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

<jats:p> 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. </jats:p>

Hematological parameters as early predictors of delayed neurological sequelae in acute carbon monoxide poisoning.

“…Concerning vital signs, this study showed that median of blood pressure (both systolic and diastolic) and oxygen saturation were significantly lower while QTc interval was significantly longer when comparing the included acute CO poisoned patients with control group. These were more or less in agreement with many previous observations in majority of centers in Egypt and across the world (Ismail et al, 2013;Abass et al, 2017;Liao et al, 2019b). The possible mechanism of QTc interval prolongation in CO poisoning is disruption of repolarization caused by late inward Na+ current resulting in action potential prolongation (Dallas et al, 2012).…”

Toxicology properties of commercial anti‐mosquitos and their effects on carboxyhemoglobin and malondialdehyde levels

“…The study results proved a linear relationship between CO-Hb and MDA levels in the blood (Abass et al, 2017;Flores et al, 2017). These results identify that an increase in CO-Hb levels was followed by MDA levels increase in the blood and vice versa.…”

“…The relationship between CO‐Hb and MDA levels in the blood was shown to have a significant correlation based on statistical analysis using Spearman's test with p ‐value = 0.000, respectively (Exhibit 6). The study results proved a linear relationship between CO‐Hb and MDA levels in the blood (Abass et al., 2017; Flores et al., 2017). These results identify that an increase in CO‐Hb levels was followed by MDA levels increase in the blood and vice versa.…”

Serum Netrin-1 and Asymmetric Dimethylarginine as Biomarkers of Acute and Chronic Carbon Monoxide Poisoning

“…Moreover, high levels of ADMA result in generation of nitric superoxide and peroxynitrite free radicals. These free radicals will inactivate mitochondrial enzymes and cause cell membrane lipid peroxidation with further damage to vascular endothelium (Abass et al, 2017).…”