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Background/Aim. Liver damage, with potentially serious consequences, is not uncommon in hospitalized cardiac patients. The aim of our study was to determine the risk factor profile for liver damage in patients hospitalized from a deterioration of their acute or chronic cardiac illness. Methods. The study had observational case-control design with retrospective data collections from medical files of adult patients hospitalized in a tertiary health care center. The cases (n = 140) were subjects with novel liver injury (which emerged during hospital stay) and three control subjects were matched (age, date) for each case subject (n = 420). The primary outcome was hepatotoxicity (present or absent) and independent variables were proposed risk factors. Statistical analysis included descriptive methods, hypothesis testing and univariate and multivariate binary logistic regression, with p ≤ 0.05. Results. In the whole study population, there were 432 (77.1%) females and the mean age of patients was 64.1 years [standard deviation (SD) = 10.7, range 24–85 years]. The most common illnesses were coronary heart disease (n = 385), hypertension (n = 334) and arrhythmia (n = 115). Mean value of Charlson Comorbidity Index (CCI) score was 3.8 (SD=1.7; range 1-10) corresponding to estimated CCI 10-years survival rate of 54.4% (SD = 33.5%). In the group of cases, 114 (81.4%) of the patients had hepatocellular, 9 (6.4%) cholestatic and 17 (12.2%) mixed type of hepatic injury. Factors independently associated with hepatotoxic event were previous occasional alcohol intake odds ratio (OR) 96.47; 95% confidence interval (CI) 28.95–321.43; p < 0.001), amiodarone (OR 3.70; 95% CI 1.82–7.53; p < 0.001), enoxaparin (OR 3.29; 95% CI 1.79–6.05; p < 0.001), obesity (OR 2.78; 95% CI 1.15– 6.71; p < 0.023), atorvastatin (OR 2.67; 95% CI 1.33–5.38; p < 0.006) and CCI total score (OR 1.89; 95% CI 1.53–2.34; p < 0.001). Conclusion. Major factors associated with acute liver damage in patients hospitalized in cardiology ward of a tertiary health care institution were patient’s constitutional and habitual characteristics (occasional alcohol intake, obesity, CCI total score) and drugs with known hepatotoxic properties (amiodarone, enoxaparin, atorvastatin).

Introduction. Myocardial infarction (MI) is characterized by a critical myocardial ischemia followed by an irreversible myocardial cell damage or death. Case report. We presented two similar clinical cases with the ST segment elevation myocardial infarction (STEMI) diagnosis due to a prolonged coronary artery spasm, but with different treatment options due to different basic patophysiological supstrates and clinical presentations. Conclusion. Coronary artery spasm is a very complex pathophysiological entity with a different medication therapy management. Although the percutaneous coronary intervention can be the first choice, the treatment strategy should be carefully planned

Background. The underlying mechanisms of N-Methyl-3,4-methylenedioxyamphetamine-MDMA-induced hepatotoxicity are still unknown. The aim of this study was to evaluate hepatic oxido-reductive status in the rats liver after the single and repeated administration of MDMA. Methods. MDMA was dissolved in distilled water and administered in the doses of 5 mg, 10 mg, 20 mg, and 40 mg/kg. The animals from the acute experiment were treated per os with the single dose of the appropriate solution, through the orogastric tube. The animals from the chronic experiment were treated per os, with the doses of 5, 10, or 20 mg/kg of MDMA every day during 14 days. The control groups were treated with water only. Eight hours after the last dose, the animals were sacrificed, dissected their livers were rapidly removed, frozen and stored at -70°C until the moment of analysis. The parameters of oxidative stress in the crude mitochondrial fractions of the livers were analyzed. Results. Superoxide dismutase (SOD) activity increased in the livers of the animals that were treated with single doses of MDMA. Chronically treated animals showed the increased SOD activity only after the highest dose (20 mg/kg). The content of reduced glutathione decreased in both groups, but the depletion was much more expressed after the single administration. Lipid peroxidation index increased in dose-dependent manner in both groups, being much higher after the single administration. Conclusion. The increased index of lipid peroxidation and the decreased reduced glutathione levels suggested that MDMA application induced the state of oxidative stress in the liver. These changes were much more expressed after the single administration of MDMA.