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T Freestone

Publications and source records attributed to T Freestone.

5 recordsLinked to original sources

Reinforcing the conventional sternal closure.

Sternal infection is a devastating complication of heart surgery. It may be the result of unstable osteosynthesis, caused by the sternal wires cutting into the cortical layers, which results in tension loss and gap formation. We describe a technique that prevents the cerclages from cutting into the sternal plates and covers the sternum with a well-capillarized barrier of major pectoralis muscle.

Aged↗

Extraperitoneal laparoscopic aortic control with endovascular visualization of a stent-graft combination.

OBJECTIVES: to demonstrate the feasibility of minimally invasive approaches to the aorta using retroperitoneal laparoscopy and to clamp the aorta to give views for perfemoral aortic angioscopy. METHODS: using retroperitoneal laparoscopy facilitated by balloon dissection the authors developed a new approach to the infrarenal abdominal aorta, in six pigs, to allow control of aortic blood flow. Aortic stent-grafts were then deployed via femoral arteriotomy, and after flushing the blood from the aorta, the stent-grafts were visualized by angioscopy. RESULTS: accurate positioning and patency of the stent-grafts was ascertained by direct vision angioscopy in all cases. CONCLUSIONS: this series shows that extraperitoneal laparoscopic aortic dissection is feasible and direct endovascular visualization of the aortic lumen can be performed. This may find a role as an adjunct to endovascular techniques such as endovascular stent-graft placement, by aortic angioscopy following minimally-invasive aortic clamping.

Animals↗

Influence of hypercholesterolemia and adventitial inflammation on the development of aortic aneurysm in rabbits.

Abdominal aortic aneurysms are characterized by intimal atherosclerosis, disruption and attenuation of the elastic media, and a variable adventitial inflammatory infiltrate. We have developed an animal model of this disorder to evaluate the contribution of hypercholesterolemia, medial injury, and adventitial inflammation to aneurysmal dilatation. To accomplish this, we used periaortic application of calcium chloride, which induced both medial injury with calcification and endothelial injury. Ultrasonography was used to demonstrate the dilatation and thickening of the aortic wall. Over the first 3 weeks after periaortic application of 0.25 mol/L CaCl2, the external aortic diameter increased from 3.5 +/- 0.5 to 4.2 +/- 0.8 mm, but the ID remained unchanged. This apparent wall thickening was accompanied by vascular remodeling, and biochemical changes included approximately 50% reduction in tissue hydroxyproline concentration and increased activity of gelatinases (matrix metalloproteinase [MMP]-2 and MMP-9). Independently, cholesterol feeding to induce hypercholesterolemia or the concomitant periaortic application of thioglycollate had little effect on the histological, biochemical, or diameter changes. Together, hypercholesterolemia and thioglycollate were associated with rapid aortic dilatation in CaCl2, treated animals but not controls: after 3 weeks, the ID and OD had doubled, the OD increasing from 3.5 +/- 0.4 to 7.1 +/- 0.4 mm, P = .005. The remarkable feature that accompanied this dilatation was the infiltration of cells, mostly foamy macrophages, into the adventitia, with a further reduction in hydroxyproline concentration. Adventitial inflammation may provide the critical stimulus to dilatation of an aorta with preexisting intimal and medial injury.

Animals↗

Inflammation and matrix metalloproteinases in the enlarging abdominal aortic aneurysm.

The risk of rupture of an abdominal aortic aneurysm increases with aortic diameter. To obtain insight into the pathological processes associated with the vascular remodeling that accompanies aortic dilatation, we compared the histological features and the activity of matrix metalloproteinases (MMPs) in biopsies from 21 small (4.0 to 5.5 cm in diameter) and 45 larger abdominal aortic aneurysms. The histological feature most clearly associated with enlarging aneurysm diameter was a higher density of inflammatory cells in the adventitia, P = .018. This inflammation was nonspecific, principally macrophages and B lymphocytes. Fibrosis of the adventitia provided compensatory thickening of the aortic wall as the aneurysm diameter increased. A combination of zymography and immunoblotting identified gelatinase A (MMP-2) as the principal metallogelatinase in small aneurysms, whereas zymography indicated an increasing activity of gelatinase B (MMP-9) in large aneurysms. Homogenates prepared from both small and large aneurysms had similar total activity against gelatin or type IV collagen. However, the concentration of gelatinase A, determined by immunoassay, was highest for small aneurysms: median concentrations, 385, 244, and 166 ng/mg protein for small aneurysms, large aneurysms, and atherosclerotic aorta, respectively. Immunolocalization studies indicated that gelatinase A was concentrated along fibrous tissue of both the acellular media and the atherosclerotic plaque. The recruitment of inflammatory cells into the adventitia, with subsequent elaboration of metalloproteinases, including gelatinase B, may contribute to the rapid growth and rupture of larger aneurysms.

Amino Acid Sequence↗