抄録
The cardiorespiratory response on multistage maximal treatdmill exercise was studied in 11 patients with effort angina pectoris and 10 age-matched normal sedentary males, whose pulmonary function revealed normal findings. Expiratory gas analysis were sequentially measured at 30 second intervals during exercise with a Respiromonitor 200 system. There were marked differences in respiratory response as well as cardiocirculatory response during exercise between these two groups.
Before exercise the heart rate (HR), oxygen intake (VO2), oxygen pulse (O2 pulse), minute ventilation (VE), oxygen removal (O2 removal) and body weight were essentially the same in both groups. Maximal HR during exercise was markedly lower in the angina group than the control group (127±16bpm v.s. 165±10bpm: p<0.001), as was maximal VO2 (1163±203ml/min vs. 1874±339ml/min: p<0.001). Maximal O2 pulse was significantly lower in the angina group than the control group (9.4±1.3ml/beat v.s. 12.2±3.1ml/beat: p<0.05), and if compared at the matched O2 of 14.0ml/kg·min during exercise in the two groups, O2 pulse tended to be lower in the angina group than the control group without statistical difference (8.0±1.0ml/beat v.s. 8.5±1.4ml/beat).
The respiration rate was higher in the angina group than the control group before exercise (16.9±2.2/min v.s. 14.3±1.5/min: p<0.01), and the tidal volume tended to be smaller in the angina group than in the control group (612±97ml v.s. 703±119ml: ns). During exercise at the matched VE of 31.31/min, the respiration rate was significantly higher in the angina group than the control group (25.5±3.4/min vs. 21.9±3.6/min: p<0.05), and tidal volume was significantly smaller in the angina group than the control group (1240±177ml v.s. 1460±268ml: p<0.05), whereas the maximal respiration tate was almost similar in both groups (32.3±5.3/min vs. 34.7±4.5/min:ns). On the contrary, the maximal tidal volume was markedly smaller in the angina group than the control group (1462±206ml vs. 2049±289ml: p<0.001). It was suggested from these results that the tidal volume showed limited increase with increments in VE during exercise, and exaggerated increase in respiration rate compensated for the decreased tidal volume responding to increasing VE in patients with effort angina pectoris.
Maximal O2 removal tended to be lower in the angina group than the control group (33.7±2.9STPD/BTPS v.s. 36.6±4.7STPD/BTPS: ns). The anaerobic threshold was markedly lower in the angina group than the control group (731±141ml/min vs. 1129±201ml/min: p<0.001). The low anaerobic threshold as well as low maximal VO2 suggested that the aerobic function was impaired in the angina group. In the control group, the anaerobic threshold closely correlated with the maximal VO2 (r=0.87: p<0.001), but it did not correlate well with the maximal VO2 in the angina group (r=0.56: ns). On the other hand in the angina group, the VO2 at the appearance of 0.1mV ischemic ST depression closely correlated with the maximal VO2 (r=0.89: p<0.001), and did so significantly with the anaerobic threshold (r=0.62: p<0.05). Thus, it was concluded from this study that the development of myocardial ischemia during exercise played an important role in influencing the aerobic function, and that respiratory responses such as the respiration rate and tidal volume were significantly altered in patients with effort angina pectoris.
