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陳旧性心筋梗塞患者に認められる梗塞部誘導の運動負荷時ST上昇は古くから論じられている心電図上の問題点である1,2)。ST上昇は前壁梗塞例に多く3),梗塞発症からの時間により変動すること4,5),運動負荷時のpres—sure rate product (PRP)に影響を受けることなどが知られているが6)その機序については梗塞部周囲における虚血によるとするもの7,8),梗塞部の壁動態異常を反映するなどの報告があり9,10),見解の一致が得られていない。近年,201—Tl心筋シンチや99m-Tc心プールシンチにより運動時に生ずる虚血の有無の検索や11,12),左室駆出率,左室容積の変化など運動負荷に伴う血行動態の評価などが試みられている13,14)。そこで,前壁梗塞例に本法を用いて運動負荷を施行しST上昇例と不変例とに分け血行動態の指標とST上昇との関連性を検討するとともに,併せて上昇例に対してはそれぞれ作用機序の異なるisosorbide dinitrate(ISDN),nifedipine(N),propranolol(P)を投与し,心電図に及ぼす影響についても検討した。
To evaluate the factors which determine exercise-induced ST elevation in infarct area, we performed 201-T1 SPECT and gated cardiac pool scans in 22 patients with old anterior myocardial infarction. Exercise-induced ST elevation was observed in 15 patients, not in 7. Redistribution of 201-Tl was shown insignificantly different in it's frequency between these two groups. Compared with patients without ST elevation, ejection fraction was signifi-cantly reduced, and left ventricular volume signifi-cantly larger in those with ST elevation. Left ventri-cular volume also increased significantly at exercise in those with ST elevation. In 7 out of 15 patients after administration of ISDN, 8 after nifedpine and 11 after propranolol, exercise-induced ST elevation was not observed. After ISDN, ESV & EDV decreased significantly, and then not increased at exercise in improved patients, unlike not improved patients. Propranolol reduced pressure rate product significantly and improved ST change in high frequency, while no significant hemodynamic changes had been found between before and after nifedipine. These findings suggest that exercise-induced ST elevation changes under cardiovascular active drugs and have stronger connection with the changes of left ventricular geometry rather than with exercise-induced ischemia.
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