Background-Ischemia modified albumin (IMA; Ischemia Technologies, Inc) blood levels rise in patients who develop ischemia during percutaneous coronary intervention (PCI). It is not known whether IMA elevations correlate with increases in other markers of oxidative stress, ie, 8-iso prostaglandin F2-A (iP). Methods and Results-We compared IMA versus iP plasma levels in 19 patients (mean age 62.8Ϯ11.9 years) undergoing PCI and 11 patients (mean age 64Ϯ13.6 years) undergoing diagnostic angiography (controls). In the PCI patients, blood samples for IMA and iP were taken from the guide catheter before PCI and after balloon inflations, and from the femoral sheath 30 minutes after PCI. IMA was measured by the albumin cobalt binding (ACB) test and plasma iP by enzyme immunoassay. During PCI, all 19 patients had chest pain and 18 had transient ischemic ST segment changes. IMA was elevated from baseline in 18 of the 19 patients after PCI. Median IMA levels were higher after PCI (101.4 U/mL, 95%CI 82 to 116) compared with baseline (72.8 U/mL, CI 55 to 93; PϽ0.0001). Levels remained elevated at 30 minutes (87.9 U/mL, CI 78 to 99; PϽ0.0001) and returned to baseline at 12 hours (70.3 U/mL, CI 65 to 87; Pϭ0.65). iP levels were raised after PCI in 9 of the 19 patients. However, median iP levels were not significantly different immediately (Pϭ0.6) or 30 minutes after PCI (Pϭ0.1). In the control group, IMA and iP levels remained unchanged before and after angiography (Pϭ0.2 and 0.16, respectively). Conclusions-IMA is a more consistent marker of ischemia than iP in patients who develop chest pain and ST segment changes during PCI. Key Words: ischemia Ⅲ proteins Ⅲ angioplasty I schemia modified albumin (IMA; Ischemia Technologies, Inc), measured by the albumin cobalt binding test (ACB; Ischemia Technologies), has been shown to be a marker of myocardial ischemia. 1 ACB measures the ability of the amino terminus (N-terminus) of human albumin to bind exogenous cobalt. Under physiological conditions, transition metals can bind tightly to the exposed N-terminus of albumin. 2 In the presence of myocardial ischemia, structural changes take place in the N-terminus of the protein, 3,4 which reduce its binding capacity, possibly, in part, as a result of exposure to reactive oxygen species (ROS). IMA rises in patients who develop myocardial ischemia during percutaneous coronary intervention (PCI). 5 PCI offers a clinical model of myocardial ischemia-reperfusion characterized by an increase in oxidative stress. 6 -8 ROS are produced after myocardial ischemia-reperfusion and result in the production of lipid and protein peroxidation products in the local myocardial environment. This occurs irrespective of the mechanism responsible for ischemia, ie, increased oxygen demand or a primary reduction of coronary blood flow. 9 8-epi prostaglandin F 2␣ (iP), a prostaglandin isomer, is formed by free-radical catalyzed oxidation of arachidonic acid esterified in membrane phospholipids. 10 It represents a chemically stable end-product of lipid peroxidat...