Key result
PPAR-alpha concentrations are ~28% lower in ACS patients alongside a predominant recessive G allele.
Why the study?
PPAR-alpha influences lipid metabolism and inflammation in ACS, but the relationship between PPAR-alpha concentration and genetic polymorphism in ACS patients needed investigation.
Is there a relationship between PPAR-alpha concentration, Leu162Val (rs1800206) genetic polymorphism, and acute coronary syndrome?
Case-Control (n=180)
Is there a relationship between PPAR-alpha concentration, Leu162Val (rs1800206) genetic polymorphism, and acute coronary syndrome?
Absolute Event Rate: 1472.2% vs 2051.8%
p-value: p=<0.05
Decreased PPAR-alpha concentration and the presence of the G allele of the Leu162Val (rs1800206) SNP are associated with acute coronary syndrome, suggesting a potential novel biomarker or target.
Should not yet change ACS practice; leaves open validation as biomarker or target in prospective studies.
BACKGROUND AND OBJECTIVE: PPAR-alpha plays a key role in acute coronary syndrome (ACS). Its activation influences lipid metabolism and inflammation, impacting cardiovascular health and potentially mitigating risks related to heart conditions. This study aims to find the relationship between PPAR-alpha concentration and genetic polymorphism in ACS patients. METHODS AND MATERIALS: The study enrolled 90 ACS patients and 90 controls aged 30-70. Blood samples were analyzed for biomarkers (troponin, CK-MB, hs-CRP, PPARα) and rs1800206 SNP via ELISA and HRM-PCR. Data were statistically analyzed using SPSS v21, ANOVA, and ROC tests. RESULTS: The results showed an increase in the levels of troponin, CK-MB, and hs-CRP for the patient groups compared to the healthy groups with significant differences between the groups (p-value <0.05). The level of (PPAR-alpha) was low in patients (1472.2 ± 74.5) and high in the healthy group (2051.8 ± 149.9) with significant differences between study groups. ROC analysis identified CK-MB, and hs-CRP as optimal biomarkers for ACS diagnosis; PPARα showed good predictive value. The study also found that the dominant genotype (CC) represented a small percentage of the patient samples while the homozygotes (CG) and the recessive (GG) represented the highest percentage, unlike the healthy group. Also, Allele (C) has a low percentage in the patients' group while allele (G) has a high percentage with considering the G allele as a risk factor. In addition, the results showed an abnormal distribution of Hardy-Weinberg equilibrium indicating the presence of factors extraneous to the community that changed the genetic pattern. The results also showed that the dominant genetic model is the best expressive for the samples of the Iraqi community infected with ACS. CONCLUSIONS: The present study demonstrated a relationship between the concentration of PPAR-alpha and the genetic polymorphism of Leu162Val (rs1800206) SNP and acute coronary syndrome with a decrease in the concentration of PPAR-alpha and the predominance of the recessive gene and the recessive allele in patients compared to healthy individuals.
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Raeef et al. (2025) conducted a case-control in Acute coronary syndrome (ACS) (n=180). PPAR-alpha concentration and Leu162Val (rs1800206) SNP vs. Healthy controls was evaluated on PPAR-alpha concentration (p=<0.05). PPAR-alpha concentration was significantly lower in ACS patients (1472.2) compared to healthy controls (2051.8), alongside a predominance of the recessive G allele.
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