Effects of acute left anterior descending occlusion on regional myocardial blood flow and wall thickening in the presence of a circumflex stenosis in dogs

Abstract

In this study, 2 hypotheses were tested: (1) Myocardium supplied by a stenosed circumflex coronary artery (LC) does not demonstrate compensatory increases in regional blood flow and systolic thickening when the left anterior descending coronary artery (LAD) is acutely occluded. (2) Blood flow to myocardium in the distribution of an acutely occluded LAD is lower in the presence of a stenosed than in the presence of an unstenosed LC. Fifty-three open-chest, anesthetized dogs were studied. Regional coronary blood flow (8 to 10-μ micro-spheres) and wall thickening (sonomicrometer crystals) were measured before and after LAD occlusion in the presence of an unstenosed LC artery, and a moderate and severe LC stenosis. Acute LAD occlusion in the presence of an unstenosed LAD was not accompanied by a significant increase in regional blood flow to the remote LC bed; posterior myocardial wall thickening, however, increased from 0.22 ± 0.02% to 0.24 ± 0.02% (p = 0.04). In the presence of a moderate LC stenosis (gradient 29 ± 1 mm Hg), LAD occlusion was associated with a 9% (p = 0.02) decrease in endocardial flow and an 11 % decrease in the endocardial/epicardial flow ratio (p = 0.002). Transmural flow was unchanged and there was no compensatory increase in posterior wall thickening. In the presence of a more severe LC stenosis (gradient 49 ± 1 mm Hg), central LC endocardial flow decreased by 32% (p = 0.0008) at the time of LAD occlusion. Similar alterations were noted in the peripheral LC region. Posterior wall thickening did not increase significantly with LAD occlusion (0.27 ± 0.01 to 0.30 ± 0.03%, p = 0.12). Stepwise regression analysis showed that the changes in remote LC blood flow were related to the distal LC pressure at the time of LAD occlusion and to changes in LC pressure and LC stenosis resistance that occurred after the LAD was occluded. Regional blood flow to the bed of the acutely occluded LAD was lower in the presence of a stenosed LC artery than in the presence of an unstenosed LC. This may have been related, in part, to an impairment of collateral flow from the stenosed LC to the distal LAD bed. Thus, acute LAD occlusion in the presence of a stenosed LC is associated with adverse blood flow alterations in the remote LC bed as well as worsening of the flow diminution in the LAD bed compared with blood flow alterations observed when the LAD is occluded in the setting of an unstenosed, fully patent LC vessel. These changes may be clinically relevant to patients with acute myocardial infarction who have underlying multivessel coronary artery disease.