Intracellular neutrophil myeloperoxidase is reduced in unstable angin and acute myocardial infarction, but its reduction is not related to ischemi

Objectives. This study sought to assess neutrophil activation in acute coronary syndromes and its relation to ischemic episodes. Background. Neutrophil activation has been reported in unstable angin and acute myocardial infarction; however, it is not clear whether it is related exclusively to ischemia-reperfusion injury. Methods. We measured the index of intracellular myeloperoxidase in 1) patients with unstable angina, myocardial infarction, variant angin and chronic stable angin and in normal subjects (protocol A); and 2) in patients with unstable angin and acute myocardial infarction during the first 4 days of the hospital period (protocol B). To assess whether neutrophil activation was triggered by ischemia, the myeloperoxidase intracellular index was analyzed before and after spontaneous ischemic episodes and before and after ischemi induced by an exercise stress test in 10 patients with chronic stable angina. In 11 patients with unstable angina, we also compared values of the myeloperoxidase intracellular index at entry with those after waning of symptoms. Results. In protocol A, the myeloperoxidase intracellular index was significantly reduced in patients with unstable angin and acute myocardial infarction compared with patients with stable and variant angin and normal subjects (p < 0.01). In protocol B, the myeloperoxidase intracellular index did not change over time in patients with unstable angin and myocardial infarction. However, in 11 patients with waning symptoms, the myeloperoxidase intracellular index was significantly higher after symptoms had waned (p < 0.05). In patients with unstable angina, 23 ischemic episodes were studied; no changes in the myeloperoxidase intracellular index were observed. In 10 patients with chronic stable angin and positive exercise stress test results, no significant differences in the myeloperoxidase intracellular index were observed after stress-induced ischemia. Conclusions. Our study confirms that neutrophils are activated in acute coronary syndromes but suggests that their activation may not be only secondary to ischemia-reperfusion injury.