INTRACELLULAR NEUTROPHIL MYELOPEROXIDASE IS REDUCED IN UNSTABLE ANGINA AND ACUTE MYOCARDIAL-INFARCTION, BUT ITS REDUCTION IS NOT RELATED TOISCHEMIA

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 angina and acute myocardial infarction; however, it is not clear whether it is related exclusively to ischemia-reperfusion injury. Methods. We measured the i ndex of intracellular myeloperoxidase in 1) patients with unstable ang ina, myocardial infarction, variant angina and chronic stable angina a nd in normal subjects (protocol A); and 2) in patients with unstable a ngina and acute myocardial infarction during the first 4 days of the h ospital period (protocol B). To assess whether neutrophil activation w as triggered by ischemia, the myeloperoxidase intracellular index was analyzed before and after spontaneous ischemic episodes and before and after ischemia induced by an exercise stress test in 10 patients with chronic stable angina. In 11 patients with unstable angina, we also c ompared values of the myeloperoxidase intracellular index at entry wit h those after waning of symptoms. Results. In protocol A, the myeloper oxidase intracellular index was significantly reduced in patients with unstable angina and acute myocardial infarction compared with patient s with stable and variant angina and normal subjects (p < 0.01). In pr otocol B, the myeloperoxidase intracellular index did not change over time in patients with unstable angina and myocardial infarction. Howev er, in 11 patients with waning symptoms, the myeloperoxidase intracell ular 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 angina and positive exercise stres s test results, no significant differences in the myeloperoxidase intr acellular index were observed after stress-induced ischemia. Conclusio ns. Our study confirms that neutrophils are activated in acute coronar y syndromes but suggests that their activation may not be only seconda ry to ischemia-reperfusion injury.