CPK流出状況からみた心筋壊死巣の成立過程と梗塞発症時胸痛の持続時間および冠動脈狭窄の関係

Evolution of myocardial infarction elucidated by serial CPK technique, connected with chest pain duration and coronary arterial stenosis

　急性心筋梗塞症のCCU内での死亡のほとんどが重症ポンプ失調によるものであることから，壊死巣の大きさ可及的小にとどめる，またはその拡大を防止するための対策が追究されている^1）。臨床的には急性心筋梗塞症例に，経過が単調で速やかに改善するものと，然らざるものがあり，心電図や心筋逸脱酵素の経過から明らかに壊死巣が拡大したと考えられる例がある。しかし，心筋梗塞症の発症とその後の壊死巣成立過程の本態が依然として不明であり，壊死巣の「拡大防止治療」の効果を判定する根拠にも確かなものがない。壊死巣の拡大が防止されたか否かを知るためには，各症例毎に壊死巣の成立過程を知る手段が得られなければならない。心電図，心筋逸脱酵素^2,3）等によるその試みが報告されている。壊死巣の大きさを測る他の方法と同様に，諸々の不備は指摘されていても，壊死巣の大きさとその過程を最も良く反映する資料が，心筋梗塞発症後の血中CPK活性の経時的変化の成績であることは，多くの論者が指摘しているとおりである^4）。壊死巣の拡大は，言葉の意味からみても，本来の，もしくは発症時に規定される壊死巣の大きさに，発症後のある時間以後，何らかの要因によってさらに壊死巣が加わるものと想定される。従って，壊死心筋から流出するCPKが，壊死の始まりから進展まで順次血中に現れてくるものならば，壊死巣の拡大は血中CPK活性の経時的変化を修飾すると考えた^5）。当研究の目的の第1は，これを解析して梗塞巣の成立過程を反映する指標を得ようとするものである。

　第2の目的は，心筋梗塞発症時の胸痛発作とその持続時間，一旦鎮痛したあと再度出現する胸痛発作という臨床上容易に観察しうる症候が壊死巣の成立過程に関わることを想定して，血中CPK活性の解析から得た指標との関係を明らかにすることである。

The serial CPK technique developed by Shell was applied on 76 patients with acute myocardial infarction (AMI) of Killip's class 1 and 2. From accumulation curve of released CPK, total released CPK (CPKr, mIU/ml), mean CPK accumulation velocity of the initial stage (Vi, mIU/ml･hr), peak serum CPK activity (CpE, mIU/ml) and its time after AMI onset (TpE, hr), total CPK releasing time (Tr, hr) and CPKr/Vi were caluculated in each patient. Vi was supposed to be related indirectly to the initial myocardial damage, and CPKr/Vi was thought to reflect the amount of infarct extension, then called as ratio of infarct size extension (Re).

CPKr, Vi, CpE were well correlated each other, and also Tr, TpE, Re revealed the same good correlation (P<0.001). However, between the former three and the latter three variables, there was no significant relationship. Mean±SD (range) of CPKr, Tr and Re were 4244±2836 (341-12833) mIU/ml, 19.5±5.5 (8.9-34.5) hoursand 18.7±5.0 (8.6-35.7), respectively.

In 76 patients, duration of chest pain after the onset of AMI (Tcp) was investigated. Average of Tcp was 5.3±2.9 (0.8-13.5) hours. Tcp was positively related to Tr, TpE and Re (P<0.001). There was no significant relation between Tcp and CPKr, Vi, CpE.

From the coronary arteriogram obtained after 3-6 weeks of AMI onset, 44 cases of the first transmural infarction were divided into two groups according to the extent of occlusion of coronary artery distributed to the infarct region, such as 17 cases of the coronary stenosis less than 90% and 27 cases of more than 99%. In the former cases, Tr, TpE, Re, Tcp were significantly less than the latter cases. As to CPKr, Vi, CpE, there was no significant difference between two groups.

The variables such as CPKr, Vi, CpE, Tr, TpE and Re calculated individually would be useful to investigate evolution of AMI, especially to evaluate the extension of myocardial infarct size. And it was apparent that Tcp related to the evolutional process of AMI, that is, the longer the Tcp was, the more tendency to extend infarct size, Furthermore, it appeared that obstruction of the coronary artery distributed to the infarct region act to prolong Tcp and time course of CPK efflux. We thought that extension of infarction was originated by the coronary arterial obstruction distributed the initial infarct region.

The results would be useful to set up principles of therapeutic limitation of infarct size and to evaluate its effects quantitatively.