ABSTRACT
Smoking is related to vascular aging. However, the hazardous effect of e-cigarette is often debatable, with limited studies available. In contrast, moderate-intensity aerobic exercise is well known to decrease aortic stiffness. We provide novel research to determine the effect of e-cigarette and aerobic moderate-intensity exercise on the aortic structure of Wistar rats. A total of 26 male Wistar rats (Rattus norvegicus) 8 weeks aged, 200-250 g b.w., were randomly divided into 4 groups, namely, K0 (normal rats), K1 (rats were given moderate-intensity aerobic exercise by animal treadmill 20 m/30 min), K2 (rats were given e-cigarette with 6 mg nicotine, 40% propylene glycol, and 60% vegetable glycerine 30 min for 5 days/week), and K3 (rats were given e-cigarette and moderate-intensity aerobic exercise). After exposure for 6 weeks, all animals were sacrificed to isolate the aorta for histopathological analysis with hematoxylin-eosin stain to evaluate the elastic fiber layer and intimal-medial thickness. The Verhoeff-Van Gieson staining was done for quantification elastic lamina fragmentation. Our study found that the e-cigarette group had the highest elastic lamina fragmentation among groups (8.14 ± 2.85). The exercise only group showed the lowest elastic lamina fragmentation (2.50 ± 1.87). Fragmentation in the e-cigarette and exercise group was higher than in the exercise only group (5.83 ± 0.753 vs. 2.50 ± 1.87, p = 0.002). There is a significant difference of NO serum between four groups. The result of post hoc analysis using LSD showed that there is a significant difference of NO serum between K0 and K2, K0 and K3, K1 and K2, and K1 and K3. Therefore, our research demonstrated that the most injury of aorta elastic lamina was in the group that was exposed to e-cigarette that leads to vascular aging while exercise is not yet proven to reverse this effect.
ABSTRACT
Coronary artery diseases (CAD), also known as coronary heart disease (CHD), are the world's leading cause of death. The basis of coronary artery disease is the narrowing of the heart coronary artery lumen due to atherosclerosis. The use of electronic cigarettes has increased significantly over the years. However, harmful effects of electronic cigarettes are still not firm. The aim of this article is to review the impact of electronic cigarette and its role in the pathogenesis of atherosclerosis from recent studies. The results showed that several chemical compounds, such as nicotine, propylene glycol, particulate matters, heavy metals, and flavorings, in electronic cigarette induce atherosclerosis with each molecular mechanism that lead to atherosclerosis progression by formation of ROS, endothelial dysfunction, and inflammation. Further research is still needed to determine the exact mechanism and provide more clinical evidence.
ABSTRACT
Coronary artery calcification is a part of atherosclerosis process associated with coronary heart disease. Recently, coronary artery calcification assessment using computed tomography (CT) is still the best noninvasive imaging with high sensitivity and specificity. Osteoprotegerin (OPG) is one of vascular calcification marker that through its role to bind receptor activator of nuclear factor-κß ligand and inhibit osteoclastogenesis is suspected of playing a role for coronary calcification in atherosclerosis process. The objective of this study was to prove a positive correlation between OPG serum level and coronary calcification using coronary artery calcium (CAC) score in patient with moderate-severe cardiovascular (CV) risk factor. This is a cross-sectional study with purposive sampling technique. Thirty-three subjects participate in this research and each subject underwent a multislice computed tomography (MSCT) examination to assess coronary calcification and their blood samples were collected for OPG measurement. This study is analyzed with Spearman's correlation test. The mean of OPG serum level in this study was 5.89 ± 2.1 pmol/L for moderate-risk Framingham risk score (FRS) and the mean of OPG serum level for high-risk FRS was 7.27 ± 3.4. There was a positive, moderate, and significant correlation between OPG serum level and coronary calcification using CAC score in patient with moderate-severe CV risk factor ( r = 0.694; p < 0.001).
