The early results show that emergent endovascular treatment of hemodynamically stable and unstable patients is associated with a limited mortality of 18% once a standardized protocol is established. There is an increased recognition of emerging complications with an endovascular approach, and a synchrony of disciplines must be developed to initiate a successful program for endovascular treatment of r-AAAs.

Mortality for females undergoing elective EVAR is significantly greater than for males. It is also more hazardous. Colon ischemia, native arterial rupture, and type 1 endoleaks are more frequent. Elective endovascular aneurysm repair benefits men more than women.

ACS is a potential complication of endovascular repair of r-AAA and negatively affects survival. Factors associated with the development of ACS include (1) use of an aortic occlusion balloon, (2) coagulopathy, (3) massive transfusion requirements, and (4) conversion of bifurcated stent grafts into aortouni-iliac devices. We recommend that, after endovascular repair of r-AAA, these patients undergo vigilant monitoring for the development of ACS.

Our long-term EVAR experience indicates that 18% of patients require additional secondary procedures, and most of these patients can be managed by endovascular means with an acceptable overall mortality of 2.9%. Most type I and II endoleaks can be successfully treated by transluminal embolization, and most patients with delayed aneurysm rupture after EVAR can be successfully managed by endovascular or open surgical repair.

Infrainguinal arterial reconstruction can be performed safely with comparable results in women and men. Although women may present older and more often for limb salvage, outcomes do not appear to be adversely affected.

For r-AAA, EVAR reduces the 30-day mortality and improves long-term survival up to 5 years. However, whereas open survivors require few graft-related interventions, up to 23% of EVAR patients will require reintervention for endoleaks or graft migration. Close follow-up of all EVAR survivors is mandatory.

Bilateral hypogastric artery interruptions can be accomplished with limited morbidity. When hypogastric artery interruption is needed during endovascular aneurysm repair, certain principles help minimize pelvic ischemia. These include hypogastric artery interruption at its origin to preserve the pelvic collateral vessels, staging bilateral hypogastric artery interruptions when possible, preserving collateral branches from the femoral and external iliac arteries, and providing adequate heparinization of the patient during these procedures.

Objective Lipid-laden macrophages or foam cells are characterized by massive cytosolic lipid droplet (LD) deposition containing mostly cholesterol ester (CE) derived from the lipoproteins cleared from the arterial wall. Cholesterol efflux from foam cells is considered to be atheroprotective. Since cholesterol is effluxed as free cholesterol (FC), CE accumulation in LDs may limit FC efflux. Our objective was to identify proteins that regulate cholesterol trafficking through LDs. Approach and results In a proteomic analysis of the LD fraction of RAW 264.7 macrophages we identified an evolutionarily conserved protein with a canonical GXSXG lipase catalytic motif and a predicted α/β-hydrolase fold, the RIKEN cDNA 1110057K04 gene, which we named lipid droplet-associated hydrolase (LDAH). LDAH association to LDs was confirmed by immunoblotting and immunocytochemistry. LDAH was labeled with a probe specific for active serine hydrolases. LDAH showed relatively weak in vitro CE hydrolase activity. However, cholesterol measurements in intact cells supported a significant role of LDAH in CE homeostasis, since LDAH upregulation and downregulation decreased and increased, respectively, intracellular cholesterol and CE in HEK293 cells and RAW 264.7 macrophages. Mutation of the putative nucleophilic serine impaired active hydrolase probe binding, in vitro CE hydrolase activity, and the cholesterol lowering effect in cells, while this mutant still localized to the LD. LDAH upregulation increased CE hydrolysis and cholesterol efflux from macrophages and, interestingly, LDAH is highly expressed in macrophage-rich areas within mouse and human atherosclerotic lesions. Conclusions The data identify a candidate target to promote reverse cholesterol transport from atherosclerotic lesions.