Biological and clinical implications of TNF-α promoter and CYP1B1 gene variations in Coronary Artery Disease susceptibility

2021 ◽  
Vol 22 ◽  
Author(s):  
Rashid Mir ◽  
Imadeldin Elfaki ◽  
Chandan K. Jha ◽  
Jamsheed Javid ◽  
Abdullatif Taha Babakr ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Gene Polymorphism ◽  
P Value ◽  
Inflammatory Disorder ◽  
Genotype Distribution ◽  
Direct Dna Sequencing ◽  
Tnf Α ◽  
Significant Difference ◽  
Artery Disease

Background: Background: Cardiovascular diseases (CVD) are important causes of death worldwide. Atherosclerosis is a chronic inflammatory disorder. It is the major cause of CVD and is manifested by ischemic heart disease or coronary artery disease (CAD). TNF-α is a pro-inflammatory cytokine that regulates immune response and promotes the development of atherosclerosis. Cytochrome p450 1B1 (CYP1B1) is an enzyme involved in the metabolism of endogenous and exogenous substrates. Objectives: This study aimed at examining the association of TNF-α rs1800629 G >A and CYP1B1 rs1056827 G>T gene polymorphisms with CAD susceptibility in an Indian cohort. Methods: AS-PCR and direct DNA sequencing were used to examine the association of TNF-α rs1800629 G >A and CYP1B1 rs1056827 G>T gene polymorphism with CAD in an Indian cohort. A total of 100 clinically confirmed cases of CAD and 110 matched apparently healthy controls were genotyped. Results: Allelic and genotypic frequencies did not deviate from Hardy-Weinberg equilibrium in the controls (p>0.05) for TNF-α G-308A and CYP1B1 rs1056827G>A. There was no significant difference between the TNF-α rs1800629 A>G genotype distribution between cases and controls (P-value >0.05). A significant difference was observed between the CYP1B1 rs1056827 G>T genotype distribution between CAD cases and controls (P<0.0003). Our result indicated that in the codominant model, the GA genotype of the CYP1B1 rs1056827 G>T was associated with CAD with OR= 2.21(1.17 to 4.15), RR=1.38(1.07 to 1.78), and P<0.013. In the dominant model, the (GA+AA) genotype was associated with CAD with OR=2.79(1.54 to 5.05) and P<0.007. The CYP1B1 rs1056827 ‘A’ allele was associated with CAD with OR = 2.30 (1.55 to 3.42) and P< 0.0001. Our results indicated that TNF-α 1800629 gene polymorphism was strongly associated with hypercholesteremia (P<0.0009), HDL (P<0.0001), TGL (P<0.039), hypertension (P<0.0001), and smoking (P<0.0001) in patients with Coronary Artery Disease. Similar correlations of CYP1B1 rs1056827 genotypes were reported with cholesterol (P<0.020), HDL (P<0.002), LDL (P<0.006), hypertension (P<0.03), and smoking (P<0.005). Conclusion: It was reported that the GA genotype of the CYP1B1 rs1056827 G>T was strongly associated with susceptibility to Coronary Artery Disease with OR= 2.21(1.17 to 4.15)) and P<0.013, and similarly, its A allele was associated with predisposition to CAD with OR = 2.30(1.55 to 3.42) and P< 0.0001. Our results indicated that TNF-α 1800629 gene polymorphism is not associated with predisposition to Coronary Artery Disease. Nevertheless, these results should be taken with caution and further validated with larger-scale studies before being introduced in the clinical setting.

scholarly journals Association of TNF-α (-308G/A) Gene Polymorphism with Circulating TNF-α Levels and Excessive Daytime Sleepiness in Adults with Coronary Artery Disease and Concomitant Obstructive Sleep Apnea

2021 ◽  
Vol 10 (15) ◽  
pp. 3413
Author(s):  
Afrouz Behboudi ◽  
Tilia Thelander ◽  
Duygu Yazici ◽  
Yeliz Celik ◽  
Tülay Yucel-Lindberg ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Obstructive Sleep Apnea ◽  
Coronary Artery ◽  
Sleep Apnea ◽  
Gene Polymorphism ◽  
Excessive Daytime Sleepiness ◽  
Daytime Sleepiness ◽  
Obstructive Sleep ◽  
Tnf Α ◽  
Artery Disease

Obstructive sleep apnea (OSA) is common in patients with coronary artery disease (CAD), in which inflammatory activity has a crucial role. The manifestation of OSA varies significantly between individuals in clinical cohorts; not all adults with OSA demonstrate the same set of symptoms; i.e., excessive daytime sleepiness (EDS) and/or increased levels of inflammatory biomarkers. The further exploration of the molecular basis of these differences is therefore essential for a better understanding of the OSA phenotypes in cardiac patients. In this current secondary analysis of the Randomized Intervention with Continuous Positive Airway Pressure in CAD and OSA (RICCADSA) trial (Trial Registry: ClinicalTrials.gov; No: NCT 00519597), we aimed to address the association of tumor necrosis factor alpha (TNF-α)-308G/A gene polymorphism with circulating TNF-α levels and EDS among 326 participants. CAD patients with OSA (apnea–hypopnea-index (AHI) ≥ 15 events/h; n = 256) were categorized as having EDS (n = 100) or no-EDS (n = 156) based on the Epworth Sleepiness Scale score with a cut-off of 10. CAD patients with no-OSA (AHI < 5 events/h; n = 70) were included as a control group. The results demonstrated no significant differences regarding the distribution of the TNF-α alleles and genotypes between CAD patients with vs. without OSA. In a multivariate analysis, the oxygen desaturation index and TNF-α genotypes from GG to GA and GA to AA as well as the TNF-α-308A allele carriage were significantly associated with the circulating TNF-α levels. Moreover, the TNF-α-308A allele was associated with a decreased risk for EDS (odds ratio 0.64, 95% confidence interval 0.41–0.99; p = 0.043) independent of age, sex, obesity, OSA severity and the circulating TNF-α levels. We conclude that the TNF-α-308A allele appears to modulate circulatory TNF-α levels and mitigate EDS in adults with CAD and concomitant OSA.

scholarly journals IL-32 Serum Levels in Coronary Artery Disease Patient and its Relationship with IL-6 and TNF-α Serum Levels

2021 ◽  
Author(s):  
Mina Mohammad-Rezaei ◽  
Reza Ahmadi ◽  
Ali Rafiei ◽  
Arsalan Khaledifar ◽  
Shohila Fatahi ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Serum Levels ◽  
Arterial Stenosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Subjects ◽  
Tnf Α ◽  
Significant Difference ◽  
Major Vessel ◽  
Artery Disease

Abstract Coronary Artery Disease (CAD) is a chronic inflammatory disease caused by atherosclerosis and arteries become clogged due to plaque formation, fat accumulation, and various sorts of immune cells. IL-32 is a new proinflammatory cytokine, which enhances inflammation through inducing different inflammatory cytokines. The purpose of current research was to assess IL-32 serum levels in coronary artery disease subjects and its relationship with serum levels of IL-6 and TNF-α. Forty-two subjects diagnosed with CAD and thirty-nine control subjects were enrolled in the research. Serum levels of IL-6, TNF-α, and IL-32 were measured using the enzyme-linked immunosorbent assay (ELISA). IL-32, TNF-α, and IL-6 serum levels were significantly higher by 2.7, 3.48, and 3.2-fold in the CAD subjects than in control subjects, respectively. Moreover, no significant difference was found in TNF-α, IL-6 and IL-32 serum levels with the clogged arteries number in the CAD group. TNF-α and IL-32 serum levels in the CAD subjects with cardiac arterial stenosis in one major vessel were significantly increased than CAD subjects with cardiac arterial stenosis in more than one major vessels. ROC curve analysis revealed that serum levels of IL-32, TNF-α, and IL-6 showed good abilities in predicting CAD. Also, Multiple logistic regression analyses suggested that TNF-α, IL-6, and IL-32, serum levels of LDL and ox-LDL were independently related to the presence of CAD, while HDL serum levels were not. TNF-α, IL-32, and IL-6 showed an increase in CAD group and serum levels of these cytokines showed good abilities in predicting CAD. Our data suggested the involvement of TNF-α and IL-32 in the early stage of CAD.

Potential Impact of MicroRNA-423 Gene Variability in Coronary Artery Disease

2019 ◽  
Vol 19 (1) ◽  
pp. 67-74 ◽  
Author(s):  
Chandan K. Jha ◽  
Rashid Mir ◽  
Imadeldin Elfaki ◽  
Naina Khullar ◽  
Suriya Rehman ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Recessive Model ◽  
Amplification Refractory Mutation System ◽  
Genotype Distribution ◽  
Healthy Controls ◽  
Increased Risk ◽  
Significant Difference ◽  
Artery Disease ◽  
Gene Variability

Aim: Studies have evaluated the association of miRNA-423 C>A genotyping with the susceptibility to various diseases such cancers, atherosclerosis and inflammatory bowel disease but the results were contradictory. However, no studies have reported the association between miRNA-423 rs6505162 C>A polymorphism and susceptibility of coronary artery disease. MicroRNAs regulate expression of multiple genes involved in atherogenesis. Therefore, we investigated the association of microRNA-423C>T gene variations with susceptibility to coronary artery disease. Methodology: This study was conducted on 100 coronary artery disease patients and 117 matched healthy controls. The genotyping of the microRNA-423 rs6505162C>A was performed by using Amplification refractory mutation system PCR method (ARMS-PCR). Results: A significant difference was observed in the genotype distribution among the coronary artery disease cases and sex-matched healthy controls (P=0.048). The frequencies of all three genotypes CC, CA, AA reported in the patient’s samples were 55%, 41% and 4% and in the healthy controls samples were 55%, 41% and 4% respectively. Our findings showed that the microRNA-423 C>A variant was associated with an increased risk of coronary artery disease in codominant model (OR = 1.96, 95 % CI, 1.12-3.42; RR 1.35(1.05-1.75, p=0.017) of microRNA-423CA genotype and significant association in dominant model (OR 1.97, 95% CI (1.14-3.39), (CA+AA vs CC) and non-significant association for recessive model (OR=1.42, 95%CI=0.42-4.83, P=0.56, AA vs CC+CA).While, the A allele significantly increased the risk of coronary artery disease (OR =1.56, 95 % CI, 1.03-2.37; p=0.035) compared to C allele. Therefore, it was observed that more than 1.96, 1.97 and 1.56 fold increased risk of developing coronary artery disease. Conclusion: Our findings indicated that microRNA-423 CA genotype and A allele are associated with an increased susceptibility to Coronary artery disease.

scholarly journals Polymer free drug-eluting stents versus durable polymer drug-eluting stents in elective percutaneous coronary interventions in patients with stable coronary artery disease patients

QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
S M A Altoukhy ◽  
A A A Rezq ◽  
B A M Anany ◽  
W A M Elhamady ◽  
M F Metwally ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Inflammatory Response ◽  
Stable Coronary Artery Disease ◽  
Drug Eluting Stents ◽  
P Value ◽  
Effort Angina ◽  
Significant Difference ◽  
Drug Eluting ◽  
Artery Disease

Abstract Aim To compare the inflammatory response of polymer-free versus permanent polymer drug-eluting stents in patients with stable coronary artery disease undergoing elective PCI, and the effect of this inflammatory response on the 6 month clinical outcomes. Methods This randomized prospective comparative study was conducted on 100 patients with stable coronary artery disease planned for elective PCI divided into 50 patients with deployed permanent polymer DES (PP-DES) groups and 50 patients with polymer free DES (PF-DES). Blood samples were taken to assess serum level of hsCRP before the procedure and the first day after the procedure. The target end points were the recurrence of effort angina, incidence of target lesion revascularization (TLR) over a period of 6 months and the inflammatory response by measuring the percentage of rise in hsCRP level. Results There was no statistically significant difference in the clinical outcome in the first six months between the patients who had PP-DES and the patients who had PF-DES regarding recurrence of effort angina (p-value = 0.822) and TLR (p-value = 0.727), with no patients developing myocardial infarction or stent thrombosis. There was a statistically significant inflammatory response after stent deployment in both groups represented by a significant rise in the serum level of hsCRP on the first day after the procedure in both groups (p-value &lt; 0.001), but there was no statistically significant difference in the inflammatory response between PP-DES and PF-DES (p-value = 0.978). The number of patients having recurrence of anginal symptoms and TLR with hsCRP rise ≥ 11.36% was higher than those having the same with hsCRP &lt; 11.36%. However, this difference was not statistically significant regarding recurrence of anginal symptoms (p = 0.057) and TLR (p = 0.092). Conclusion The PF-DES was proved to be non-inferior to PP-DES regarding the short-term clinical outcome and the early inflammatory response. It was concluded that the presence of polymeric coating in PP-DES did not add to the magnitude of the inflammatory response and it did not significantly increase the incidence of recurrence of anginal symptoms and TLR in this group of patients.

Glutamine-Arginine 192 Polymorphism of Paraoxonase 1 Gene in Coronary Artery Disease Patients Compared to Healthy Controls in a Study from Kerala

2021 ◽  
Vol 8 (03) ◽  
pp. 136-140
Author(s):  
Rakhi Sasidharan Nair ◽  
Roshni Hareendra Babu ◽  
Shajee Sivasankaran Nair ◽  
Saboora Beegum
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Paraoxonase 1 ◽  
Control Group ◽  
Case Group ◽  
Genotype Distribution ◽  
Healthy Controls ◽  
Allele Distribution ◽  
Significant Difference ◽  
Artery Disease

BACKGROUND Coronary artery disease is multifactorial in origin. Coronary artery disease predisposition is attributed to genetic factors also. Many gene polymorphisms are implicated out of which paraoxonase 1 (PON 1) gene is an important one. The product of paraoxonase gene is paraoxonase enzyme which is seen in serum associated with high density lipoprotein (HDL). This enzyme is mainly synthesised by the liver. The protective effect of HDL is attributed to the presence of such enzymes on it. Gln to Arg polymorphism at position 192 confers a risk of developing atherosclerosis and coronary artery disease (CAD). This study is done to assess the genotype distribution of PON 1 gene in CAD patients compared to healthy controls in a population from Kerala. METHODS The case group consists of 100 angiographically proven CAD patients with no history of hypertension, diabetes mellitus, hepatic disease or smoking. The control group had 100 healthy controls from the general population. PON 1 gene was amplified by a polymerase chain reaction (PCR) technique already reported and restriction fragment length polymorphism by the restriction enzyme Alwl was done to assess the polymorphism. to assess the polymorphism. RESULTS In this study, the frequency of heterozygous genotype QR was 86 % in control and 76 % in cases. Though there was no significant difference in allele distribution of Q or R, RR genotype was significantly higher in the case group ( 2 = 8.82; p value = .012). With binary logistic regression model, adjusting for age and sex, RR genotype is independently associated with CHD. Adjusted odds ratio of RR was 5.24 with 95 % confidence interval (CI) 1.41 - 19.47 for developing CHD (p < 0.05). CONCLUSIONS The RR genotype is more frequently seen in CAD patients than in controls. The QR genotype is more frequent than QQ or RR in both cases and controls. KEYWORDS Coronary Artery Disease, Paraoxonase, Gene Polymorphism

scholarly journals NO Level and Endothelial NO Synthase Gene Polymorphism (Glu298Asp) in the Patients with Coronary Artery Disease from the Turkish Population

2004 ◽  
Vol 36 (10) ◽  
pp. 661-666 ◽  
Author(s):  
Lale Afrasyap ◽  
Guler Ozturk
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Gene Polymorphism ◽  
Turkish Population ◽  
Control Group ◽  
Enos Gene ◽  
Nitric Oxide Level ◽  
Significant Difference ◽  
Artery Disease

Abstract Nitric oxide is synthesized from L-arginine by endothelial nitric oxide synthase encoded by eNOS gene. This study was performed to investigate the relationship between the serum nitric oxide level and eNOS gene polymorphism in the Turkish population with angiographically diagnosed coronary artery disease (63.47 ± 9.10 years old, n=250) and control subjects without any history and/or risk factors of coronary artery disease (60.71 ± 9.14 years old, n=150). Griess assay and PCR-RFLP analysis were used to measure the serum nitric oxide metabolites and genotypes, respectively. It was found that Glu/Glu, Glu/Asp and Asp/ Asp genotype frequencies of the eNOS were 49.3%, 41.3% and 9.3% respectively in the control group, and 45.6%, 41.2% and 13.2% in the patient group. Serum nitric oxide levels were (32.56 ± 17.26) μM in controls and (29.84 ± 11.88) μM in patients. Neither the frequencies of the Glu298Asp genotypes nor the serum nitric oxide levels showed a significant difference between the groups. There was also no correlation between serum nitric oxide levels and the frequencies of the eNOS genotypes. Result showed that the coronary artery disease of the Turkish population seemed to develop without any alterations in eNOS Glu298Asp genotype frequency and the serum nitric oxide level.

scholarly journals ApoB gene polymorphism (rs676210) and its pharmacogenetics impact on atorvastatin response among Iraqi population with coronary artery disease

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Shaimaa Y. Abdulfattah ◽  
Salwa J. Al-Awadi
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Gene Polymorphism ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Genotype Distribution ◽  
Anova Analysis ◽  
Atorvastatin Therapy ◽  
Artery Disease

Abstract Background Drug response is below genetic influence, proven by the genetic variants. Pharmacogenetics trials are performed in many diseases, including coronary artery disease. This study was designed to determine the genetic polymorphism (rs676210) Pro2739leu G > A in the lipid metabolism-related gene (ApoB gene) and its pharmacogenetic role in the response to atorvastatin drug in a sample of Iraqi population with coronary artery disease (CAD). Results Significant differences of genotype distribution in CAD patients and controls were observed in ApoB+ 8216 in Iraqi population from Hardy Weinberg Analysis. It also found that dramatic difference of low-density lipoprotein (LDL-C) level in response to 40 mg/day of atorvastatin therapy, the minor allele (A) observed a greater LDL-C lowering than the wild type allele (G). In ANOVA analysis, the result showed that the rs676210, Pro2739Leu, in ApoB gene increased non significantly, but gradually in plasma level of total cholesterol (TC), triglyceride (TG), very low-density lipoprotein (VLDL), and oxidize low-density lipoprotein (oxLDL) in the order of genotype AA, GA, and GG in response to 40 mg atorvastatin. Conclusion We found the results highlighted the function of the rs676210, Pro2739Leu, in the ApoB gene in CAD etiology, and the findings support this variant’s impact in predicting the response of (LDL-C) to 40 mg of atorvastatin therapy. ApoB gene polymorphism (rs676210, Pro2739Leu), specifically the AA genotype, may help to identify individuals who will profit from atorvastatin's lowering effects.

scholarly journals Comparison of Tumor Necrosis Factor-α Level in Coronary Artery Disease and Coronary Slow Flow of Thrombolysis in Myocardial Infarction

2019 ◽  
Vol 11 (3) ◽  
pp. 299-303
Author(s):  
Muhammad Diah ◽  
Rahmawati Rahmawati ◽  
Aznan Lelo ◽  
Zulfikri Muhktar ◽  
Dharma Lindarto ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Healthy Subjects ◽  
Slow Flow ◽  
Timi Frame Count ◽  
Tnf Α ◽  
Significant Difference ◽  
Coronary Slow Flow ◽  
Artery Disease ◽  
Α Level

BACKGROUND: Tumor necrosis factor (TNF)-α, an important primary pro-inflammatory cytokine, has a crucial role in the pathogenesis of atherosclerosis. Since the pathophysiological mechanism of coronary slow flow (CSF) is not fully understood, we investigated the level of TNF-α in coronary artery disease (CAD), CSF and healthy subjects.METHODS: This study was conducted in cross-sectional design involving 16 CAD, 18 CSF and 18 healthy subjects. Coronary angiography was recorded at the left anterior oblique, cranial, right anterior oblique, caudal, and horizontal positions. The flow in coronary arteries of the subjects were assessed using Thrombolysis in the Myocardial Infarction (TIMI) frame count method. Peripheral blood-derived serum was collected and level of TNF-α was determined by using highly sensitive enzymelinked immunosorbent assay (ELISA).RESULTS: No significant difference in level of TNF-α in CAD, CSF and healthy subjects (2.72±2.64 pg/mL, 1.88±0.8 pg/mL, 1.64±0.35 pg/mL, respectively) (p=0.087). In addition, there was no correlation between the concentration of TNF-α and TIMI frame count (r<0.2, p>0.05).CONCLUSION: There was no significant difference of TNF-α level in CAD, CSF and healthy subjects. In addition, there was no correlation between the TNF-α level with TIMI frame count as well. Nevertheless, further clinical studies with more subjects are needed.KEYWORDS: TNF-alpha, coronary artery disease, coronary slow flow 

MicroRNA-224 (rs188519172 A>G) Gene Variability is Associated with a Decreased Susceptibility to Coronary Artery Disease: A Case-Control Study

MicroRNA ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 198-205 ◽  
Author(s):  
Rashid Mir ◽  
Chandan K. Jha ◽  
Imadeldin Elfaki ◽  
Suriya Rehman ◽  
Jamsheed Javid ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Recessive Model ◽  
Amplification Refractory Mutation System ◽  
Genotype Distribution ◽  
Healthy Controls ◽  
Significant Difference ◽  
Mutation System ◽  
Artery Disease ◽  
Gene Variability

Aim: The microRNAs regulate the expression of multiple genes involved in diseases such as cancer, diabetes and cardiovascular disease. In this study, we have investigated the association between the miR-224 gene polymorphism (rs188519172A>G) and susceptibility of coronary artery disease CAD. Methodology: Hundred CAD patients and 100-matched healthy control were included. Genotyping of the miR-224 (rs188519172A>G) polymorphism was performed using Amplification refractory mutation system PCR method (ARMS-PCR). Results: A significant difference was observed in the genotype distribution among CAD patients and healthy controls (P=0.018). The frequencies of all three genotypes GG, GA, AA reported in the patient’s samples were 33%, 66% and 01%, and in the healthy controls samples, were 16%, 82% and 2% respectively. A multivariate analysis based on logistic regression was conducted for each group to estimate the association between miR-224 rs188519172 genotypes and risk to coronary artery disease. Results show that the miR-224 (rs188519172 A>G) polymorphism was associated with a decreased risk to CAD in a codominant model, GA genotype vs. GG (OR = 0.39 (95 % CI, 0.19-0.76), RR 0.58 (0.38-0.90, P=0.006). In the dominant model, (GA+AA vs. GG), there was also a significant association with the OR=0.38 (95 % CI (0.19-0.76), RR 0.58 (0.38-0.89), and P=0.006. Whereas, in the recessive model, (GG+GA vs. AA), there was no significant association of CAD with OR=0.49 (95% CI (0.044-5.54), RR 0.74 (0.33-1.68), and P=0.48. Conclusion: Our findings indicated that miR-224 (rs188519172) GA genotype is associated with a decreased susceptibility to CAD.

scholarly journals Impact of free fatty acids on prognosis in coronary artery disease patients under different glucose metabolism status

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Jing-Lu Jin ◽  
Ye-Xuan Cao ◽  
Hui-Hui Liu ◽  
Hui-Wen Zhang ◽  
Yuan-Lin Guo ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Fatty Acids ◽  
Coronary Artery ◽  
Glucose Metabolism ◽  
Free Fatty Acids ◽  
Cox Model ◽  
Stable Coronary Artery Disease ◽  
P Value ◽  
Significant Difference ◽  
Artery Disease

Abstract Background The aim of the present study is to examine the effects of free fatty acids (FFAs) on major cardiovascular events (MACEs) in patients with stable coronary artery disease (CAD) and different glucose metabolism status. Methods In this study, we consecutively enrolled 5443 patients from March 2011 to May 2015. Patients were categorized according to both status of glucose metabolism status [diabetes mellitus (DM), pre-diabetes (Pre-DM), normal glycaemia regulation (NGR)] and FFAs levels. All subjects were followed up for the occurrence of the MACEs. Results During a median of 6.7 years’ follow-up, 608 MACEs occurred. A twofold higher FFAs level was independently associated with MACEs after adjusting for confounding factors [Hazard Ratio (HR): 1.242, 95% confidence interval (CI) 1.084–1.424, p value = 0.002]. Adding FFAs to the Cox model increased the C-statistic by 0.015 (0.005–0.027). No significant difference in MACEs was observed between NGR and Pre-DM groups (p > 0.05). When patients were categorized by both status of glucose metabolism and FFAs levels, medium and high FFAs were associated with significantly higher risk of MACEs in Pre-DM [1.736 (1.018–2.959) and 1.779 (1.012–3.126), all p-value < 0.05] and DM [2.017 (1.164–3.494) and 2.795 (1.619–4.824), all p-value < 0.05]. Conclusions The present data indicated that baseline FFAs levels were associated with the prognosis in DM and Pre-DM patients with CAD, suggesting that FFAs may be a valuable predictor in patients with impaired glucose metabolism.

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