Primary outcomes were 30-day and 5-year survival. Preoperative, intraoperative, and postoperative variables were assessed for their influence on outcomes using univariate and multivariate analysis, as appropriate. One- and 5-year survival were determined by Kaplan-Meier analysis.
Results: Four hundred eight patients (289 men; 70.8%) with a mean age of 72.4 +/- 8.3 years underwent open AAA repair. Sixty-seven patients (16.4%) underwent nonelective repair. The clamp site was infrarenal in 137 patients (33.6%), suprarenal in 97 patients (23.8%), and supraceliac 8-Bromo-cAMP supplier in 174 patients (42.6%). Thirty-day
survival was 95.6%. One- and 5-year survival were 90.0% +/- 1.5% and 65.1% +/- 3.0%, respectively. Seventy-nine patients (19.4%) had decreased renal function postoperatively compared to preoperatively, 71 patients (17.4%) sustained cardiac complications, and 45 patients (11.0%) sustained pulmonary complications. Patients with chronic obstructive learn more pulmonary disease (91.9% vs 97.2%; P = .004) and chronic renal insufficiency (92.0% vs 98.3%; P = .009) had decreased 30-day survival. Patients with chronic obstructive pulmonary disease (55.8% +/- 5.8% vs 67.3%
+/- 3.6%; P = .013), chronic renal insufficiency (51.2% +/- 5.2% vs 72.8% +/- 3.7%; P = .043), and cerebrovascular disease (46.8% +/- 7.4% vs 67.4% +/- 3.4%; P = .003) had decreased 5-year survival. Patients who had decreased postoperative renal function (41.0% +/- 7.4% vs 72.2% +/- 3.4%; P =.004), and patients who sustained pulmonary complications (45.6% +/- 8.8% vs 66.3% +/- 3.3%; P = .042) had worse 5-year survival.
Conclusions: Open AAA repair can be done with low morbidity and mortality in the era of endovascular aneurysm repair. Careful consideration should be given to preoperative optimization and perioperative care in patients with chronic obstructive pulmonary disease, chronic renal insufficiency, and cerebrovascular disease. Postoperative decrease in renal function and pulmonary complication portend
Dipeptidyl peptidase decreased 5-year survival; strategies to ameliorate these factors should be sought. (J Vase Surg 2011;54:1237-43.)”
“Pharmacological control of seizure activity following nerve agent exposure is critical in reducing neuropathology and improving survival in casualties. Three classes of drugs, anticholinergics, benzodiazepines and excitatory amino acid (EM) antagonists, have been shown to be effective at moderating nerve agent-induced seizures. However, little is known about which brain structures are involved in producing the anticonvulsant response. This study evaluated drugs from each class, injected directly into one of three specific brain structures, the perirhinal cortex, the entorhinal cortex, or the mediodorsal thalamus, for their ability to modulate seizures induced by the nerve agent soman. The drugs evaluated were the anticholinergic scopolamine, the benzodiazepine midazolam, and the EM antagonist MK-801.