労作性狭心症におけるProstacyclinの効果—トレッドミル運動負荷試験による検討

Therapeutic efficacy of prostacyclin in the patients with effort angina

　虚血性心疾患の病態発生機序として，冠動脈の器質的狭窄に加えて血栓とspasmの関与が重要視されており，近年これらのmediatorとして冠循環におけるprosta—noid代謝異常が大きな関心を集めている。すなわち，血小板で生成されるthromboxane A₂（TXA₂）は強力な血小板凝集作用と血管収縮作用を有することが知られているが，冠血管の硬化性病変により血小板が活性化され冠循環に放出されたTXA₂が微小血栓ないしspasmを誘発し，これによりさらに冠血流の低下と血小板凝集が促進され，ついには心筋虚血が誘発されるといった一連の機序が推定されている^1,2）。

　一方，血管壁で生成されるprostacyclin （PGI₂）は，その血小板凝集抑制作用と血管拡張作用とからTXA₂に拮抗することが知られており，虚血性心疾患への臨床応用が期待されている^2,3）。

The equilibrium of thromboxane A2(TXA2) and prostacyclin (PGI2) may modulate platelet aggregability and coronary arterial tone, which have been implicated as pathogenetic factors of myocardial ischemia. We evaluated the therapeutic potential of PGI2 in 8 patients with effort angina by exercise stress test. All patients underwent tread-mill exercise test according to the standard Bruce protocol before and after PGI2 6-10ng/kg/min infu-sion. Plasma levels of ,3-thromboglobulin (8-TG), an index of in vivo platelet activation, and TXB2 at rest and post-exercise were measured in each ex-ercise test.

Though mean blood pressure fell significantly, double product at peak exercise did not change after PGI2 infusion. Exercise duration prolonged from 321±58 to 353±50 sec, and treadmill exer-cise score which quantifies the time coures of ST depression improved from 4.8±11.7 to 3.5±1.2, respectively (p<0.05). The elevation of β-TG induced by exercise (36.2±6.5 to 54.4±12.9 ng/ ml, p<0.02) was not seen after PGI2 infusion (35.0 ±6.0 to 27.8±7.0 ng/ml, NS). But TXB2 level did not change during exercise and after PGI2 infu-sion.

These observation indicate the effectiveness of PGI2 for inhibition of exercise-induced platelet activation and improvement of exercise tolerance in effort angina.