A subset of 7 patients (14%) underwent placement of the EndoSure wireless pressure measurement system (CardioMEMS, Inc, Atlanta, Ga) in the false lumen adjacent to the primary tear for monitoring aneurysm sac/false selleck inhibitor lumen pulse pressure after thoracic endovascular aortic repair.

Results: Mean patient age was 57 +/- 12 years (range, 30-82 years); 14 patients (28%) were female. Mean aortic diameter was 6.2 +/- 1.4 cm. There were no in-hospital/30-day deaths, strokes, or permanent paraplegia/paresis. There were no complications related to compromise of downstream branch vessels arising from the false lumen. Two patients (3.9%) who had preexisting ascending

aortic dilation had retrograde acute type A aortic dissection; both were repaired successfully. Median postoperative length of stay was 4 days. Mean follow-up is 27.0 +/- 16.5 months (range, 2-60 months). Actuarial overall survival is 77.7% at 60 months with an actuarial aorta-specific survival of 98% over this same time period. Actuarial freedom from reintervention is 77.3% at 60 months. find more All patients with the EndoSure wireless

pressure measurement system exhibited a decrease in aneurysm sac/false lumen pulse pressure indicating a depressurized false lumen. The aneurysm sac/false lumen pulse pressure ratio decreased from 52% +/- 27% at the predischarge measurement to 14% +/- 5% at the latest follow-up reading (P = .029).

Conclusions: Thoracic endovascular aortic repair for chronic type B dissection with associated aneurysm is safe and effective at midterm follow-up. Aneurysm sac/false lumen pulse pressure measurements demonstrate a significant reduction in false lumen endotension, thus ruling out unless clinically significant persistent retrograde false lumen perfusion and provide proof of concept for a thoracic endovascular aortic repair-based approach. Longer-term follow-up is needed to determine the durability of thoracic endovascular aortic repair for

this aortic pathology. (J Thorac Cardiovasc Surg 2011;141:322-7)”
“Murine transgenic models of Alzheimer’s disease (Tg-AD) have been useful to analyze the contribution of beta-amyloid precursor protein (beta APP), A beta 42 peptide deposition, and the proinflammatory mechanisms that characterize Alzheimer-type neuropathology. In this report, we have studied the levels of beta APP, A beta 40 and A beta 42 peptide, as well as the innate immune and inflammatory response-regulator complement factor H in the brain and retina in four different Tg-AD models including Tg2576, PSAPP, 3xTg-AD, and 5xFAD. Aged, symptomatic 5xFAD mice showed the highest retinal abundance of A beta 42 peptides and the highest deficits in complement factor H. This may be a useful model to study the mechanisms of amyloid-mediated inflammatory degeneration.