Effects of acute left anterior descending occlusion on regional myocardial blood flow and wall thickening in the presence of a circumflex stenosis in dogs.
Effects of acute left anterior descending occlusion on regional myocardial blood flow and wall thickening in the presence of a circumflex stenosis in dogs.
复制标题
犬旋支狭窄时急性左前降支闭塞对局部心肌血流和壁增厚的影响。
DOI：
10.1016/0002-9149(84)90205-4
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Beller,GA
中科院分区：
文献类型：
--
作者：
Gascho,JA;Lesnefsky,EJ;Mahanes,MS;Kaiser,DL;Beller,GA
本研究检验了两个假设：(1)当左冠状动脉前降支（LAD）急性闭塞时，狭窄的旋冠状动脉（LC）供应的心肌不表现出局部血流量和收缩增厚的代偿性增加。(2)急性闭塞的前冠状动脉狭窄时流向心肌的血流量低于未狭窄的前冠状动脉。对53只开胸麻醉犬进行了研究。在未狭窄的LC动脉和中度和重度LC狭窄存在的LAD闭塞前后，测量局部冠状动脉血流（8至10 μ微球）和壁增厚（声微米晶体）。在LAD未狭窄的情况下，急性LAD闭塞不伴有远端LC床的局部血流显著增加；心肌后壁增厚由0.22±0.02%增加至0.24±0.02% （p = 0.04）。在存在中度LC狭窄（梯度为29±1mmHg）的情况下，LAD闭塞与心内膜血流减少9% （p = 0.02）和心内膜/心外膜血流比减少11% （p = 0.002）相关。跨壁血流无变化，后壁增厚无代偿性增加。当存在更严重的LC狭窄（梯度为49±1 mm Hg）时，LAD闭塞时中央LC心内膜血流减少32% （p = 0.0008）。外周LC区域也有类似的改变。LAD闭塞后壁增厚无明显增加（0.27±0.01 ~ 0.30±0.03%,p = 0.12）。逐步回归分析显示，远端LC血流的变化与LAD闭塞时远端LC压力的变化以及LAD闭塞后LC压力和LC狭窄阻力的变化有关。在急性闭塞的LAD中，狭窄的LC动脉比未狭窄的LC动脉的血流要少。这可能部分与从狭窄的LC到远端LAD床的侧支血流受损有关。因此，与在未狭窄、完全通畅的LC血管中闭塞LAD时观察到的血流改变相比，在LC狭窄存在下的急性LAD闭塞与远端LC床的不利血流改变以及LAD床血流减少的恶化有关。这些变化可能与伴有多支冠状动脉疾病的急性心肌梗死患者有临床相关性。
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 ± 1mmHg), 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.