This study was undertaken to quantitàte the lateral extension that occurs concomitantly with the transmural extension of a subendocardial infarction. A subendocardial infarct was produced in 12 dogs by a 40 minute temporary coronary artery occlusion. Infarct extension was induced 7 days later by permanent occlusion of the same vessel. Regional myocardial blood flows confirmed that ischemia had been produced with both coronary artery occlusions. The vascular boundaries between the normally perfused and ischemic beds were defined by perfusion with different-colored Microfil solutions. The extent of subendocardial infarction and subsequent transmural and lateral extensions were assessed by point counting of histologic specimens. The initial temporary occlusion produced a 30.0 ± 4.2% transmural infarct and the subsequent permanent occlusion a 29.2 ± 3.5% transmural extension in a risk region of 39 ± 4 g. Lateral extension was not measured in four dogs because the initial subendocardial infarct was patchy with markedly irregular lateral borders. In eight dogs the size of the measured lateral infarct extension from each lateral margin from two histologic sections was 0.63 ± 0.013 cm2. The area of both lateral extensions was 1.7 ± 0.1% of the cross-sectional area of its risk region as determined by planimetry. Using a model of the risk region; the mass of the lateral extension was estimated to be 1.4 ± 0.3 g or 3.5 ± 0.6% of the region at risk. Thus, at the lateral margin of a subendocardial infarct there is a border zone that is small relative to the size of the region at risk and ihfafcted myocardium. This border zone is not a site at which a significant volume of myocardium can be salvaged or into which significant extension can occur.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine