No abstract

The aim of this study was to investigate the protective effects of fish omega-3 (n-3) fatty acids on doxorubicin (DOX)-induced acute cardiotoxicity. A total of 24 rats were divided into three groups: control, DOX-treated, and DOX treated with fish n-3 fatty acids. Control group received 0.4 ml/kg/day of saline intragastrically. The rats in the fish n-3 fatty acid-pretreated group were given 400 mg/kg/day fish n-3 fatty acids for 30 days by intragastric intubation. To induce acute cardiotoxicity, DOX (30 mg/kg) was injected intraperitoneally by a single dose and the rats were killed after 48 h. DOX treatment caused severe damage in heart tissues. Disorganization of myocardial muscle fibers, myofibrillar loss, and cardiotoxic myocardial fibers with cytoplasmic vacuoles were seen. Fish n-3 fatty acid-treated rats showed an improved histological appearance in the DOX-treated group. Our data indicate a significant reduction in the activity of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling in cardiomyocytes of the DOX-treated group with fish n-3 fatty acids therapy. The DOX-treated with fish n-3 fatty acids group showed a significant decrease in malondialdehyde levels, and an increase in superoxide dismutase and glutathione peroxidase activities in comparison with the DOX-treated group. This study showed that fish n-3 fatty acids may be a suitable cardioprotector against acute toxic effects of DOX.

The aim of this study was to investigate the antioxidant and anti-apoptotic effects of onion (Allium cepa) extracts (ACE) on doxorubicin (DOX)-induced cardiotoxicity. The rats in the ACE-pretreated group were given a daily dose of 1 ml ACE for 14 days. To induce cardiotoxicity, DOX (30 mg kg(-1) body weight) was injected intraperitoneally by a single dose and the rats were sacrificed after 48 h. To date, no such studies have been performed on the cardioprotective and anti-apoptotic potential of ACE on DOX-induced cardiotoxicity. Our data indicate a significant reduction in the activity of in situ identification of apoptosis using terminal dUTP nick end-labeling in cardiomyocytes of the DOX-treated group with ACE therapy. The DOX-treated with ACE groups showed a significant decrease in malondialdehyde levels, and increased activities of superoxide dismutase, glutathione and glutathione peroxidase in comparison with the DOX-treated group. Creatine kinase, creatine kinase MB, lactate dehydrogenase activities and cardiac troponin I levels were significantly decreased in the DOX + ACE group in comparison with the DOX group. These biochemical and histological disturbances were effectively attenuated on pretreatment with ACE. The present study showed that ACE may be a suitable cardioprotector against toxic effects of DOX.

Objective: We investigated whether post-exercise first minute abnormal heart rate recovery (HRR1) helps to predict the presence and severity of CAD, because of some confounding data. Methods: A cross-sectional, retrospective study was performed. Two hundred individuals were included. Gensini scores and the number of coronary artery involvements were used to evaluate the severity of CAD. Student's t-test, Mann-Whitney U test and chi-square test were used for the analysis continuous and categorical data. Spearman's correlation analysis was used to determine whether there is correlation between Gensini scoring and HRR1. Univariate and multivariate logistic regression were used to determine predictors for abnormal HRR1. ROC curve analysis was performed to detect the best sensitivity and specificity value of HRR1 in predicting CAD presence. Results: Seventy subjects (35%) did not have CAD, and CAD was present in 130 patients (65%). HRR1 ≤21 beats with ROC analysis was determined to be the best cut off point. After adjustment between the two groups in terms of age, gender, diabetes, hypertension, dyslipidemia or smoking (all p>0.05), there was relationship CAD presence and abnormal HRR1 (OR=2.1, 95% CI: 1.1-3.9, p=0.02), but not between CAD severity and HRR1 (r=-0.13, p=0.112). The sensitivity, specificity, and the positive and negative predictive values of abnormal HRR1 ≤21 beats at first minute for predicting CAD presence were 76.1%, 41.3% (AUC=0.588, CI 95%: 0.517-0,657, p=0.039), 70.7% and 48.3%, respectively. Conclusion: In the study abnormal HRR1 predicted the presence of CAD, but not the severity of it. (Anadolu Kardiyol Derg 2014; 14: 351-6)

Psoriasis is a disease that can contribute to a risk of atherosclerosis. In several studies, impaired endothelial dysfunction (ED) is correlated with psoriasis. Serum YKL-40 is a new inflammatory biomarker of vascular damage, like ED and cardiovascular diseases. The aim of the study was to compare relevance of serum YKL-40 levels in psoriasis patients and healthy subjects according to ED diagnosis and identifiable cardiovascular risk factors. Sixty (31 female, 29 male) patients with plaque psoriasis, and 30 (18 female, 12 male) healthy controls were selected according to whether they had at least one or no identifiable risk factors for cardiovascular disease. All subjects were evaluated ultrasonographically for endothelial function and diagnosed as with or without ED and all groups compared for serum YKL-40 levels. YKL-40 levels of psoriatic patients with ED were higher than healthy controls with ED (P = <0.05). There were no statistical differences in between subjects without ED. YKL-40 levels of patients over age of 40 were higher than younger ones (P < 0.05). But in healthy controls, there were no differences. In comparison of cardiovascular risk-positive (RP) patients and RP healthy subjects, YKL-40 levels were higher in RP patients (P = <0.05). The elevation of plasma YKL-40 in psoriasis can be associated not only with inflammation of the disease, but also with ED. YKL-40 can be used as a marker for predicting and preventing cardiovascular diseases in RP psoriatic patients with age above 40.