Carbon monoxide (CO) intoxication is the most common cause of accidental poisoning in developed countries and, although most published data relate to its neurological manifestations, it often leads to cardiac damage. Myocardial hypoxia due to the formation of carboxyhemoglobin is not enough to explain such damage fully as a major role is played by the direct effect of CO on the heart as a result of the reversible inhibition of mitochondrial respiration and oxidative stress. Cardiac damage secondary to CO poisoning can be detected not only in patients with known ischemic heart disease but also in subjects with undamaged coronary arteries. Given the wide range of cardiovascular manifestations (the entity of which is related to the severity of intoxication), useful information can be obtained by carefully recording the patient's medical history, analyzing electrocardiographic alterations, and determining the biochemical markers of cardiac necrosis. Moreover, echocardiographic examination may highlight the extent of the alterations in left ventricular function due to myocardial stunning associated with CO intoxication and evaluate its evolution over time. Clinical studies suggest that all patients admitted to hospital with moderate to severe CO poisoning should routinely undergo ECG and serial evaluation of cardiac markers, and that those with positive signs of myocardial cytonecrosis or preexisting ischemic heart disease should also undergo echocardiography. A finding of myocardial damage in patients with CO poisoning seems to indicate an unfavorable long-term prognosis, although it needs further confirmation.