title: Asymmetric dimethylarginine and heart-type fatty acid-binding protein 3 are risk markers of cardiotoxicity in carbon monoxide poisoning cases in Zagazig university hospitals.
abstract: Carbon monoxide (CO) poisoning is a leading cause of toxicity-related mortality and morbidity worldwide. Recent studies focused on CO-induced cardiovascular toxicity. Oxidative stress plays an important role in the pathophysiology of CO toxicity. The aim of this study was to elucidate the relationship between cardiac damage biomarkers and oxidative stress biomarkers in patients with CO-induced cardiotoxicity. This study was carried out on 36 CO-poisoned patients admitted to Zagazig University Hospitals. Forty healthy individuals (age- and sex-matched) were selected as a control group. Clinical examination and electrocardiography (ECG) were performed for CO-poisoned patients. These patients have been investigated for carboxyhaemoglobin percent (COHB%) and cardiac damage biomarkers; cardiac troponin I (cTn-I), heart-type fatty acid-binding protein 3 (H-FABP3). Oxidative stress biomarkers comprising malondialdehyde (MDA), asymmetric dimethylarginine (ADMA), and total antioxidant capacity (TAC) have been also assessed. All biomarkers have been assessed on admission (0 h) and 6 h after treatment of CO-poisoned patients with high-flow oxygen and compared with those of the control groups. ECG findings were abnormal in 31 patients (86.11%), where sinus tachycardia was the commonest finding (58.33%). There was a statistically significant increase of COHB%, MDA, ADMA, and H-FABP3 levels, and a significant decrease of TAC level in CO-poisoned patients compared to controls with no significant changes in cTn-I. Six hours following treatment, all measured parameters were significantly improved except for cTn-I, which was significantly increased when compared with admission status (0 h). Furthermore, H-FABP3 showed a significant positive correlation with COHB%, MDA, ADMA, and a negative correlation with TAC, while cTn-I was significantly correlated with COHB% only. ADMA and MDA seem to be the strongest determinants for the prediction of H-FABP3 changes and hence cardiovascular toxicity. Thus, cardiac damage in patients with CO poisoning could be partially mediated by CO-induced oxidative stress, where H-FABP3 level was directly and strongly associated with MDA and ADMA levels.
authors.affiliation: 1 Department of Forensic Medicine & Clinical Toxicology, Faculty of Medicine, Zagazig University, Zagazig, Skarkia, Egypt.
authors.forename: Marwa A
authors.initials: MA
authors.lastname: Abass
authors.affiliation: 1 Department of Forensic Medicine & Clinical Toxicology, Faculty of Medicine, Zagazig University, Zagazig, Skarkia, Egypt.
authors.forename: Manar H
authors.initials: MH
authors.lastname: Arafa
authors.affiliation: 2 Department of Medical Biochemistry, Faculty of Medicine, Zagazig University, Zagazig, Skarkia, Egypt.
authors.forename: Amal S
authors.initials: AS
authors.lastname: El-Shal
authors.affiliation: 3 Department of Biochemistry, Faculty of Pharmacy, Zagazig University, Zagazig, Skarkia, Egypt.
authors.forename: Hebatallah H
authors.initials: HH
authors.lastname: Atteia
mesh_terms: D000328:Adult; D001120:Arginine / Q000031:analogs & derivatives* / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism*; D002249:Carbon Monoxide Poisoning / Q000378:metabolism* / Q000503:physiopathology; D002263:Carboxyhemoglobin / Q000378:metabolism; D016022:Case-Control Studies; D004534:Egypt; D004562:Electrocardiography; D000074026:Fatty Acid Binding Protein 3; D050556:Fatty Acid-Binding Proteins / Q000378:metabolism*; D005260:Female; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology*; D006801:Humans; D008297:Male; D012307:Risk Factors; D055815:Young Adult
chemical_list: D015415:Biomarkers; C493408:FABP3 protein, human; D000074026:Fatty Acid Binding Protein 3; D050556:Fatty Acid-Binding Proteins; C018524:N,N-dimethylarginine; D002263:Carboxyhemoglobin; D001120:Arginine
keywords: ADMA; H-FABP3; cTn-I; carbon monoxide; cardiotoxicity; oxidative stress