Pathological Evidence of Native Aortic Valve Injury After Impella Support
Pathological Evidence of Native Aortic Valve Injury After Impella Support
复制标题
叶轮支撑后原生主动脉瓣损伤的病理证据
DOI：
10.1161/circheartfailure.120.007571
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Yamaguchi Osamu
中科院分区：
文献类型：
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作者：
Higashi Haruhiko;Nishimura Takashi;Aono Jun;Sakaue Tomohisa;Kurata Mie;Izutani Hironori;Yamaguchi Osamu
在手术过程中直接观察到的自体主动脉瓣在临床上看起来是健康的。然而，术中经食管超声心动图在Impella取出后立即显示轻度主动脉瓣关闭不全，即使在体外循环期间血压非常低（数据补充中的电影III）。我们在LVAD植入术中增加了使用生物瓣膜的主动脉瓣置换术，因为我们预计患者的主动脉瓣关闭不全在LVAD植入术后会恶化。令人惊讶的是，切除的自体主动脉瓣的肉眼观察结果显示，瓣膜的某些区域呈红色，尤其是在非冠状瓣尖（图1）。非冠状动脉瓣尖的病理学检查（图2A）显示内皮剥脱和红细胞外渗至间质空间，无新生血管形成（图2B和2C），表明主动脉瓣损伤是由Impella的机械损伤引起的，而不是炎症过程。然而，在右冠状动脉尖中观察到CD 34阳性细胞（成纤维细胞）、CD 68阳性细胞（巨噬细胞）和α-SMA（平滑肌肌动蛋白）阳性细胞（肌成纤维细胞）（图3A至3E）。在内皮细胞裸露的瓣膜表面观察到大量成纤维细胞和肌成纤维细胞（图3C和3E）。此外，在左冠状动脉瓣尖表面检测到微血栓（图4A和4 B）。这些发现表明，机械损伤和通过炎症和间质细胞的组织修复过程在每个瓣膜中都有进展，这反过来可能加速了瓣膜的损伤。
The native aortic valve, which was observed directly during the operation, appeared clinically healthy. However, intraoperative transesophageal echocardiography immediately after removal of Impella revealed mild aortic insufficiency, even with very low blood pressure during extracorporeal circulation (Movie III in the Data Supplement). We added the procedure of aortic valve replacement using a bioprosthetic valve to the LVAD implantation because we anticipated the patient’s aortic insufficiency to deteriorate after LVAD implantation. Surprisingly, macroscopic findings of the explanted native aortic valve showed that some areas of the valve were reddish, especially in the noncoronary cusp (Figure 1). Pathological examinations of the noncoronary cusp (Figure 2A) showed endothelial denudation and red blood cell extravasation into the interstitial space without neovascularization (Figure 2B and 2C), suggesting that the damage to the aortic valve was caused by mechanical injury from Impella rather than the inflammatory process. However, CD34-positive cells (fibroblasts), CD68-positive cells (macrophages), and α-SMA (smooth muscle actin)–positive cells (myofibroblasts) were seen in the right coronary cusp (Figure 3A through 3E). A large number of fibroblasts and myofibroblasts were observed at the valve surface where endothelial cells were denuded (Figure 3C and 3E). Furthermore, microthrombi were detected on the surface of the left coronary cusp (Figure 4A and 4B). These findings implied that mechanical injury and the tissue repair process through the inflammatory and interstitial cells had been progressing in each of the valves, which in turn might have accelerated the