Discussion The cardiovascular manifestations of CO poisoning have been limited to case reports and presented variable

type of myocardial dysfunction and injury. Until recently, the various mechanisms have been proposed. Myocardial injury from CO poisoning results from tissue hypoxia as well as damage at the cellular level. The affinity of hemoglobin for CO is 200 to 250 times greater than its affinity for oxygen. This results in competitive Inhibitors,research,lifescience,medical inhibition of oxygen release due to a shift in the oxygen-hemoglobin dissociation curve, reduced oxygen delivery, and subsequent tissue hypoxia.2),5) Also, CO may bind to heme proteins, including myoglobin and cytochrome C oxidase.6) And, it may bind to cytochrome C oxidase, which is an enzyme in the mitochondrial electron-transport system chain that produces adenosine triphosphate by KRX-0401 cell line catalyzing the reduction of

oxygen to water.7) In a study by Satran et al.,2) different Inhibitors,research,lifescience,medical clinical patterns of myocardial injury were found. The pattern seen in younger patients with few coronary risk factors but severe CO poisoning was global LV dysfunction by TTE, which improved or resolved. This was consistent with stunned myocardium as a result of CO poisoning. The second pattern was seen in older patients with higher Inhibitors,research,lifescience,medical coronary risk factors. These Inhibitors,research,lifescience,medical patients had regional wall motion abnormalities suggesting that CO poisoning unmasks underlying coronary artery disease by creating supply/demand mismatch.2),3) To our knowledge, this is the first Korean case of acute CO poisoning induced acute heart failure complicated with LV thrombus. However, stress induced cardiomyopathy associated with LV thrombus is not a rare but well known complication. De Gregorio et al.8) reported that LV thrombus formation results in about 2.5% of all the patients with documented stress induced cardiomyopathy. In general, LV thrombus disappears together with or before LV functional recovery.8),9) We experienced

a case of acute CO poisoning induced transient LV dysfunction, Inhibitors,research,lifescience,medical which is apical ballooning form complicated with LV thrombus. The patient in this case has significant coronary artery disease, but he is fully recovered from segmental wall motion abnormality and LV thrombus within three weeks. In conclusion, although the optimal therapy for stress induced cardiomyopathy found with LV thrombus is still unknown, the use of anticoagulant therapy in the acute phase and until complete resolution of wall motion abnormalities appears to be appropriate in patients with apical thrombus.8),9) Because TTE can evaluate rapid change in cardiac condition, frequent follow-up using this technique is recommended for patients with stress induced cardiomyopathy, especially when anticoagulant therapy is difficult.