Two‐dimensional Echocardiography in Experimental Coronary Stenosis: II. Relationship Between Systolic Wall Thinning and Regional Myocardial Perfusion in Severe Coronary Stenosis
Two‐dimensional Echocardiography in Experimental Coronary Stenosis: II. Relationship Between Systolic Wall Thinning and Regional Myocardial Perfusion in Severe Coronary Stenosis
复制标题
实验性冠状动脉狭窄中的二维超声心动图：II. 严重冠状动脉狭窄时收缩期壁变薄与局部心肌灌注的关系
作者：
N. Pandian;R. Kieso;R. Kerber
为了确定在中度和重度冠状动脉狭窄的情况下，收缩期收缩异常（通过二维超声心动图证实）和心肌灌注减少之间是否存在定量关系，我们在开胸犬中建立了70%或90%的回旋冠状动脉直径减少。短暂性缺血是通过在存在狭窄的情况下叠加增加的心肌需氧量（静脉注射异丙肾上腺素、主动脉缩窄）或通过减少冠状动脉灌注（静脉注射硝普钠、硝酸甘油或出血降低动脉压）诱导的。二维超声心动图或植入式心肌声学测微计显示的急性收缩期室壁变薄被视为心肌缺血的功能证据。当心肌壁明显变薄时，用放射性标记微球测定心肌灌注。当冠状动脉狭窄程度仅为70%时，这些干预措施不能诱导血管壁变薄。只有当心肌需氧量增加或主动脉压降低叠加在90%的冠状动脉狭窄时，才会发生心肌管壁变薄。在这些条件下，心肌灌注降低至28 ± 27 ml/100 g/min（平均值± SD），为对照组的15-25%。主动脉舒张压是缺血的主要决定因素，因为90%狭窄和血管扩张剂或出血产生的收缩异常可以通过叠加急性主动脉收缩而急性逆转，这会升高动脉压;心肌灌注相应增加。因此，在压力干预过程中通过二维超声心动图显示的短暂收缩期壁变薄表明存在严重的冠状动脉狭窄，并且急性运动障碍心肌区域的灌注为对照的25%或更少。
To determine if there is a quantitative relationship between systolic contraction abnormalities (demonstrated by two-dimensional echocardiography) and reduced myocardial perfusion in a setting of moderate and severe coronary stenosis, we created 70% or 90% reduction in circumflex coronary artery diameter in open-chest dogs. Transient ischemia was induced by superimposing increased myocardial oxygen requirements (i.v. isoproterenol, aortic constriction) in the presence of the stenosis or by decreased coronary perfusion (lowering arterial pressure with i.v. nitroprusside, nitroglycerin, or hemorrhage). Acute systolic wall thinning shown by two-dimensional echocardiography or by implanted myocardial sonomicrometers was taken as functional evidence of myocardial ischemia. Myocardial perfusion was determined by radiolabeled microspheres when wall thinning was apparent. Systolic wall thinning could not be induced by these interventions when the degree of coronary stenosis was only 70%. Systolic wall thinning occurred only when increased myocardial oxygen requirements or decreased aortic pressure were superimposed on 90% coronary stenosis. Under these conditions, myocardial perfusion was reduced to 28 ± 27 ml/100 g/min (mean ± SD), 15-25% of control. Aortic diastolic pressure was a major determinant of ischemia in that contraction abnormalities produced by a 90% stenosis and vasodilators or hemorrhage could be acutely reversed by superimposing acute aortic constriction, which elevated arterial pressure; myocardial perfusion increased correspondingly. Thus, the demonstration of transient systolic wall thinning by two-dimensional echocardiography during a stressful intervention indicated that severe coronary stenosis was present, and that the perfusion of the acutely dyskinetic myocardial area was 25% of control or less.