Since its introduction in Japan in 1980, the extracorporeal left ventricular assist device has been used as a bridge to the recovery of cardiac function or to heart transplantation by many institutions. In this case report, we describe a 23-year-old female with peripartum cardiomyopathy. She had a persistently low cardiac index despite intensive care with intravenous inotropes, intra-aortic balloon pumping and extracorporeal membrane oxygenation; thus, we implanted an extracorporeal left ventricular assist device. Thereafter, her cardiac function gradually improved; the device was removed 2 months after the implantation. She currently has good heart function.
Decellularization of non-autologous biological implants reduces the immune response against foreign tissue. Striving for in vivo repopulation of aortic prostheses with autologous cells, thereby improving the graft biocompatibility, we examined surface coating with laminin in a standardized rat implantation model. Detergent-decellularized aortic grafts from donor rats (n = 37) were coated with laminin and systemically implanted into Wistar rats. Uncoated implants served as controls. Implant re-colonization and remodeling were examined by scanning electron microscopy (n = 10), histology and immunohistology (n = 18). Laminin coating persisted over eight weeks. Two weeks after implantation, no relevant neoendothelium formation was observed, whereas it was covering the whole grafts after eight weeks, with a significant acceleration in the laminin group (p = 0.0048). Remarkably, the intima-to-media ratio, indicating adverse hyperplasia, was significantly diminished in the laminin group (p = 0.0149). No intergroup difference was detected in terms of medial recellularization (p = 0.2577). Alpha-smooth muscle actin-positive cells originating from the adventitial surface invaded the media in both groups to a similar extent. The amount of calcifying hydroxyapatite deposition in the intima and the media did not differ between the groups. Inflammatory cell markers (CD3 and CD68) proved negative in coated as well as uncoated decellularized implants. The coating of decellularized aortic implants with bioactive laminin caused an acceleration of the autologous recellularization and a reduction of the intima hyperplasia. Thereby, laminin coating seems to be a promising strategy to enhance the biocompatibility of tissue-engineered vascular implants.
An emergency thoracic endovascular aortic repair (TEVAR) with zone 2 landing without revascularization of the left subclavian artery was performed due to the impending rupture of a distal arch aneurysm in an old patient presenting hemoptysis. Two months later, the patient had recurrent massive hemoptyses and continued after additional zone 0 TEVAR. The lung parenchyma was considered to be the bleeding source and transcatheter pulmonary artery embolization was performed, and the episodes of massive hemoptysis appeared to have ceased. However, the patient died of sudden recurrent massive hemoptysis 40 days later. Inflammation and/or infection of the lung parenchyma adjunct to the aortic aneurysm could be cause of fatal hemoptysis, and aggressive therapy such as lung resection should be considered in such patients.
Optimized biocompatibility is crucial for the durability of cardiovascular implants. Previously, a combined coating with fibronectin (FN) and stromal cell-derived factor 1α (SDF1α) has been shown to accelerate the in vivo cellularization of synthetic vascular grafts and to reduce the calcification of biological pulmonary root grafts. In this study, we evaluate the effect of side-specific luminal SDF1α coating and adventitial FN coating on the in vivo cellularization and degeneration of decellularized rat aortic implants. Aortic arch vascular donor grafts were detergent-decellularized. The luminal graft surface was coated with SDF1α, while the adventitial surface was coated with FN. SDF1α-coated and uncoated grafts were infrarenally implanted (n = 20) in rats and followed up for up to eight weeks. Cellular intima population was accelerated by luminal SDF1α coating at two weeks (92.4 ± 2.95% versus 61.1 ± 6.51% in controls, p < 0.001). SDF1α coating inhibited neo-intimal hyperplasia, resulting in a significantly decreased intima-to-media ratio after eight weeks (0.62 ± 0.15 versus 1.35 ± 0.26 in controls, p < 0.05). Furthermore, at eight weeks, media calcification was significantly decreased in the SDF1α group as compared to the control group (area of calcification in proximal arch region 1092 ± 517 μm2 versus 11 814 ± 1883 μm2, p < 0.01). Luminal coating with SDF1α promotes early autologous intima recellularization in vivo and attenuates neo-intima hyperplasia as well as calcification of decellularized vascular grafts.
A Kommerell’s diverticulum is a rare congenital aortic arch anomaly associated with a high rate of aortic rupture or dissection. Therefore, surgical or endovascular repair should be considered early. A 64-year-old man was incidentally found to have an aortic arch anomaly, Kommerell’s diverticulum, with a right aberrant subclavian artery and distal arch aneurysm. Hybrid total arch replacement with bilateral extra-anatomical axillary artery bypass and frozen elephant trunk technique was performed. This particular surgical approach would be a treatment option for any type of Kommerell’s diverticulum.
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