Allman K C, Wieland D M, Muzik O, Degrado T R, Wolfe E R, Schwaiger M
Department of Internal Medicine, University of Michigan, Ann Arbor.
J Am Coll Cardiol. 1993 Aug;22(2):368-75. doi: 10.1016/0735-1097(93)90039-4.
The purpose of this study was to assess the extent and reversibility of neuronal abnormalities in patients with an acute myocardial infarction.
Previous experimental studies have described ischemic injury to sympathetic neurons exceeding the area of myocardial necrosis. Carbon-11 (C-11) hydroxyephedrine (HED) is a norepinephrine analogue that can be used for the noninvasive evaluation of neuronal integrity using positron emission tomography.
We studied 14 volunteers and 16 patients experiencing a first acute myocardial infarction. Positron emission tomographic imaging was used to quantitatively compare regional perfusion, as assessed with nitrogen-13 ammonia, with myocardial retention of C-11 hydroxyephedrine early after myocardial infarction as well as > 6 months after the acute event.
C-11 hydroxyephedrine and flow images demonstrated homogeneous tracer retention in volunteers but were abnormal in all patients. C-11 hydroxyephedrine abnormalities were more extensive than those for blood flow assessed by semiquantitative polar map analysis (31 +/- 15% vs. 17 +/- 17% left ventricle; p < 0.05), particularly in five patients with non-Q wave infarction (31 +/- 11% vs. 3.5 +/- 2.5% left ventricle; p = 0.008). Eleven patients with Q wave infarction had matched defects (28 +/- 17% vs. 21 +/- 17% left ventricle; p = NS). C-11 hydroxyephedrine tissue retention fraction was quantified in three tissue zones: zone 1 (abnormal rest flow) had retention fraction 0.037 +/- 0.022-min; zone 2 (normal rest flow but decreased carbon-11 hydroxyephedrine retention) had retention fraction 0.068 +/- .034-min, and zone 3 (normal flow and carbon-11 hydroxyephedrine retention) had retention fraction 0.087 +/- 0.041-min (p = 0.0004). Follow-up studies at 8 +/- 3 months in eight patients revealed no change in extent of abnormalities or absolute tissue tracer retention in infarct and peri-infarct territories.
The results of abnormal regional sympathetic innervation in patients with infarction confirm previous experimental data and suggest persistent neuronal damage in infarct and peri-infarct territories, without evidence of reinnervation of reversibly injured myocardium.
本研究旨在评估急性心肌梗死患者神经元异常的程度及可逆性。
先前的实验研究已描述了交感神经元的缺血性损伤超过心肌坏死区域。碳-11（C-11）羟基麻黄碱（HED）是一种去甲肾上腺素类似物，可用于使用正电子发射断层扫描对神经元完整性进行无创评估。
我们研究了14名志愿者和16名首次发生急性心肌梗死的患者。使用正电子发射断层扫描成像来定量比较用氮-13氨评估的区域灌注与心肌梗死后早期以及急性事件发生>6个月后C-11羟基麻黄碱在心肌中的滞留情况。
C-11羟基麻黄碱和血流图像显示志愿者体内示踪剂滞留均匀，但所有患者均异常。通过半定量极坐标图分析，C-11羟基麻黄碱异常比血流异常更广泛（左心室分别为31±15%对17±17%；p<0.05），特别是在5名非Q波梗死患者中（左心室分别为31±11%对3.5±2.5%；p = 0.008）。11名Q波梗死患者有匹配的缺损（左心室分别为28±17%对21±17%；p = 无显著差异）。在三个组织区域对C-11羟基麻黄碱组织滞留分数进行了定量：区域1（静息血流异常）的滞留分数为0.037±0.022 - 分钟；区域2（静息血流正常但C-11羟基麻黄碱滞留减少）的滞留分数为0.068±.034 - 分钟，区域3（血流和C-11羟基麻黄碱滞留正常）的滞留分数为0.087±0.041 - 分钟（p = 0.0004）。8名患者在8±3个月时的随访研究显示梗死和梗死周边区域的异常程度或绝对组织示踪剂滞留无变化。
梗死患者区域交感神经支配异常的结果证实了先前的实验数据，并提示梗死和梗死周边区域存在持续性神经元损伤，无可逆性损伤心肌再支配的证据。
