Aims: Paraoxonase-1 (PON-1) gene polymorphisms and carotid intima-media thickness (cIMT) in adults have been associated to increased incidence of cardiovascular diseases (CVD). Possible relation of cIMT to PON-1 polymorphisms and to markers of inflammation and oxidation, in children with family history of premature CVD, was investigated.
Place of the Study: Laboratory for Lipids and Cardiovascular Disease Prevention, 2nd Pediatric Department, AHEPA University Hospital, Thessaloniki, Greece.
Methodology: Eighty four healthy children of normal BMI, were recruited; 42 with positive family history of premature CVD, median age 10 (7-15) years old (study group) and 42 age- and gender-matched controls. Levels of lipid profile parameters, high sensitivity CRP (hsCRP) and oxidized LDL (oxLDL) were determined. cIMT was measured by ultrasounds and PON-1 gene polymorphisms, Q192R and L55M, were investigated using standard PCR-RFLP.
Results: Median cIMT was higher in study group than in controls [0.45 (0.30-0.65) vs 0.4 (0.30-0.60)]. Only ApoA-I presented significant difference between the three subgroups with different PON-1 SNP of the L55M polymorphism (P=.03). Regression analysis showed that there was no statistically significant dependence of cIMT on age, lipid profile parameters or markers of inflammation and oxidation.
Conclusion: Family history of premature CVD and PON-1 gene polymorphism are not related with significant differences in cIMT in children. Inflammation and oxidation do not markedly affect cIMT in children with family history of premature CVD.
Aim: To evaluate the cardioprotective effects of resveratrol during hyperglycemic conditions in in vitro and in vivo models.
Study Design: H9c2 cardiomyocyte cells were used as in vitro models and adult male Wistar strain albino rats were used as in vivo models. Activities of LDH and levels of lipid peroxides, total reduced glutathione were the end point indicators for the in vitro studies. For the in vivo studies the activities of membrane bound ATPases, levels of lipid peroxides, enzymic and non enzymic antioxidants were the end point indicators.
Place and Duration of Study: The study was conducted at the Department of Microbiology and Biotechnology, Bangalore University, Bangalore, between January 2014 and June 2014.
Methodology: To mimic myocardial injury during diabetic conditions (in vitro), the H9c2 cells were maintained in high glucose environment followed by isoproterenol challenge. For in vivo studies the animals were segregated as follows: Untreated control; Myocardial stress induced animals (Isoproterenol 150 mg/kg body wt i.p); Diabetic rats (Streptozotocin, 50 mg/kg body wt,i.p); Myocardial stress induced diabetic rats; resveratrol per se (5 mg/kg.body wt. orally for 21 days), and resveratrol pretreated prior to induction of diabetes and myocardial stress.
Results: H9c2 cells given glucose insult and challenged with isoproterenol showed severe cytotoxicity and stress as elicited by increased LDH release, increased lipid peroxides and depleted GSH levels. These changes were prevented in the cells pretreated with resveratrol prior to isoproterenol/glucose challenge. The diabetic rats induced with myocardial stress showed significant alterations in the activity of membrane bound phosphatases, levels of lipid peroxides, enzymic and non enzymic antioxidants. Pre-treatment with resveratrol prevented these alterations thereby implicating cardioprotective effects during hyperglycemic conditions
Conclusion: Resveratrol could combat myocardial stress during experimental hyperglycemia in in vitro and in vivo models.
Cadmium (Cd) is a toxic element that can produce reactive oxygen species. Fruits and vegetables are natural sources of various bioactive compounds. Watermelon contains nutritional agents like lycopene, citrulline and arginine and Aloe vera is used for therapeutic purposes. This study was carried out to investigate the antioxidant property of watermelon and Aloe vera against cadmium damaging effect on the heart tissues using Haematoxylin and Eosin (H/E) stain. Thirty five (35) Wistar rats were obtained and acclimatized for two weeks. They were divided into seven (7) groups, five (5) rats each. Group 1 normal control received 3 mg/kg/bw of phosphate buffer (pH 7.4) intraperitoneally. Group 2, received 3 mg/kg/bw of Cd (3CdSO4.8H2O) intraperitoneally. Group 3 (therapeutic control) received 100 mg/kg/bw of vitamin C and 300 mg/kg/bw of vitamin E orally once daily. Group 4 (therapeutic control and induced) received same as group 3 with Cd induction intraperitoneally two days before sacrifice. Group 5, 6 and 7 treatment groups were induced with 3 mg/kg/bw of Cd intraperitoneally before treatment with 80 mg/kg/bw of watermelon, 80 mg/kg/bw of Aloe vera and 40 mg/kg/bw of both extract orally and twice daily respectively. The experiment lasted for 4 weeks. The histomorphological result obtained showed normal cardiac features in group 1, damage in myofibril, displaced nuclei in group 2, displaced striation in group 5 and 6 but, improvement was observed as compared to group 2 rats, little displacement of nuclei in group 4, normal morphology in groups 3 and 7 animals were evident. The result from this experiment demonstrated the high degree of potency in the action of Aloe vera and watermelon combined in preventing oxidative tissues damage to the heart due to cadmium interaction.
Aims: Serum eicosapentaenoic acid (EPA) to arachidonic acid (AA) ratio (EPA/AA) in Japanese is rapidly changing according to the senescence and food westernization, and sonographic carotid artery intima-media thickness (IMT) is increasingly used as a surrogate of systemic atherosclerosis. However, the relationship between IMT and EPA/AA in Japanese remains unclear.
Place of the Study: Vascular Laboratory of Heart Center, Kyushu University Hospital, Fukuoka, Japan.
Methodology: Seventy consecutive Japanese atherosclerotic patients (69.7±7.8 years) hospitalized for elective endovascular therapy without purified EPA agent administration were enrolled in this study. IMT was estimated by high-resolution duplex ultrasonography in vascular laboratory. Conventional vascular risk factors were under the intensive treatment. Demographic variables were extracted from medical records after obtaining informed consent.
Results: IMT was strongly age-dependent (P = .003) and age-adjusted multiple correlation analyses revealed no significant correlations among vascular risk factors, although positive partial correlation between serum EPA/AA and IMT (r = .277, P = .056) and negative partial correlation between EPA/AA and HbA1c (r = -.281, P = .053) were marginal. Stepwise multiple regression analyses demonstrated age and serum EPA/AA as positive contributors to the IMT (P < .001). EPA/AA was a seemingly paradoxical positive contributor to IMT due to age-dependent complicated profile of EPA/AA. Multiple correlation analyses were performed by multiple adjustments, which yielded significant negative correlation between EPA/AA and IMT (r = -.262, P = .049).
Conclusions: This study demonstrated that EPA/AA is a determinant of IMT among other vascular risk factors at least in Japanese atherosclerotic patients hospitalized for endovascular therapy.
Coronary artery angiography became the golden tool for coronary artery disease management. Transient cortical blindness following coronary angiography (TCBCA) is a rare complication of coronary artery angiography, in comparison with the other common complications. The neurotoxic effect of contrast medium is the possible cause of this clinical phenomenon, by disrupting blood brain barriers (BBB). TCBCA usually occurs during or immediately after coronary artery angiography. The clinical picture includes loss of vision that progressively resolves within hours or days. Ophthalmologic examination reveals normal structural findings, while computed tomography scan (CT scan) may show contrast accumulation in the occipital area. No current clinical protocols to manage this condition, except of excluding other possible causes of blindness after coronary artery angiography. Further well-organized studies are recommended to understand this clinical phenomenon, and more effort is needed to set a variety of interventional strategies regarding TCBCA management.
