp(a) levels (Model 1: betars10455872 per allele: 1.56 [1.46; 1.65], p < 0.0001 and betars3798220 per allele: 1.51 [1.33; 1.69], p < 0.0001)). The Mendelian randomization analysis showed that Lp(a) is a causal risk factor for CAC (estimate per log-unit increase in Lp(a) levels (95% CI), p: 0.27 [0.11; 0.44], p = 0.001). The IL1F9 SNP did not show any statistically significant association with Lp(a) levels or with CAC.ConclusionsWe provide evidence for the association of LPA rs10455872 with higher levels of Lp(a) and CAC in our study. The results of our study suggest that rs10455872, mediated by Lp(a) levels, might play a role in promoting the development of atherosclerosis leading to cardiovascular disease events.

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Relationship Between Lipoprotein (a) [Lp(a)] and Cognition in Different Ischemic Stroke Subtypes.

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