Pathological mechanism for delayed hyperenhancement of chronic scarred myocardium in contrast agent enhanced magnetic resonance imaging.
Pathological mechanism for delayed hyperenhancement of chronic scarred myocardium in contrast agent enhanced magnetic resonance imaging.
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慢性瘢痕心肌造影剂增强磁共振成像迟发性超增强的病理机制
DOI：
10.1371/journal.pone.0096463
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Tian G
中科院分区：
文献类型：
--
作者：
Wang J;Xiang B;Lin HY;Liu H;Freed D;Arora RC;Tian G
目的 通过研究造影剂（CA）首过和延迟增强模式与组织病理学变化的关系，评估疤痕心肌延迟过度增强的可能机制。材料和方法 对 18 头猪进行为期 4 周的 1 或 2 条对角冠状动脉结扎以诱发慢性梗塞。然后取出心脏并在 Langendorff 装置中灌注。心脏首先经历了磷 31 MR 光谱分析。 I组（n = 9）和II组（n = 9）的心脏分别接受二亚乙基三胺五乙酸钆（0.05 mmol/kg）和钆基高分子药物（P792，15 µmol/kg）的推注。使用梯度回波序列获取第一遍 T2 * MRI。通过反转恢复序列获得延迟增强 T1 MRI。进行马森三色和抗血管性血友病因子（vWF）染色以表征梗塞。结果两种CA的洗入均导致疤痕心肌与正常心肌相似的T2*信号急剧下降。 4周龄疤痕组织中心肌血流量和微血管密度显着恢复。 Gd-DTPA 的稳态分布体积（ΔR1 弛豫率）在疤痕心肌中显着高于正常心肌，而 P792 的 ΔR1 弛豫率在疤痕心肌和正常心肌之间没有显着差异。疤痕心肌中细胞外体积与总水体积的比率显着大于正常心肌。伤痕累累的心肌含有大量残留的毛细血管和扩张的血管。组织学染色表明疤痕心肌中存在广泛离散的基质沉积和细胞结构的缺乏。结论 侧枝循环的形成和残余血管有效地将CA输送到疤痕心肌中。然而，没有异常渗透性过高的残余血管允许 Gd-DTPA 而不是 P792 渗透到血管外室。离散的胶原纤维网和细胞结构的丧失扩大了 Gd-DTPA 可进入的细胞外空间，导致延迟性超增强疤痕。
Objectives To evaluate possible mechanism for delayed hyperenhancement of scarred myocardium by investigating the relationship of contrast agent (CA) first pass and delayed enhancement patterns with histopathological changes. Materials and Methods Eighteen pigs underwent 4 weeks ligation of 1 or 2 diagonal coronary arteries to induce chronic infarction. The hearts were then removed and perfused in a Langendorff apparatus. The hearts firstly experienced phosphorus 31 MR spectroscopy. The hearts in group I (n = 9) and II (n = 9) then received the bolus injection of Gadolinium diethylenetriamine pentaacetic acid (0.05 mmol/kg) and gadolinium-based macromolecular agent (P792, 15 µmol/kg), respectively. First pass T2 * MRI was acquired using a gradient echo sequence. Delayed enhanced T1 MRI was acquired with an inversion recovery sequence. Masson's trichrome and anti- von Willebrand Factor (vWF) staining were performed for infarct characterization. Results Wash-in of both kinds of CA caused the sharp and dramatic T2 * signal decrease of scarred myocardium similar to that of normal myocardium. Myocardial blood flow and microvessel density were significantly recovered in 4-week-old scar tissue. Steady state distribution volume (ΔR1 relaxation rate) of Gd-DTPA was markedly higher in scarred myocardium than in normal myocardium, whereas ΔR1 relaxation rate of P792 did not differ significantly between scarred and normal myocardium. The ratio of extracellular volume to the total water volume was significantly greater in scarred myocardium than in normal myocardium. Scarred myocardium contained massive residual capillaries and dilated vessels. Histological stains indicated the extensively discrete matrix deposition and lack of cellular structure in scarred myocardium. Conclusions Collateral circulation formation and residual vessel effectively delivered CA into scarred myocardium. However, residual vessel without abnormal hyperpermeability allowed Gd-DTPA rather than P792 to penetrate into extravascular compartment. Discrete collagen fiber meshwork and loss of cellularity enlarged extracellular space accessible to Gd-DTPA, resulting in the delayed hyper-enhanced scar.
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影响因子：
3.3
作者：
JOHNSTON, DL;HOMMA, S;OKADA, RD
通讯作者：
OKADA, RD
影响因子：
24
作者：
Saeed, Maythern;Weber, Oliver;Higgins, Charles B.
通讯作者：
Higgins, Charles B.
影响因子：
3.7
作者：
Morales, C;González, GE;Gelpi, RJ
通讯作者：
Gelpi, RJ
DOI：
10.1016/s0735-1097(97)00245-3
发表时间：
1997-10-01
影响因子：
24
作者：
Schwitter, J;Saeed, M;Higgins, CB
通讯作者：
Higgins, CB
DOI：
10.1067/mlc.2000.105971
发表时间：
2000-04-01
期刊：
JOURNAL OF LABORATORY AND CLINICAL MEDICINE
影响因子：
--
作者：
Sun, Y;Zhang, JQ;Lamparter, S
通讯作者：
Lamparter, S