Key result
Higher lipid and oxidative genetic risk score linked to ~31% higher MACE risk in metabolic syndrome.
Why the study?
Metabolic syndrome is a major health hazard with genetic susceptibility regions identified, but the value of a genetic risk score in predicting cardiovascular outcomes in MetS patients was unclear.
Does a higher genetic risk score involving lipidic and oxidative pathways predict MACE and cardiovascular mortality in coronary patients with metabolic syndrome?
Cohort (n=1,101)
Does a higher genetic risk score involving lipidic and oxidative pathways predict MACE and cardiovascular mortality in coronary patients with metabolic syndrome?
A genetic risk score comprising variants in lipidic and oxidative pathways can serve as a useful stratification tool to predict worse prognosis over time in coronary patients with metabolic syndrome.
Answers are grounded in this paper and cite their sources.
May support risk stratification in metabolic syndrome; leaves open prospective validation and outcome impact.
Background Metabolic syndrome (MetS), characterized by a cluster of cardiovascular risk factors, is considered to be the major health hazard of modern world and a 21st century epidemic. Recent GWAS have identified several susceptibility regions involved in lipid metabolism and oxidation, also associated with MetS. Genetic risk score (GRS) is an emerging method that attempts to establish correlation between SNPs and clinical phenotypes. Aim Evaluate the value of a GRS encompassing SNPs involved in lipidic metabolism and oxidation pathways, in predicting CAD outcome (MACEs and long-term cardiovascular Mortality) in a coronary population with MetS. Methods 1101 coronary patients and MetS, were selected from the GENEMACOR study. Genotyping was performed by TaqMan allelic discrimination assay. A Multiplicative score (mGRS) was constructed according to the multiplicative model with variants belonging to the lipid and oxidative axes (PSRC1, PCSK9, KIF6, ZNF259, LPA, APO E, PON192, PON108, PON55, MTHFR677, MTHFR1298, MTHFD1L). This GRS was categorized using the mean (higher vs lower than mean). Cumulate Mortality Hazards Model (Cox regression) adjusted for age, gender, smoking, hypertension, dyslipidaemia, diabetes, hsCRP, eGFR, Ejection fraction (EF), and multivessel disease) was used to find independent predictors of cardiovascular outcome. We performed Kaplan-Meier Survival curves for both groups (higher vs lower than mean GRS) and log-rank test to compare survival distributions in both groups. Results The following variables have emerged independently associated with time to MACE occurrence: mGRS (HR=1.31 95% CI (1.07; 1.59); p=0.008), male gender, EF and multivessel disease. Concerning cardiovascular mortality, mGRS also remained an independent predictor (HR=1.44 (1.04–1.99); p=0.028) alongside age, smoking, diabetes and EF. The Log-Rank test showed significant differences between the two curves related to MACE occurrence and cardiovascular mortality (p=0.001 and 0.002, respectively). The Kaplan-Meier survival showed that as mGRS increases, patient survival decreases. Conclusion In patients with MetS, a GRS comprising variants in lipidic and oxidative pathways, proved to be a useful stratification tool, identifying patients likely to have a worst prognosis over time. Our data further underlines the additive potential and clinical utility of genetic information in shaping secondary prevention.
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Sousa et al. (2020) conducted a cohort in Coronary disease with metabolic syndrome (MetS) (n=1,101). Multiplicative genetic risk score (mGRS) for lipidic and oxidative pathways vs. Lower than mean mGRS was evaluated on MACE occurrence (HR 1.31, 95% CI 1.07-1.59, p=0.008). A higher multiplicative genetic risk score for lipid and oxidative pathways independently predicted MACE in coronary patients with metabolic syndrome (HR 1.31; 95% CI 1.07-1.59; p=0.008).
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