Methods: Patients hospitalized with rAAA who underwent either OAR or EVAR, were derived from the Medicare inpatient dataset (1995-2004)

using ICD9 codes. We evaluated long-term survival after OAR and EVAR in the entire fee-for-service Medicare population, and then in patients matched by propensity score to create two similar cohorts for comparison with Kaplan-Meier analysis. Annual surgeon and hospital volumes of EVAR (elective and ruptured), OAR (elective and ruptured), and rAAA (EVAR and OAR) were divided into quintiles to determine if increasing volumes correlate with decreasing mortality. Predictors of survival were VX-809 nmr determined by Cox modeling.

Results: A total of 43,033 Medicare beneficiaries had rAAA repair: 41,969 had OAR and 1,064 had

EVAR. The proportions of patients with diabetes, hypertension, cardiovascular, cerebrovascular, renal disease, hyperlipidemia, and cancer were statistically S63845 higher in the EVAR than in the OAR group, whereas lower extremity vascular disease was higher in the OAR group. The initial evaluation of EVAR vs OAF, prior to propensity matching, showed no statistical advantage in EVAR-survival after 90 days. The survival analysis of patients matched by propensity score showed a benefit of EVAR over OAR that persisted throughout the 4 years of follow-up (P = .0042). Perioperative and long-term survival after rAAA repair correlated with increasing annual surgeon and hospital volume in OAR and EVAR and also with rAAA experience. EVAR repair had a protective effect (HR = 0.8.57, P = .0061) on long-term

survival controlling for comorbidities, demographics, and hospital and surgeon volume.

Conclusion:When AZD4547 cell line EVAR and OAR patients are compared using a reliable statistical technique such as propensity analysis, the perioperative survival advantage of rAAA repaired endovascularly is maintained over the long term. Institutional experience with rAAA is critical for survival after either OAR or EVAR. (J Vasc Surg 2008;48:1092-1100.)”
“Prior studies have demonstrated that both nicotine administration and cigarette smoking lead to dopamine (DA) release in the ventral striatum/nucleus accumbens. In tobacco-dependent individuals, smoking denicotinized cigarettes leads to reduced craving, but less pleasure, than smoking regular cigarettes. Using denicotinized cigarettes and (11)C-raclopride positron emission tomography ( PET) scanning, we sought to determine if nicotine is necessary for smoking-induced DA release. Sixty-two tobacco-dependent smokers underwent (11)C-raclopride PET scanning, during which they smoked either a regular or denicotinized cigarette (double-blind). Change in (11)C-raclopride binding potential (BP) in the ventral striatum from before to after smoking was determined as an indirect measure of DA release. Cigarette craving, anxiety, and mood were monitored during scanning.