Background: Previous studies have suggested an increased risk of myocardial infarction associated with physical exercise. Activated neutrophils may contribute to the triggering mechanisms.
Methods: Fifteen patients with stable angina pectoris underwent symptom-limited bicycle ergometry. In neutrophils obtained from serial blood samples, superoxide anion production (SOP) was determined by superoxide dismutase-inhibited reduction of cytochrome C and chemotactic mobility in the microchemotaxis chamber. The same ergometry was repeated after successful balloon angioplasty [percutaneous transluminal coronary angioplasty (PTCA)].
Results: Rate-pressure products and systemic lactate concentrations were similar in both ergometries. Angina was induced in all exercise tests before PTCA, but in none after PTCA. Before the ergometries, systemic neutrophil counts, SOP and chemotactic mobility were essentially the same. Compared with baseline, exercise-induced angina immediately after 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 cells per vision field (P < 0.01). In the ergometry after PTCA this increase 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 increase 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 myocardial ischaemia.