Dilsizian Vasken, Bateman Timothy M, Bergmann Steven R, Des Prez Roger, Magram Martin Y, Goodbody Anne E, Babich John W, Udelson James E
Division of Nuclear Medicine, University of Maryland Hospital and School of Medicine, Baltimore, MD 21201-1595, USA.
Circulation. 2005 Oct 4;112(14):2169-74. doi: 10.1161/CIRCULATIONAHA.104.530428. Epub 2005 Sep 26.
After myocardial ischemia, prolonged suppression of fatty acid metabolism may persist despite restoration of blood flow, which is called metabolic stunning. We hypothesized that a branched-chain fatty acid, beta-methyl-p-[(123)I]-iodophenyl-pentadecanoic acid (BMIPP), might identify the presence of myocardial ischemia late after demand ischemia at rest up to 30 hours later.
In 32 patients with exercise-induced ischemia on thallium SPECT, BMIPP was injected at rest within 30 hours of ischemia. SPECT images were acquired beginning 10 minutes after injection (early) and again 30 minutes after injection (delayed). Thallium and BMIPP SPECT data were read separately by 3 observers blinded to other imaging and clinical data. Agreement between BMIPP and thallium data for the presence of an abnormality on the patient level was 91% (95% CI, 75 to 98) for the early BMIPP data and 94% (95% CI, 79 to 99) for the delayed BMIPP data. Agreement between delayed BMIPP and thallium was 95% among 21 patients studied on the same day, a mean of 6.2+/-1.4 hours after exercise-induced ischemia, and 91% among the 11 patients studied on the next calendar day, a mean of 24.9+/-2.6 hours after ischemia (P=NS). The magnitude of resting BMIPP metabolic defect by semiquantitative visual analysis was correlated to the magnitude of exercise-induced thallium perfusion defect (r=0.6, P<0.001 for early BMIPP; r=0.5, P=0.005 for delayed BMIPP).
Metabolic imaging with BMIPP identifies patients with recent exercise-induced myocardial ischemia. These findings support the concept that BMIPP imaging can successfully demonstrate the metabolic imprint of a stress-induced ischemic episode, also known as ischemic memory.
心肌缺血后,尽管血流已恢复,但脂肪酸代谢的长期抑制可能仍然存在,这被称为代谢顿抑。我们推测一种支链脂肪酸,β-甲基-p-[(123)I]-碘苯基-十五烷酸(BMIPP),可能在静息状态下需求性缺血后长达30小时的晚期识别心肌缺血的存在。
在32例铊单光子发射计算机断层扫描(SPECT)显示运动诱发缺血的患者中,在缺血后30小时内静息状态下注射BMIPP。注射后10分钟(早期)开始采集SPECT图像,注射后30分钟(延迟期)再次采集。铊和BMIPP SPECT数据由3名对其他影像和临床数据不知情的观察者分别读取。在患者层面,早期BMIPP数据显示异常时,BMIPP与铊数据的一致性为91%(95%可信区间,75至98),延迟期BMIPP数据为94%(95%可信区间,79至99)。在同一天进行研究的21例患者中,延迟期BMIPP与铊的一致性为95%,运动诱发缺血后平均6.2±1.4小时;在次日进行研究的11例患者中,一致性为91%,缺血后平均24.9±2.6小时(P=无显著性差异)。通过半定量视觉分析得出的静息BMIPP代谢缺损程度与运动诱发的铊灌注缺损程度相关(早期BMIPP,r=0.6,P<0.001;延迟期BMIPP,r=0.5,P=0.005)。
BMIPP代谢成像可识别近期运动诱发心肌缺血的患者。这些发现支持了BMIPP成像能够成功显示应激诱发缺血事件的代谢印记(也称为缺血记忆)这一概念。