抄録
Relevant to the cause of the acute myocardial infarction, the theoretical assumption whether coronary thrombosis or coronary spasms will play more important factors offers much debate nowadays. The matter has been a subject of vigorous investigation in our laboratory and noteworthy results have been obtained to support coronary functional derangementas one of the most important causative factors of the myocardial infarction. Based on these observations, the author made an investigation to elucidate the above-mentioned subject, utilizing autopsy subjects which suffered from non-thrombotic, non-occlusive myocardial infarctions and related coronary impaired heart diseases.
Twenty five cases of non-thrombotic, non-occlusive myocardial infarctions and four cases of related coronary impaired diseases were studied. Moreover, one hundred and twenty cases of heart with coronary thrombosis served as a control. The most common site of thrombosis formation is assumed to be the point 2.5 cm from the origin of the coronary orifice and the site was excised at 3 mm interval.
Several sections were cut and embedded in paraffin.
Approximately ten sections were cut and stained routinely with HE, Azan and PAM stainings. Representative sections were also processed for a transmission electron microscopic investigation. The results obtained were as follows :
1) The morphological study of the non-thrombotic, non-occlusive myocardial infarction disclosed a frequent occurence of the mechanical destruction of the vascular wall as well as the imbibition of the serous component in the mural layer which could be justifiable as pre-thrombotic lesion of the coronary arteries.
2) The above-mentioned change disclosed various alterations based on the extent of coronary atherosclerosis and the amount and degree of the imbibed serous component. They were categorized as slightly destructive, collagenous network formative, serous component imbibitive, intimal thickening with mural hemorrhage and destructive types with atheroma.
Moreover, occlusion by soft atheroma was confirmed and might be subclassified as one of the variants of the destructive type with atheroma.
The last type was encountered in patients who received cardiac massage at the terminalstage and intensification of mechanical destruction due to manipulation should be taken into consideration.
3) The above-mentioned acute changes may result from a rapid increase of intra-luminal pressure which cause marked coronary circulatory derangement. However, this fails to give adequate explanation for the interpretation of the most common occurrence of pre-thrombotic lesion which frequently observed at 2.5 cm from the orifice.
The common occurrence of this pre-thrombotic lesion was confirmed with the cine-angiography of the patients suffering from the angina pectoris which revealed persisting spastic change at that site. In this context, it is worthwhile to consider the concept of coronary post-spastic failed and good reflow to give adequate explanation for it. The concept was initially proposed by Sheehan and Davis in the renal arterial trees based on observation of the blood flow after release from the renal arterial ligation.
4) This proposal is obviously substantiated by the acute circulatory disturbance, which is manifested by the cytoplasmolytic edematous lesion in the medial smooth muscle cells and the persisting ischemic change of the arteriolo-small arterial trees.
5) Occasional aggregates of the coagulative necrotic foci in relatively broad range were noted in the non-thrombotic, non-occlusive acute myocardial infarction. In other instances, necrotic foci were surrounded by far advanced degenerative regions.
6) The cases which had related coronary impaired heart diseases revealed similar changes to a lesser extent.
