Methodology This case control study was conducted in Poison Control Center, Ain Shams university Hospital, Cairo, Egypt. Patients with coronary artery disease or other known heart disease, patients with renal failure and individuals subjected to drugs or supplements with antioxidant effect as well as smoker subjects were excluded. This study was conducted on 50 patients diagnosed as acute carbon monoxide poisoning according to medical history, examination, and/or COHb level>3% at the time of

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... sentation. They were 30 males and 20 females. Their age ranged between 15-45 years (26.5 ± 8.3 years). Apparently healthy 40 individuals, 20 males and 20 females, matched for age and sex were the control group. Consent for examination was taken from these subjects. On admission to the emergency department, blood samples were withdrawn from patients, after detailed clinical examination, to perform the following investigations; blood gases analysis, troponin I, BNP, SOD, MDA and (NO) synthase products (nitrate & nitrite) levels were measured. Baseline 12-lead ECGs were recorded with a paper speed of 25mm/s from each of the patients at the admission. Arterial blood gases and Carboxyhemoglobin measurements were Abstract Background: Myocardial injury is a frequent consequence of carbon monoxide (CO) poisoning. Oxidative stress affection seems to be a relevant mechanism in the patho-physiology of patients with acute CO poisoning. Methodology: Cardiovascular system examination and Electrocardiography (ECG) were performed for fifty CO intoxicated patients admitted to Poison Control Center, Ain Shams university Hospital for whom some oxidative stress indices have been investigated through the assessment of plasma level of malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO). Both cardiac enzymes; troponin I and beta natriuretic peptide (BNP) have been also assessed in addition to carboxyhemoglobin (COHb) levels. The investigated parameters were compared with those of 40 non-smoker healthy controls (comparable in terms of age and gender). Results: ECG changes were present in 96% of patients, whereas only 4% had a normal ECG. In intoxicated patients, a statistical significant increase in plasma level of COHb level, MDA, NO, troponin I, and BNP peptide was reported compared to control individuals, while SOD enzyme was significantly decreased. BNP showed a significant positive correlation with COHb level and a negative correlation with SOD, while SOD showed a significant negative correlation with COHb level. Conclusions and recommendations: Myocardial injury occurs frequently in patients hospitalized for CO poisoning. The oxidative stress indices are significantly affected after acute CO poisoning. We suggested that such affection could be partially mediated by CO. Patients admitted to the hospital with CO poisoning should have a baseline ECG and serial cardiac biomarkers.