Abstract W MP67: Non-traditional Serum Lipid Indices and Recurrent Stroke Risk

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Jong-Ho Park ◽  
Bruce Ovbiagele

Background: Expert consensus guidelines recommend low-density lipoprotein (LDL) cholesterol as the primary serum lipid target for recurrent stroke risk reduction. Indeed, emerging evidence suggests that non-traditional serum lipid indices may be better predictors of vascular risk than LDL. Triglycerides (TG)/high-density lipoprotein (HDL) is a powerful independent predictor of all-cause mortality and cardiovascular events. Furthermore, total cholesterol (TC)/HDL ratio, LDL/HDL and non-HDL have all been independently linked with greater coronary heart disease (CHD) risk. Little is known about the effects non-traditional serum lipid indices on recurrent vascular risk after a recent stroke. Method: We analyzed the Vitamin Intervention for Stroke Prevention study database comprising 3680 recent (<120 days) ischemic stroke patients followed up for 2 years. Independent associations of each 4 lipid index (TG/HDL, TC/HDL, LDL/HDL, and non-HDL) with recurrent stroke (primary outcome) and stroke/coronary heart disease (CHD)/vascular death (secondary outcome) were analyzed. Each of the 4 groups was stratified into quintiles according to the distribution of lipid indices. Results: Of all indices evaluated only TG/HDL was consistently and independently related to both outcomes: compared with the lowest quintile (≤1.93), the highest TG/HDL quintile (≥6.22) was associated with stroke [adjusted hazard ratio (AHR), 1.56; 95% CI, 1.05–2.32] and stroke/CHD/vascular death (AHR 1.39, 95% CI, 1.05–1.83), including adjustment for lipid modifier use. Compared with the lowest quintile (≤3.50), the highest TC/HDL quintile (≥5.98) was associated with stroke/CHD/vascular death (AHR 1.44, 95% CI, 1.03–2.01). LDL/HDL, non-HDL, elevated TG alone, and low HDL alone, were not independently linked to either outcome. Conclusions: Of various non-traditional serum lipid indices, elevated baseline TG/HDL and TC/HDL predict future vascular risk after a stroke, but only elevated TG/HDL is related to risk of recurrent stroke. Future studies should assess the role of TG/HDL as a potential therapeutic target for global vascular risk reduction after stroke.

Stroke ◽  
2011 ◽  
Vol 42 (12) ◽  
pp. 3397-3402 ◽  
Author(s):  
Bruce Ovbiagele ◽  
Philip M. Bath ◽  
Daniel Cotton ◽  
Richard Vinisko ◽  
Hans-Christoph Diener

Background and Purpose— Although obesity is an established risk factor for the occurrence of a primary stroke, little is known about the impact of baseline obesity on recurrent vascular risk among patients with recently symptomatic cerebrovascular disease. We evaluated the association of obesity with future vascular risk in patients with a recent history of stroke. Methods— We analyzed the database of a multicenter trial involving 20 332 patients with recent ischemic stroke followed for 2.5 years. Subjects were divided into 3 groups according to recognized body mass index categories representing lean, overweight, and obese. Primary outcome was time to first recurrent stroke and secondary outcome time to stroke, myocardial infarction, or vascular death. The independent association of obesity with outcome was assessed by controlling for other known risk factors. Results— Of 20 246 eligible subjects, 4805 (24%) were obese. After adjusting for confounders, compared with the lean group, being overweight (hazard ratio, 0.95; 95% CI, 0.85–1.06) or obese (hazard ratio, 0.95; 95% CI, 0.83–1.08) was not associated with increased recurrent stroke risk, but being overweight (hazard ratio, 0.84; 95% CI, 0.77–0.92) or obese (hazard ratio, 0.86; 95% CI, 0.77–0.96) was associated with lower risk of a major vascular event. Conclusions— Obesity is not related to recurrent stroke risk, but obese patients with stroke are at lower overall vascular risk than their leaner counterparts, supporting the widely held notion of the existence of a cardiovascular “obesity paradox.”


2018 ◽  
Vol 38 (1) ◽  
Author(s):  
Qing-Hui Zhang ◽  
Rui-Xing Yin ◽  
Wu-Xian Chen ◽  
Xiao-Li Cao ◽  
Yu-Ming Chen

Little is known about the association of the TIMD4 (T-cell immunoglobulin and mucin domain 4 gene)-HAVCR1 (hepatitis A virus cellular receptor 1) variants and lipid metabolism, the risk of coronary heart disease (CHD) and ischemic stroke (IS). The present study aimed to determine the TIMD4-HAVCR1 variants, their haplotypes and gene–environment interactions on serum lipid levels, the risk of CHD and IS, and the lipid-lowering efficacy of atorvastatin in a southern Chinese Han population. Genotypes of three variants in 622 controls, 579 CHD, and 546 IS patients were determined by the Snapshot technology. Atorvastatin calcium tablet (20 mg/day) was given in 724 hyperlipidemic patients for 8 weeks after genotyping. The rs12522248 genotypic and allelic frequencies were different between controls and patients, and were associated with the risk of CHD and IS. The rs1501908G-rs12522248T-rs2036402T haplotype was associated with an increased risk of CHD; the G-C-T haplotype was associated with lower risk of CHD; and the C-C-C haplotype was associated with an increased risk of IS. Variants and their haplotypes in controls were associated with triglyceride (rs1501908), low-density lipoprotein cholesterol (LDL-C, rs1501908, G-T-T), high-density lipoprotein cholesterol (HDL-C, rs12522248, C-C-C) and the ratio of total cholesterol (TC) to HDL-C (C-C-C). Interactions of rs1501908- and rs2036402-alcohol (HDL-C); rs1501908- and rs12522248-high body mass index (hBMI, ≥24 kg/m2; TC); and TIMD4-HAVCR1 variants-atorvastatin on several lipid parameters were detected. Interactions of rs12522248TC/CC-hBMI, G-T-T-, and C-C-C-smoking on the risk of CHD; and C-C-C-smoking, C-C-C-, and G-C-T-hBMI on the risk of IS were also observed. These findings suggest that the TIMD4-HAVCR1 variants may be the genetic risk factors for CHD and IS.


2021 ◽  
pp. jech-2020-214358
Author(s):  
Pekka Martikainen ◽  
Kaarina Korhonen ◽  
Aline Jelenkovic ◽  
Hannu Lahtinen ◽  
Aki Havulinna ◽  
...  

BackgroundGenetic vulnerability to coronary heart disease (CHD) is well established, but little is known whether these effects are mediated or modified by equally well-established social determinants of CHD. We estimate the joint associations of the polygenetic risk score (PRS) for CHD and education on CHD events.MethodsThe data are from the 1992, 1997, 2002, 2007 and 2012 surveys of the population-based FINRISK Study including measures of social, behavioural and metabolic factors and genome-wide genotypes (N=26 203). Follow-up of fatal and non-fatal incident CHD events (N=2063) was based on nationwide registers.ResultsAllowing for age, sex, study year, region of residence, study batch and principal components, those in the highest quartile of PRS for CHD had strongly increased risk of CHD events compared with the lowest quartile (HR=2.26; 95% CI: 1.97 to 2.59); associations were also observed for low education (HR=1.58; 95% CI: 1.32 to 1.89). These effects were largely independent of each other. Adjustment for baseline smoking, alcohol use, body mass index, igh-density lipoprotein (HDL) and total cholesterol, blood pressure and diabetes attenuated the PRS associations by 10% and the education associations by 50%. We do not find strong evidence of interactions between PRS and education.ConclusionsPRS and education predict CHD events, and these associations are independent of each other. Both can improve CHD prediction beyond behavioural risks. The results imply that observational studies that do not have information on genetic risk factors for CHD do not provide confounded estimates for the association between education and CHD.


2018 ◽  
Vol 275 ◽  
pp. e215
Author(s):  
S. Kutkiene ◽  
Z. Petrulioniene ◽  
A. Laucevicius ◽  
U. Gargalskaite ◽  
A. Saulyte ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document