Scharf S M, Woods B O, Brown R, Parisi A, Tow D E, Miller M, McIntyre K
Department of Medicine, Brockton/West Roxbury VA Medical Center, MA 02132.
Ann Biomed Eng. 1987;15(3-4):297-310. doi: 10.1007/BF02584285.
Decreasing pleural pressure impedes the ejection of blood from the left ventricle (LV), may lead to decreased LV compliance because of interdependence effects and leads to increased transmural LV systolic and diastolic pressure. Previous work from this laboratory has shown that patients with coronary artery disease (CAD) often develop akinetic segments of the LV wall during the Mueller maneuver. In the presence of increased LV transmural pressure regional akinesis could be caused either by the development of regional ischemia or by mechanical inhibition of motion of an area of nonfunctional myocardium as would be caused by previous myocardial infarction (MI). The present study was designed to distinguish between these two mechanisms by determining if the presence of CAD alone is sufficient to lead to regional akinesis or if prior MI is necessary. We used first pass radionuclide ventriculography (RVG) in the 30 degrees LAD supine position to measure LV ejection fraction (EF), end-diastolic (EDV) and end-systolic (ESV) volumes, heart rate and to assess regional wall motion during the Mueller maneuver. This was done in four groups of subjects: 13 normal subjects, 25 patients with CAD but no prior MI, 13 patients with prior nontransmural MI and 36 patients with prior transmural MI. All subjects had angina pectoris and underwent contrast coronary arteriography. Most also underwent routine contrast left ventriculography as well. There were no significant differences among the three patient groups as regards medications, extent and severity of CAD, and response to routine exercise tolerance testing. EF decreased significantly in the three patient groups (4%-9%, p less than 0.01) but not in the normals during the Mueller maneuver. Heart rate increased (5-10 bpm, p less than 0.05) in the normals and in patient groups 2 and 4. EDV decrease in all four subject groups (8%-10%, p less than 0.01), while ESV remained unchanged. Akinesis of the LV wall developed during the Mueller maneuver only in one group-2 patient, but did so in 17/36 patients with prior transmural MI (group 4, p less than 0.001). One-half of the akinetic LV wall segments seen during the Mueller maneuver on RVG were not seen on routine contrast ventriculography. We tested the effects of posture (supine versus upright) on the response to the Mueller maneuver in six normal subjects and found no changes in the response of EDV and ESV to the Mueller maneuver.(ABSTRACT TRUNCATED AT 400 WORDS)
胸膜腔内压降低会阻碍左心室(LV)射血,由于相互依存效应可能导致左心室顺应性降低,并导致左心室跨壁收缩压和舒张压升高。本实验室先前的研究表明,冠心病(CAD)患者在米勒动作过程中左心室壁常出现运动不能节段。在左心室跨壁压力升高的情况下,局部运动不能可能是由局部缺血的发展引起的,也可能是由先前心肌梗死(MI)导致的无功能心肌区域运动的机械性抑制引起的。本研究旨在通过确定仅CAD的存在是否足以导致局部运动不能,或者先前的MI是否是必需的,来区分这两种机制。我们在30度左前降支仰卧位使用首次通过放射性核素心室造影(RVG)来测量左心室射血分数(EF)、舒张末期(EDV)和收缩末期(ESV)容积、心率,并评估米勒动作过程中的局部壁运动。这在四组受试者中进行:13名正常受试者、25名有CAD但无先前MI的患者、13名有先前非透壁MI的患者和36名有先前透壁MI的患者。所有受试者均有胸痛并接受了冠状动脉造影。大多数受试者还接受了常规的对比剂左心室造影。在药物治疗、CAD的范围和严重程度以及对常规运动耐量测试的反应方面,三组患者之间没有显著差异。在米勒动作过程中,三组患者的EF显著降低(4%-9%,p<0.01),而正常受试者则没有。正常受试者以及第2组和第4组患者的心率增加(5-10次/分钟,p<0.05)。所有四组受试者的EDV均降低(8%-10%,p<0.01),而ESV保持不变。仅在一组2名患者中,米勒动作过程中出现了左心室壁运动不能,但在36名有先前透壁MI的患者中有17名出现了这种情况(第4组,p<0.001)。在RVG上米勒动作过程中看到的左心室壁运动不能节段的一半在常规对比剂心室造影中未看到。我们在6名正常受试者中测试了姿势(仰卧位与直立位)对米勒动作反应的影响,发现EDV和ESV对米勒动作的反应没有变化。(摘要截短至400字)