Myoglobin and Carbonic Anhydrase III

Abstract

Currently, the diagnosis of acute myocardial infarction (AMI)* in the first 6-8 h after the infarction is based on the clinical presentation of the patient with typical chest pain and electrocardiogram (ECG). However, chest pain is a nonspecific presentation. Only about 32.5% of patients admitted with chest pain are eventually diagnosed as having AMI. Among the patients with chest pain, typical ECG abnormalities, such as Q-wave changes and ST-T-wave elevation, are observed in 73% of AMI patients (sensitivity 73%) (1–3). Thus, a clinical need has been created to have an adjunctive biochemical marker that can aid in more efficient early diagnosis of AMI. In response to this need, several biochemical markers, such as myoglobin, CK-MM isoforms, CK-MB isoforms, and myosin light chain, are being evaluated for their early diagnostic utility (4,5). Attempts are also being made to enhance the diagnostic efficiency of myoglobin by combining its results with ECG (6–8), CK-MB (9), or carbonic anhydrase III (CAIII) (10–12). Myoglobin is a 17.8-kDa oxygen binding heme protein present in both cardiac and skeletal muscle. It constitutes about 2% of the total muscle protein and is located in the cytoplasm. Although structurally similar to hemoglobin subunits, its physiological role is not well understood. Cell injury during AMI releases myoglobin into the blood circulation. The relationship between myoglobinemia and myocardial infarction was first reported in 1975 (13).