Differentiation of acute and four-week old myocardial infarct with Gd(ABE-DTTA)-enhanced CMR.
Differentiation of acute and four-week old myocardial infarct with Gd(ABE-DTTA)-enhanced CMR.
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DOI：
10.1186/1532-429x-12-22
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发表时间：
2010-04-07
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影响因子：
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通讯作者：
Elgavish GA
中科院分区：
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作者：
Kirschner R;Toth L;Varga-Szemes A;Simor T;Suranyi P;Kiss P;Ruzsics B;Toth A;Baker R;Brott BC;Litovsky S;Elgavish A;Elgavish GA
标准的细胞外心血管磁共振(CMR)造影剂(CA)不能区分急性和陈旧性心肌梗死(MI)。本研究的目的是开发一种新的低分子质量造影剂的心肌晚增强(LE)CMR鉴别急性和陈旧性心肌梗死的方法。犬(n=6)采用闭胸式再灌流双心肌梗死模型。用血管成形术球囊闭塞左前降支(LAD)180min，4周后闭塞左回旋支(Lcx)180min，造成心肌梗死。在第二次心肌梗死后第3天和第4天分别用Gd(DTPA)(标准细胞外造影剂)和Gd(ABE-DTTA)(新型低分子质量造影剂)进行LE成像。三苯基四氮唑氯化铵(TTC)组织形态计量学证实了梗塞的存在和位置。苏木精-伊红染色和Masson三色染色提供了梗死灶的组织学评价。Gd(ABE-DTTA)或Gd(DTPA)显示急性脑梗塞，而Gd(DTPA)显示4周龄脑梗塞，而Gd(ABE-DTTA)不显示。Gd(ABE-DTTA)对急性脑梗塞和4周龄脑梗塞的平均信号强度增强(SIE)分别为366±166%和24±59%(P<0.05)。后者与正常心肌的信号强度无显著差异(P=NS)。Gd(DTPA)在急性脑梗塞(431±124%)和四周龄脑梗塞(400±124%，P=NS)引起的信号增强相似，与Gd(ABE-DTTA)诱发的急性脑梗塞SIE无统计学差异。氯化三苯基四氮唑(TTC)法证实了两种脑梗塞的存在和定位。组织学检查显示，4天龄脑梗塞大鼠出现凝固性坏死、炎症和多灶性钙化，而晚期亚急性脑梗塞则表现为肉芽组织和早期胶原沉积。通过分别给予标准细胞外造影剂Gd(DTPA)和新型低分子造影剂Gd(ABE-DTTA)的晚期增强CMR，可以在再灌流的双梗死犬模型中区分急性和晚期亚急性梗死区。
Standard extracellular cardiovascular magnetic resonance (CMR) contrast agents (CA) do not provide differentiation between acute and older myocardial infarcts (MI). The purpose of this study was to develop a method for differentiation between acute and older myocardial infarct using myocardial late-enhancement (LE) CMR by a new, low molecular weight contrast agent. Dogs (n = 6) were studied in a closed-chest, reperfused, double myocardial infarct model. Myocardial infarcts were generated by occluding the Left Anterior Descending (LAD) coronary artery with an angioplasty balloon for 180 min, and four weeks later occluding the Left Circumflex (LCx) coronary artery for 180 min. LE images were obtained on day 3 and day 4 after second myocardial infarct, using Gd(DTPA) (standard extracellular contrast agent) and Gd(ABE-DTTA) (new, low molecular weight contrast agent), respectively. Triphenyltetrazolium chloride (TTC) histomorphometry validated existence and location of infarcts. Hematoxylin-eosin and Masson's trichrome staining provided histologic evaluation of infarcts. Gd(ABE-DTTA) or Gd(DTPA) highlighted the acute infarct, whereas the four-week old infarct was visualized by Gd(DTPA), but not by Gd(ABE-DTTA). With Gd(ABE-DTTA), the mean ± SD signal intensity enhancement (SIE) was 366 ± 166% and 24 ± 59% in the acute infarct and the four-week old infarct, respectively (P < 0.05). The latter did not differ significantly from signal intensity in healthy myocardium (P = NS). Gd(DTPA) produced signal intensity enhancements which were similar in acute (431 ± 124%) and four-week old infarcts (400 ± 124%, P = NS), and not statistically different from the Gd(ABE-DTTA)-induced SIE in acute infarct. The existence and localization of both infarcts were confirmed by triphenyltetrazolium chloride (TTC). Histologic evaluation demonstrated coagulation necrosis, inflammation, and multiple foci of calcification in the four day old infarct, while the late subacute infarct showed granulation tissue and early collagen deposition. Late enhancement CMR with separate administrations of standard extracellular contrast agent, Gd(DTPA), and the new low molecular weight contrast agent, Gd(ABE-DTTA), differentiates between acute and late subacute infarct in a reperfused, double infarct, canine model.