NEUTROPHIL HYPERREACTIVITY AFTER EXERCISE-INDUCED ANGINA-PECTORIS

Background: Previous studies have suggested an increased risk of myoca rdial infarction associated with physical exercise. Activated neutroph ils may contribute to the triggering mechanisms. Methods: Fifteen pati ents with stable angina pectoris underwent symptom-limited bicycle erg ometry. In neutrophils obtained from serial blood samples, superoxide anion production (SOP) was determined by superoxide dismutase-inhibite d reduction of cytochrome C and chemotactic mobility in the microchemo taxis chamber. The same ergometry was repeated after successful balloo n angioplasty [percutaneous transluminal coronary angioplasty (PTCA)]. Results: Rate-pressure products and systemic lactate concentrations w ere similar in both ergometries. Angina was induced in all exercise te sts before PTCA, but in none after PTCA. Before the ergometries, syste mic neutrophil counts, SOP and chemotactic mobility were essentially t he same. Compared with baseline, exercise-induced angina immediately a fter the first ergometry was associated with an increase in neutrophil count by 0.8+/-0.1 nl(-7) (P<0.01), an increase in N-formyl-methionyl -leucyl-phenylalanine (FMLP)-stimulated SOP by 2.44+/-0.49 nmol/15 min /5000 cells (P< 0.01) and an increase in chemotaxis by 10.28+/-1.65 ce lls per vision field (P<0.01). In the ergometry after PTCA this increa se in SOP and in chemotaxis disappeared (0.26+/-0.39 nmol/15 min/5000 cells and 2.15+/-1.52 cells per vision field; NS), whereas the increas e in neutrophil count was not significantly different from that in the ergometry before PTCA. Conclusion: This study reveals that neutrophil hyper-reactivity after exercise-induced angina can be attributed to m yocardial ischaemia.