Detection of reperfusion after thrombolytic therapy by the analysis of released biochemical markers.
Although the advent of thrombolytic therapy for acute coronary occlusion has substantially reduced the mortality of acute myocardial infarction (AMI), the best available thrombolytic regimens only achieve adequate reperfusion in a little over half the patients who are treated. The ability to detect failure of reperfusion by non-invasive means would permit further therapy in this patient group who currently have a high mortality. As coronary reperfusion causes a rapid release of many myocardial proteins into the blood stream, analysis of the rate of release of markers such as myoglobin, troponin, and creatine kinase (CK) during the first 90 minutes after thrombolytic therapy can identify about 80% of the patients in whom thrombolytic therapy has been ineffective. An ideal marker of reperfusion would be rapidly released after reperfusion, rapidly cleared from the circulation, highly myocardial specific, and amenable to rapid quantitative assay to permit 'real time' determination of coronary patency status. At present myoglobin and cardiac troponins appear most promising for detection of reperfusion, but other markers such as CK isoforms may prove useful if reliable rapid assays become available.
Cross
D B
DB
Cardiology Department, Royal Brisbane Hospital, Qld.
D003402:Creatine Kinase / Q000097:blood*; D006801:Humans; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy*; D009211:Myoglobin / Q000097:blood*; D011237:Predictive Value of Tests; D020033:Protein Isoforms / Q000097:blood; D012680:Sensitivity and Specificity; D015912:Thrombolytic Therapy; D014336:Troponin / Q000097:blood*
D009211:Myoglobin; D020033:Protein Isoforms; D014336:Troponin; D003402:Creatine Kinase