Background: Carbon monoxide (CO) poisoning is a common cause of toxicological morbidity and mortality. Myocardial injury is a frequent consequence of CO poisoning. Oxidative stress affection seems to be a relevant mechanism in the pathophysiology of patients with an acute carbon monoxide (CO) poisoning.Methodology: Cardiovascular system examination and Electrocardiography were done in fifty carbon monoxide intoxicated patients admitted to Poison Control Center, Ain Shams university Hospital. We have investigated the oxidative stress indices through the assessment of plasma level of malondialdehyde, superoxide dismutase and nitric oxide. We have also assessed the cardiac enzymes such as troponine I, beta natriuretic peptide. The carboxyhaemoglobin (COHb) levels and the relationships with electrocardiographic parameters, cardiac markers (troponin I and beta natriuretic peptide) and oxidative stress indices (superoxide dismutase, malondialdehyde and nitric oxide) were studied. Data were compared with those from 40 non-smoker healthy controls comparable in terms of age and gender.Results : In intoxicated patients, we have found a significant increase of COHb level, malondialdehyde, nitric oxide , beta natriuretic peptide , compared to control individuals, as well as a superoxide dismutase enzyme was significantly decreased. Beta natriuretic peptide showed a positive, significant correlation with COHb level, superoxide dismutase showed a negative, significant correlation with COHb level. Electrocardiogram (ECG) changes were present in 96% of patients, whereas only 4% had a normal ECG. Conclusions: Myocardial injury occurs frequently in patients hospitalized for CO poisoning. The oxidative stress indices are significantly affected after acute CO poisoning. We suggest 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.