RESUMO
BACKGROUND: Post-coarctoplasty aortic pseudoaneurysms constitute a lethal problem occurring in up to 38% of patients with a history of aortic coarctation surgical repair. Such pseudoaneurysms are prone to rupture if managed conservatively and high mortality and morbidity if treated with open surgery. Therefore, the endovascular approach has been proposed for their management. CASE REPORT: We describe a patient with a post-coarctoplasty aortic pseudoaneurysm complicated by an aortobronchial fistula. The case was treated via the endovascular approach (thoracic endovascular aortic repair and endovascular coarctoplasty) with an atrial septal defect occluder device. CONCLUSIONS: Endovascular repair is a feasible, safe, and promising treatment for thoracic aortic pseudoaneurysms secondary to coarctation repair.
RESUMO
BACKGROUND: Mounting evidence indicates an association between endothelial dysfunction and the coronary slow flow phenomenon (CSFP). In the present study, we aimed to evaluate the possible role of endothelial nitric oxide synthase (eNOS) 894G/T and interleukin-1ß (IL-1ß) 315C/T polymorphisms as possible risk factors for CSFP. METHODS: This prospective study enrolled patients with CSFP and individuals with normal coronary arteries. Genotypes were assessed using regular polymerase chain reaction and direct Sanger-sequencing techniques. RESULTS: The study population consisted of 267 individuals: 180 patients with CSFP (49 women [27.2%]) at a median age of 55 (48-62) years and 87 controls with normal coronary arteries (56 women [64.4%]) at a median age of 47 (41-58) years. The allelic distribution of eNOS 894G/T was significantly associated with CSFP (odds ratio [OR], 1.58; 95% confidence interval (CI), 1.04-2.42; P = 0.03). This polymorphism increased the risk of CSFP under the dominant model (OR 1.73; 95% CI I.02-2.95; P = 0.04). However, the allelic frequencies (1.05; 95% CI 0.68-1.59; P = 0.83) and genotypic frequencies (0.88; 95% CI 0.52-1.49; P = 0.63) of the IL-1ß 315C/T polymorphism were not associated with the incidence of CSFP in the Iranian population. CONCLUSIONS: The CSFP and control groups were statistically different regarding the eNOS 894G/T polymorphism. Our findings also demonstrated that the IL-1ß 315C/T polymorphism was not a risk factor for CSFP.