Determinants of the release pattern of ischaemia-modified albumin in acute ST-elevation myocardial infarction treated with primary PCI

Background. Ischaemia-modified albumin (IMA) is proposed as a marker of cardiac ischaemia. Release kinetics of IMA have not been investigated during ongoing acute coronary syndrome. We evaluated IMA kinetics in patients with ongoing ST-segment elevation MI (STEMI) and revascularization by primary percutaneous coronary intervention (pPCI) as a model. Methods. Twenty-five patients with STEMI undergoing successful pPCI (Age: median 65 y, range 41 79 y; symptoms duration: median 4 h, range 1-7 h). Fourteen blood samples were collected (11 during the first 24 h following pPCI) and analyzed for IMA, cardiac troponin T, CKMBmass, myoglobin, and heart-type fatty acid binding protein. Results. Following pPCI, mean IMA increased to 16% above baseline, normalizing within less than 3 h. At the time of pPCI, patients with TIMI 0 flow in the infarct artery had low levels of IMA and only exhibited a rise in IMA levels after pPCI, whereas patients with TIMI 1-3 flow had high IMA levels on arrival with a subsequent decrease (p < 0.036). There was no statistically significant association between IMA and other variables, e. g. ECG, symptoms duration, sex, age, blood pressure, and number of vessels affected. Relative concentrations of IMA were low compared with other cardiac biomarkers. Conclusions. Our results indicate that IMA release may depend on reperfusion-induced events rather than ischaemia per se. Further, we find a narrow diagnostic time window and a low sensitivity of the IMA assay. Improved understanding of the release mechanisms of IMA is needed before clinical application of the test.