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Chronic rejection has several histological appearances, depending on the type of organ graft Common to all of them is transplant arteriosclerosis associated with an ongoing inflammatory response in the transplanted graft. To the contrary of classical atherosclerosis, in which the manifestations are mostly focal, proximal, and asymmetric, transplant arteriosclerosis is generalized, and the intimal thickening is concentric In this article, we describe an experimental animal model whereby transplant arteriosclerosis may be investigated in the inbred rat Aortic allografts were transplanted from DA (RTF) to major histocompatibility complex-incompatible WF (RTF) rats or, for control, to rats of the DA strain. Transplantation was followed by an acute inflammation episode in the aortic adventitia of the allograft, largely lacking in the syngeneic graft, with a prominence of lymphoid activation markers (Cd25) in the cells of the inflammatory infiltrate. The inflammation episode peaked at 2 months after transplantation, became attenuated, and was followed by a proliferative response of myocytes in the allograft media. An increase in the migration of myocytes to the subendothelial space (presumably through small breaks generated in the internal elastic lamina) was observed thereafter, and myocyte proliferation continued in the intima with some intermingled macrophages. Finally, necrosis and disappearance of myocytes and their replacement by fibrous tissue were observed in the media. These alterations are virtually identical with the vascular lesion of chronically rejecting parenchymal organ transplants in human subjects. We suggest that aortic allografts exchanged between histoincompatible rat strains may be used as an experimental model for transplant arteriosclerosis. (Arteriosclerosis and Thrombosis 1991;ll:671-680)

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Acute type A aortic dissection (ATAAD) is still one of the most challenging diseases that cardiac surgeons encounter. This review is based on the current literature and includes the results from the Nordic Consortium for Acute Type-A Aortic Dissection (NORCAAD) database. It covers different aspects of ATAAD and concentrates on the outcome of surgical repair. The diagnosis is occasionally delayed, and ATAAD is usually lethal if prompt repair is not performed. The dynamic nature of the disease, the variation in presentation and clinical course, and the urgency of treatment require significant attentiveness. Many surgical techniques and perfusion strategies of varying complexity have been described, ranging from simple interposition graft to total arch replacement with frozen elephant trunk and valve-sparing root reconstruction. Although more complex techniques may provide long-term benefit in selected patients, they require significant surgical expertise and experience. Short-term survival is first priority so an expedited operation that fits in with the surgeon's level of expertise is in most cases appropriate. ARTICLE HISTORY Definitions and classification systemsDissection of the aorta occurs when the aortic media is separated, usually by pulsatile flow that penetrates the intimal layer of the aortic wall [14] (Figure 1(b)). This allows blood to flow between the layers of the aortic wall, forcing the layers apart, creating a false lumen parallel to the native (i.e. true) aortic lumen (Figure 1(b)). Consequently, the false lumen can propagate in both directions from the tear of intima and affect most of its distal branches, including the coronary, cerebral, and mesenteric arteries [15]. Another-but less common-CONTACT Tomas Gudbjartsson

Objectives: To evaluate the effect of preoperative malperfusion on 30-day and late mortality and postoperative complications using data from the Nordic Consortium for Acute Type A Aortic Dissection (ATAAD) registry.Methods: We studied 1159 patients who underwent ATAAD surgery between January 2005 and December 2014 at 8 Nordic centers. Multivariable logistic and Cox regression analyses were performed to identify independent predictors of 30-day and late mortality.Results: Preoperative malperfusion was identified in 381 of 1159 patients (33%) who underwent ATAAD surgery. Thirty-day mortality was 28.9% in patients with preoperative malperfusion and 12.1% in those without. Independent predictors of 30-day mortality included any malperfusion (odds ratio, 2.76; 95% confidence interval [

Endotension after EVAR may cause subsequent aneurysm rupture. Endotension is evidently not associated with endoleak I to III provided that the endovascular graft is maintained in appropriate position and that free endovascular flow is observed. We propose to consider a nonoperative approach in the clinically asymptomatic patient with aneurysm enlargement after EVAR if endoleak is excluded by well-performed imaging techniques.

Cardiovascular diseases due to atherosclerosis are the leading cause of death globally. We aimed to investigate the potentially altered gene and pathway expression in advanced peripheral atherosclerotic plaques in comparison to healthy control arteries. Gene expression analysis was performed (Illumina HumanHT-12 version 3 Expression BeadChip) for 68 advanced atherosclerotic plaques (15 aortic, 29 carotid and 24 femoral plaques) and 28 controls (left internal thoracic artery (LITA)) from Tampere Vascular Study. Dysregulation of individual genes was compared to healthy controls and between plaques from different arterial beds and Ingenuity pathway analysis was conducted on genes with a fold change (FC) > ±1.5 and false discovery rate (FDR) < 0.05. 787 genes were significantly differentially expressed in atherosclerotic plaques. The most up-regulated genes were osteopontin and multiple MMPs, and the most down-regulated were cell death-inducing DFFA-like effector C and A (CIDEC, CIDEA) and apolipoprotein D (FC > 20). 156 pathways were differentially expressed in atherosclerotic plaques, mostly inflammation-related, especially related with leukocyte trafficking and signaling. In artery specific plaque analysis 50.4% of canonical pathways and 41.2% GO terms differentially expressed were in common for all three arterial beds. Our results confirm the inflammatory nature of advanced atherosclerosis and show novel pathway differences between different arterial beds.