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1.
Ann Vasc Surg ; 85: 156-166, 2022 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-35304297

RESUMO

BACKGROUND: Critical limb ischemia (CLI) is considered the most severe pattern of peripheral artery disease. CLI is associated with high rates of morbidity and mortality with high risk of limb amputation. In the absence of appropriate autologous grafts, unsuitability of prosthetic bypasses, and endovascular methods, fresh cold-stored venous allografts is an option. Endovascular interventional methods are essential methods for maintaining primary and secondary patency. METHODS: A single-centre retrospective analysis of 82 surgical revascularizations using allogeneic vascular grafts and rescue endovascular techniques restoring and maintaining the patency of these allogeneic revascularizations in the period between July 2005 and July 2021. RESULTS: We have performed 82 allogeneic revascularizations in 75 patients (52 reconstructions in men/63.4%/, 30 reconstructions in women/36.6%/). The median age of patients was 68 years (49 min, 87 max). We subsequently had to intervene a total of 26 bypasses. We intervened in 30 acute occluded allogeneic bypass grafts and 9 failing stenotic bypass grafts. We performed 52 angiographies. The success rate of rescue endovascular procedures in primary allogeneic reconstruction with distal anastomosis to the popliteal artery is statistically significant (P < 0.02) compared to procedures with distal anastomosis to the tibial and pedal bed. The cumulative patency (primary at time) of allogeneic reconstructions in our group was 89% after 1 month, 51.9% after 12 months, 24.2% after 3 years, 9.8% after 5 years. Limb salvage was 72.6% in 1 year, 53% in 3 years, 36.5% in 5 years, respectively. CONCLUSIONS: Cold-stored venous allografts may be used for performing below-the-knee revascularization for CLI with acceptable results, despite the poor long-term patency. Rescue endovascular techniques are an essential method for restoring or maintaining the patency of these reconstructions. These techniques have a high success rate and no other alternative.


Assuntos
Procedimentos Endovasculares , Doença Arterial Periférica , Idoso , Aloenxertos/cirurgia , Procedimentos Endovasculares/efeitos adversos , Feminino , Humanos , Isquemia/diagnóstico por imagem , Isquemia/cirurgia , Salvamento de Membro , Masculino , Doença Arterial Periférica/diagnóstico por imagem , Doença Arterial Periférica/cirurgia , Estudos Retrospectivos , Resultado do Tratamento , Grau de Desobstrução Vascular
2.
Int J Angiol ; 18(2): 99-102, 2009.
Artigo em Inglês | MEDLINE | ID: mdl-22477503

RESUMO

BACKGROUND: Approximately 10% of patients who undergo surgery for aortic valve disease (stenosis or regurgitation) suffer from ascending aortic dilation (AAD). A possible genetic etiology of AAD associated with aortic valve disease has been repeatedly mentioned in the literature, but a specific responsible gene mutation has not been described. METHODS: In the present study, two groups of patients were compared, all of whom underwent surgery for aortic valve disease. Group A was a cohort of 27 patients who suffered from aortic valve disease associated with AAD. Group B was a cohort of 29 patients with structural aortic valve disease, but without concomitant AAD (control group). Genomic DNA was extracted from the white blood cells of peripheral blood samples and was amplified using primers specific for chosen exons of the fibrillin-1 gene, including their intron/exon boundaries. Exons 26 and 27 were selected for analysis. RESULTS: Analysis of the intronic part situated close to exon 27 showed insertion of cytosine between nucleotide 37 682 and 37 683 of query sequence. This insertions was classified as IVS 37 682 and 37 683insC. This mutation was found in all 27 patients from group A (patients with structural aortic valve disease accompanied by significant AAD). The abovementioned mutation was not found in any of the 29 patients from group B. CONCLUSIONS: This finding has potential implications for risk stratification and therapeutic targeting not only for patients with existing disease, but also for the general population. Future studies are needed to determine the clinical utility of the finding; however, the present hypothesis needs to be verified by further molecular studies.

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