The association between angiotensin-converting enzyme insertion/deletion (ACE I/D) polymorphisms and plasma ACE levels may allow for the optimization of a preventive intervention to reduce cardiovascular morbidity and mortality in the chronic kidney disease (CKD) population. In this study, we aimed to analyze the association between ACE I/D polymorphism and cardiovascular mortality risk among non-hemodialyzed chronic kidney disease patients. This cross-sectional study examined 70 patients of Javanese ethnic origin with stable CKD who did not receive hemodialysis. ACE I/D polymorphisms, plasma ACE levels, atherosclerotic cardiovascular disease (ASCVD) risk, and cardiovascular mortality risk were investigated. As per our findings, the I allele was found to be more frequent (78.6) than the D allele (21.4), and the DD genotype was less frequent than the II genotype (4.3 vs. 61.4). The ACE I/D polymorphism had a significant direct positive effect on plasma ACE levels (path coefficient = 0.302, p = 0.021). Similarly, plasma ACE levels had a direct and significant positive effect on the risk of atherosclerotic cardiovascular disease (path coefficient = 0.410, p = 0.000). Moreover, atherosclerotic cardiovascular disease risk had a significant positive effect on cardiovascular mortality risk (path coefficient = 0.918, p = 0.000). The ACE I/D polymorphism had no direct effect on ASCVD and cardiovascular mortality risk. However, our findings show that the indirect effects of high plasma ACE levels may be a factor in the increased risk of ASCVD and cardiovascular mortality in Javanese CKD patients.

Interleukin-6 (IL-6) has been identified as an important pro-inflammatory factor involved in mediating the severity of chronic kidney disease (CKD). This study sought to determine the effect of plasma IL-6 levels on atherosclerotic cardiovascular disease (ASCVD) and cardiovascular mortality risk scores in Javanese CKD patients. We also analyzed the frequency of IL-6 G174C single nucleotide polymorphism (SNP) in the population. This study was a cross-sectional study involving seventy-three patients of Javanese ethnic origin with stable chronic kidney disease. We assessed the ASCVD risk score, cardiovascular mortality score, genotyping of IL-6 G174C SNP, and plasma IL-6 levels in these patients. The genotype distribution and allele frequencies of the IL-6 G174C SNP were predominated by the G genotype/allele (GG: 97.26%, GC: 1.37%, CC: 1.37%, G-allele: 97.95%, and C-allele: 2.05%). Despite the fact that plasma IL-6 levels did not directly affect cardiovascular mortality risk, further analysis revealed its direct effect on the ASCVD risk score (path coefficient = 0.184, p = 0.043, 95% CI = 0.018–0.380), which in turn affected cardiovascular mortality risk (path coefficient = 0.851, p = <0.01, 95% CI = 0.714–0.925). In conclusion, plasma IL-6 levels play important roles on ASCVD risk and cardiovascular mortality risk in Javanese patients with CKD.

Objectives: The aim of the study was to evaluate the correlation between left ventricular hypertrophy and the gene polymorphism of angiotensin-converting enzyme (ACE) intron deletion (I/D) and ACE G2350A. Methods: Information related to the sample size and genotype frequencies was extracted from each study. Results: Our results found that the D allele (p = 0.0180) and DD genotype (p = 0.0110) of ACE I/D had a significant association with increasing the risk of left ventricular hypertrophy, whereas the I allele (p = 0.0180), but not II (p = 0.1660) and ID genotypes (p = 0.1430), was associated with decreasing the risk of left ventricular hypertrophy. On other hand, we found that the A allele (p = 0.0020) and GA genotype of ACE G2350A (p = 0.0070) had the correlation with increasing the risk of left ventricular hypertrophy. Conclusions: Our meta-analysis reveals that the D allele of ACE I/D and the A allele of ACE G2350A are associated with increasing the risk of left ventricular hypertrophy.

Background. Cigarette smoking could induce endothelial dysfunction and the increase of circulating markers of inflammation by activation of monocytes. This can lead to increased intima media thickness (IMT) of entire blood vessels and result in acceleration of the atherosclerosis process. However, to our knowledge, little is known about the role of cigarette smoking in this atherosclerotic inflammatory process. The aim of this study is to explore the link between cigarette smoking and its effect on endothelial nitric oxide synthase (e-NOS) and vascular cell adhesion molecule 1 (VCAM-1). Methods. An experimental study with a post-test only controlled group design was used. We used 18 Wistar rats (Rattus norvegicus) randomly subdivided into two groups: group K (-) were not exposed to tobacco smoke, whereas group K (+) were exposed to smoke equivalent of more than 40 cigarettes for 28 days daily. After 28 days, samples were analyzed for e-NOS, VCAM-1 and aortic IMT. Results . Our results indicate that tobacco smoke can enhance the expression of VCAM-1 on rat cardiac vascular endothelial cells, resulting in a decreased expression of e-NOS level and increase of aortic IMT. Linear regression model found that eNOS level negatively correlated wiith aortic IMT (r 2 = 0.584, β = -0.764, p < 0.001), whereas VCAM-1 expression did not correlate with aortic IMT (r 2 = 0.197, p = 0.065). Conclusion. Low e-NOS level and high VCAM-1 level observed after cigarette smoke exposure which may increase aortic IMT.

Interleukin 6 (IL-6) and C-Reactive Protein (CRP) play an important role in chronic periodontitis with coronary artery disease (CAD). Genetic factors can affect a person’s risk of CAD, which affects one-third of the population. This study investigated the role of IL-6 -572 C/G, CRP -757 A/G, and CRP -717 T/C gene polymorphisms. IL-6 and CRP levels on the severity of periodontitis in CAD in Indonesia were also evaluated. This case-control study was conducted with mild and moderate–severe chronic periodontitis groups. A path analysis test was conducted with Smart PLS with a 95% confidence interval to determine the significant variable for chronic periodontitis. Our study revealed that the effects of IL-6 -572 C/G, CRP -757 A/G, and CRP -717 T/C gene polymorphisms on IL-6 levels and CRP levels were not significant. IL-6 and CRP levels were not significantly different between the two groups. We found that IL-6 levels had a significant effect on CRP levels in periodontitis patients with CAD (path coefficient 0.322, p = 0.003). IL-6 -572 C/G, CRP -757 A/G, and CRP -717 T/C gene polymorphisms had no effect on the severity of chronic periodontitis in CAD patients in the Indonesian population. We also observed no apparent effects of the influence of gene polymorphisms in IL-6 -572 C/G, CRP -757 A/G, and CRP -717 T/C genes. Although the IL-6 and CRP levels were not significantly different between the two groups, IL-6 levels affected CRP levels in periodontitis patients with CAD.

Background: Cigarette smoking could induce endothelial dysfunction and increase of circulating markers of inflammation by activation of monocytes. This can lead to the increased of intima media thickness (IMT) of entire blood vessel and result acceleration of atherosclerosis process. However, to our knowledge, little is known about the role of cigarette smoking in this atherosclerotic inflammatory process. Objective: The aim of this study is to explore the link between cigarette smoking on endothelial nitric oxide synthase (e-NOS) and vascular cell adhesion molecule 1 (VCAM-1). Methods: An experimental study with post-test only controlled group design was used in this study. We used 18 Wistar rats ( Rattus norvegicus ) randomly subdivided into 2 groups, group K (−) were given no tobacco smoking exposed, whereas group K (+) were exposed to 40 cigarettes smokes daily. After 28 days, samples were analyzed for e-NOS, VCAM-1 and aortic IMT. Results: Our results indicate that tobacco smoke can enhance the expression of VCAM-1 on mouse cardiac vascular endothelial cell, resulting in decreased expression of e-NOS level and increased of aortic IMT. Linear regression model found that eNOS level negatively correlated wiith aortic IMT (r ² = 0.584, β = −0.764, p < 0.001), whereas VCAM-1 expression did not correlate with aortic IMT (r ² = 0.197, p = 0.065). Conclusion: Low e-NOS level and high VCAM-1 level observed following after cigarette smoke exposure may increase aortic IMT. Clinical significance: Increasing evidence suggests that cigarette smoke exposure could induce VCAM-1 (enhance pro-atherogenic property),and decreased of e-NOS level (anti-atherogenic depletion). Thus, cigarette smoke may represent a significant risk factor for atherosclerosis by increasing aortic IMT. This evidence is discussed herein.