Anna Fashandi

Isolated Hemorrhagic Pericardial Effusion after Foreign Body Ingestion

Foreign body ingestion is one of the many potential causes of esophageal perforation. In this case report we describe a man who presented with chest pain and was found to have an isolated hemorrhagic pericardial effusion secondary to occult ingestion and pericardial migration of a metallic foreign body. Surgical management was successful, and the patient has recovered well.

Tamsulosin attenuates abdominal aortic aneurysm growth

Background Tamsulosin, an &agr;1A‐adrenergic receptor inhibitor, is prescribed to treat benign prostatic hyperplasia in men >60 years of age, the same demographic most susceptible to abdominal aortic aneurysm. The goal of this study was to investigate the effect of tamsulosin on abdominal aortic aneurysm pathogenesis. Methods Abdominal aortic aneurysms were induced in WT C57BL/6 male mice (n = 9‐18/group), using an established topical elastase abdominal aortic aneurysm model. Osmotic pumps were implanted in mice 5 days before operation to create the model, administering either low dose (0.125 &mgr;g/day tamsulosin), high dose (0.250&mgr;g/day tamsulosin), or vehicle treatments with and without topical application of elastase. Blood pressures were measured preoperatively and on postoperative days 0, 3, 7, and 14. On postoperative day 14, aortic diameter was measured before harvest. Sample aortas were prepared for histology and cytokine analysis. Results Measurements of systolic blood pressure did not differ between groups. Mice treated with the low dose of tamsulosin and with the high dose of tamsulosin showed decreased aortic diameter compared with vehicle‐treated control (93% ± 24 versus 94% ± 30 versus 132% ± 24, respectively; P = .0003, P = .0003). Cytokine analysis demonstrated downregulation of pro‐inflammatory cytokines in both treatment groups compared with the control (P < .05). Histology exhibited preservation of elastin in both low‐ and high‐dose tamsulosin‐treated groups (P = .0041 and P = .0018, respectively). Conclusion Tamsulosin attenuates abdominal aortic aneurysm formation with increased preservation of elastin and decreased production of pro‐inflammatory cytokines. Further studies are necessary to elucidate the mechanism by which tamsulosin attenuates abdominal aortic aneurysm pathogenesis.

A novel reproducible model of aortic aneurysm rupture

Introduction Given the unknown biologic antecedents before aortic aneurysm rupture, the purpose of this study was to establish a reproducible model of aortic aneurysm rupture. Methods We fed 7‐week‐old apolipoprotein E deficient mice a high‐fat diet for 4 weeks and osmotic infusion pumps containing Angiotensin II were implanted. Angiotensin II was delivered continuously for 4 weeks at either 1,000 ng/kg/min (n = 25) or 2,000 ng/kg/min (n = 29). A third group (n = 14) were given Angiotensin II at 2,000 ng/kg/min and 0.2% &bgr;‐aminopropionitrile dissolved in drinking water. Surviving mice were killed 28 days after pump placement, aortic diameters were measured, and molecular analyses were performed. Results Survival at 28 days was significantly different among groups with 80% survival in the 1,000 ng/kg/min group, 52% in the 2,000 ng/kg/min group, and only 14% in the Angiotensin II/&bgr;‐aminopropionitrile group (P = .0001). Concordantly, rupture rates were statistically different among groups (8% versus 38% versus 79%, P < .0001). Rates of abdominal aortic aneurysm were 48%, 55%, and 93%, respectively, with statistically higher rates in the Angiotensin II/&bgr;‐aminopropionitrile group compared with both the 1,000 ng and 2,000 ng Angiotensin II groups (P = .006 and P = .0165, respectively). Rates of thoracic aortic aneurysm formation were 12%, 52%, and 79% in the 3 groups with a statistically higher rate in the Angiotensin II/&bgr;‐aminopropionitrile group compared with 1,000 ng group (P < .0001). Conclusions A reproducible model of aortic aneurysm rupture was developed with a high incidence of abdominal and thoracic aortic aneurysm. This model should enable further studies investigating the pathogenesis of aortic rupture, as well as allow for targeted strategies to prevent human aortic aneurysm rupture.