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下壁梗塞急性期にみられる前胸部ST低下の臨床的意義についてはまだ議論の多いところである1)。このST低下は,下壁梗塞に合併した後壁梗塞の反映2〜4),下壁梗塞に伴う電気的ないわゆるreciprocalな変化5,6),下壁梗塞に同時に存在する前壁の虚血7)などの見解がある。しかし,これらの研究のST低下のcriteriaにも差があり,発症後時間,I,aVLの扱い,ST低下の程度が問題となる。今回,我々は当院CCUに急性下壁梗塞で入院した患者につき,前胸部ST低下を検討し,その意義を評価した。
Implications of anterior ST depression in acute inferior myocardial infarction are controversial. We evaluated 37 patients with acute inferior infarction who admitted within 8 hours (mean 3.4 hours) after the onset of symptom. Thirty-five patients (94.6%) had ST depression greater than 0.1 mV in leads I, aVL or V1-6. The maximal ST elevation in II, III, aVF correlated well with the maximal ST depression in I, aVL (r=0.73) and did not correlate with the maximal ST depression in V1-4 (r=0.15). Patients with the maximal ST depression greater than 0.2 mV in V1-4 (ST↓(+) group, n= 27) had greater peak CPK and peak CPK-MB than those without such ST depression (ST↓(-) group, n=10) (CPK 1588±662 vs 838+388 IU)/l p<0.01, CPK-MB 407±203 vs 228+163 IU/l p<0.05). ST↓(+) group had larger technetium 99 m pyro-phosphate uptake than ST↓(-) group (1452±1450 vs 535±505 mm2 p<0.05). LV posterior wall uptake of technetium) 99m pyrophosphate was seen in 91.3% of ST↓(+) group and in 40% of ST↓(-) group (p<0.005). Stenosis of left anterior descending artery was seen in 55.6% of ST↓(+) group and in 70% of ST↓(-) group in coronary arteriography (NS). These data suggest that ST depression greater than 0.1 mV in leads I, aVL or V1-6 is commonly seen in acute phase of inferior myocardial infarction and ST depression in I, aVL is an electrically reciprocal phenomenon of ST elevation in II, III, aVF. But ST depression greater than 0.2 mV in V1-4 indicates a larger infarct size extended to LV posterior wall. These findings may detect high risk subset of patients in acute phase of inferior infarction and an aggressive therapy would be favorable to such patients.
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