Rochitte C E, Lima J A, Bluemke D A, Reeder S B, McVeigh E R, Furuta T, Becker L C, Melin J A
Department of Medicine, Johns Hopkins University, Baltimore, MD, USA.
Circulation. 1998 Sep 8;98(10):1006-14. doi: 10.1161/01.cir.98.10.1006.
Microvascular obstruction within an area of myocardial infarction indicates worse functional recovery and a higher risk of postinfarction complications. After prolonged coronary occlusion, contrast-enhanced MRI identifies myocardial infarction as a hyperenhanced region containing a hypoenhanced core. Because the time course of microvascular obstruction after infarction/reperfusion is unknown, we examined whether microvascular obstruction reaches its full extent shortly after reperfusion or shows significant progression over the following 2 days.
Seven dogs underwent 90-minute balloon occlusion of the left anterior descending coronary artery (LAD) followed by reflow. Gadolinium-DTPA-enhanced MRI performed at 2, 6, and 48 hours after reperfusion was compared with radioactive microsphere blood flow (MBF) measurements and myocardial staining to define microvascular obstruction (thioflavin S) and infarct size (triphenyltetrazolium chloride, TTC). The MRI hypoenhanced region increased 3-fold during 48 hours after reperfusion (3.2+/-1.8%, 6.7+/-4.4%, and 9.9+/-3.2% of left ventricular mass at 2, 6, and 48 hours, respectively, P<0.03) and correlated well with microvascular obstruction (MBF <50% of remote region, r=0.99 and thioflavin S, r=0.93). MRI hyperenhancement also increased (21.7+/-4.0%, 24.3+/-4.6%, and 28.8+/-5.1% at 2, 6, and 48 hours, P<0.006) and correlated well with infarct size by TTC (r=0.92). The microvascular obstruction/infarct size ratio increased from 13.0+/-4.8% to 22.6+/-8.9% and to 30.4+/-4.2% over 48 hours (P=0.024).
The extent of microvascular obstruction and the infarct size increase significantly over the first 48 hours after myocardial infarction. These results are consistent with progressive microvascular and myocardial injury well beyond coronary occlusion and reflow.
心肌梗死区域内的微血管阻塞表明功能恢复较差且梗死后并发症风险较高。在冠状动脉长时间闭塞后,对比增强磁共振成像(MRI)将心肌梗死识别为包含低增强核心的高增强区域。由于梗死/再灌注后微血管阻塞的时间进程尚不清楚,我们研究了微血管阻塞在再灌注后不久是否达到其最大程度,或者在接下来的2天内是否有显著进展。
7只犬接受了左前降支冠状动脉(LAD)90分钟的球囊闭塞,随后再灌注。将再灌注后2小时、6小时和48小时进行的钆喷酸葡胺增强MRI与放射性微球血流(MBF)测量及心肌染色进行比较,以确定微血管阻塞(硫黄素S)和梗死面积(氯化三苯基四氮唑,TTC)。MRI低增强区域在再灌注后48小时内增加了3倍(分别为左心室质量的3.2±1.8%、6.7±4.4%和 在2小时、6小时和48小时时分别为9.9±3.2%,P<0.03),并且与微血管阻塞(MBF<远隔区域的50%,r=0.99;硫黄素S,r=0.93)相关性良好。MRI高增强也增加(在2小时、6小时和48小时时分别为21.7±4.0%、24.3±4.6%和28.8±5.1%,P<0.006),并且与TTC测定的梗死面积相关性良好(r=0.92)。微血管阻塞/梗死面积比值在48小时内从13.0±4.8%增加到22.6±8.9%,再增加到30.4±4.2%(P=0.024)。
心肌梗死后最初48小时内,微血管阻塞程度和梗死面积显著增加。这些结果与冠状动脉闭塞和再灌注后微血管和心肌的进行性损伤一致。