Identification and quantification of histochemical border zones during the evolution of myocardial infarction in the rat

Abstract

Several interventions have been shown to preserve ischaemic myocardium after coronary artery occlusion; yet there is uncertainty concerning the location, extent and very existence of the potentially salvageable myocardium. This study was undertaken to identify and to quantify by planimetry, histochemically different zones of myocardium in evolving infarcts. Serial frozen sections of the left ventricle from 98 rats killed at different time intervals ranging from 5 min to 72 h after coronary artery occlusion were stained for glycogen, neutral lipids and oxidative enzyme activity. From 5 to 20 min after occlusion, the ischaemic area (measured as a percentage of the cross-sectional area at the midventricular level) showed progressive glycogen loss which was, paradoxically, more severe at the periphery than at the center. By 30 min glycogen loss was uniform and complete. Three hours after occlusion 3 abnormal zones were observed: (1) a central zone of severe glycogen loss and severe loss of enzyme activity comprising 21 ± 3% (mean ± SE) of the left ventricular cross-sectional area; (2) a peripheral zone showing severe glycogen loss but only mild loss of enzyme activity comprising 21 ± 4% of the ventricle; and (3) a surrounding lipid-containing, but otherwise normal, zone comprising 9 ± 1% of the ventricle. The zone of mild loss of enzyme activity was smaller but still present 6 h after occlusion, but disappeared by 9 h as the zone of more severe loss of enzyme activity enlarged to equal the size of the glycogen-depleted zone. The lipid-containing zone persisted for 72 h. Thus, 2 histochemical border zones were observed: an outer histochemical border zone which contained lipid but was otherwise normal which was present up to 72 h after coronary occlusion, and an inner histochemical border zone with severe glycogen loss but delayed loss of enzyme activity presented at 3 and 6 h but which disappeared 9 h after coronary artery occlusion. These data support the concept that a myocardial infarction is not a homogeneous, static structure, but rather a dynamic temporally-related phenomenon with different zones that change in size and character as the infarct evolves.