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Aortic dissection is an uncommon diagnosis that typically presents with acute onset of severe pain. It rarely presents with minimal to no symptoms, which carries a higher mortality risk given the delay in diagnosis. An adequate interpretation of risk factors, clinical findings and auxiliary tests constitutes a greater value for clinicians to detect this life-threatening condition. This report describes a case of type A aortic dissection in an asymptomatic patient presenting with an abnormal electrocardiogram (ECG).

Cryptogenic stroke represents 40% of ischemic strokes. Intra-cardiac source is a main concern in this group, but the need of routine trans-esophageal echocardiogram (TEE) in the work-up remains unclear. Retrospective review from February 2015 to February 2019 of all the TEEs done at our institution

Aims The origin of post-injury neointimal cells is still a matter of debate. This study aims to determine the anatomic source of neointimal cells in one of the most important animal models for the study of vascular stenosis in response to injury, the rat balloon injury model. Methods and results Chimeric rats were generated by rescuing lethally irradiated animals with green fluorescent protein (GFP)+ bone marrow (BM) cells from transgenic rats. Neointimal formation was induced in the right iliac artery of these animals using a balloon angioplasty catheter. Injured and non-injured contra-lateral arteries were harvested at 7, 14, and 30 days post-surgery. BM-derived monocytes/macrophages (CD68+ GFP+) were abundant in the media and adventitia of injured vessels harvested at 7 days as determined by immunofluorescence and confocal microscopy. The number of GFP+ cells declined in the vascular wall with time. Post-injury neointimal cells were mostly GFP−/smooth muscle actin (SMA)+, which indicated that those cells originated in the recipient. Only a few neointimal cells seemed to come from circulating progenitors (GFP+ SMA+, 2.34% ± 1.61). The vascular origin of cells in the neointima was further confirmed by transplanting injured GFP arteries into wild-type recipients. In these grafts, 94.23 ± 0.44% of medial and 92.95 ± 19.34% of neointimal cells were GFP+ SMA+. Finally, we tested the capacity of vascular smooth muscle cells (VSMC) to migrate through the vascular wall using a novel in vivo assay. As expected, VSMC migrated and populated the neointima only in response to injury. Conclusion Our results suggest that neointimal cells in the rat balloon injury model mostly derive from pre-existing vascular cells and that only a small population of those cells come from BM-derived progenitors.

Background. Almost half of all transplanted vascularized organ grafts will be lost to transplant arteriosclerosis sometime posttransplantation. Organ shortage for primary transplants and retransplants has led to donor-pool expansion to include elderly donors, knowing that aging per se promotes arteriosclerosis. The current understanding that donor age negatively affects organ and/or patient survival outcome is undermined by variables such as the use of immunosuppressive drugs, their toxicity to the graft, degree of donor-recipient histocompatibility, and the resulting chronic rejection. The purpose of this study was to determine whether the donor's age or recipient's age matters the most in transplant arteriosclerosis in the absence of such variables. Methods. A syngeneic combination was used where young (2-month-old) and old (22-month-old) donor aortas were injured to initiate neointimal thickening, then transplanted into age-mismatched recipients for 14, 60, and 90 days and then assessed for neointimal thickening. Base level injury response due ischemia and surgery was evaluated in agematched and noninjured aortic grafts, respectively. Results. Young aortas invariably developed thicker neointima when transplanted into old recipients than when transplanted into young ones. Correspondingly, old aortas transplanted in young recipients consistently developed less neointimal thickening than when transplanted into old recipients. Conclusions. Our findings strongly suggest that the severity of age-related neointima formation is primarily determined by the recipient's age rather than the donor's age. Therefore, in addition to focusing on donor-specific tolerance induction, strategies aiming at increasing the lifespan of vascularized organ grafts also have to take into consideration the recipient's aging milieu.