Intersurgeon variations in postoperative length of stay after video-assisted thoracoscopic surgery lobectomy.

Objectives: To identify factors associated with prolonged postoperative length of stay (LOS) after VATS lobectomy (VATS-L), explore potential intersurgeon variation in LOS and ascertain whether or not early discharge influences hospital readmission rates. Methods: We conducted a retrospective analysis of patients who underwent VATS-L at a single academic center between 2018 and 2021. Each VATS lobectomy procedure was performed by 1 of 7 experienced thoracic surgeons. The primary end point of interest was prolonged LOS, defined as an index LOS >3 days. Results: Among 1006 patients who underwent VATS lobectomy, 632 (63%) had a prolonged LOS. On multivariate analysis, the factors independently associated with prolonged LOS were: surgeon (P < .001), patient age (odds ratio [OR], 1.03; 95% CI, 1.02-1.06), operation time (OR, 1.01; 95% CI, 1.01-1.01), postoperative complication (OR, 3.60; 95% CI, 2.45-5.29), and prolonged air leak (OR, 8.95; 95% CI, 4.17-19.23). There was no significant association between LOS and gender, body mass index, coronary artery disease, prior atrial fibrillation, American Society of Anesthesiologists score >3, and prior ipsilateral thoracic surgery or sternotomy. There was no association between LOS ≤3 days and hospital readmission (20 [5.3%] vs 39 [5.9%]; OR, 0.88; 95% CI, 0.50-1.53). Conclusions: An intersurgeon variation in postoperative LOS after VATS-L exists and is independent of patient baseline characteristics or perioperative complications. This variation seems to be more closely related to differences in postoperative management and discharge practices rather than to surgical quality. Postoperative discharge within 3 days is safe and does not increase hospital readmissions.

Neoadjuvant sutent induction therapy may effectively down-stage renal cell carcinoma atrial thrombi.

A 75-yr-old previously healthy woman presented with gross hematuria, European Cooperative Oncology Group 0, and an 11-cm renal mass with right atrial thrombus. The patient refused the sternotomy. She was offered two cycles of sunitinib maleate (Sutent) induction therapy to down-stage the thrombus and to reduce the extent of the surgery.

Differential regulation of matrix metalloproteinase activities in abdominal aortic aneurysms.

BACKGROUND: The increased synthesis of matrix metalloproteinases (MMPs) by aortic smooth muscle cells (SMCs) is thought to be involved in the etiopathogenesis of abdominal aortic aneurysms (AAAs), but the functional regulation and the activation states of these MMPs remain unclear. In this study, we assessed the expression levels and the functional regulation of several MMPs in the pathogenesis of AAAs. METHODS: Human healthy aorta and AAA specimens were homogenized, and the proteolytic activities of MMP-2 and MMP-9 and of the macrophage metalloelastase (MMP-12) were assessed with zymography. Protein expression of MMP-1, MMP-12, membrane-type 1 MMP (MT1-MMP), tissue inhibitor of MMP 1 (TIMP-1), TIMP-2, TIMP-3, alpha-actin, and beta-actin was analyzed with electrophoresis on sodium dodecyl sulfate gels and immunoblotting. RESULTS: MMP-1, MMP-9, and MMP-12 zymogen levels and proteolytic activities were increased in AAAs when compared with healthy aorta. A severe reduction in alpha-actin--positive vascular SMCs was observed in all the AAA specimens and was correlated with an increase in TIMP-3 but not TIMP-1 or TIMP-2 potential activities. Although pro--MMP-2 activity was decreased, the extent of activated MMP-2 remained unaffected in the AAAs. In accordance with this result, a highly activated MT1-MMP form was also observed in AAAs. CONCLUSION: These data suggest that chronic aortic wall inflammation is mediated by macrophage infiltration, which may account for the destruction of medial elastin, as reflected by SMC down regulation, through increased levels of active MMP-1 and MMP-12. Moreover, altered MT1-MMP proteolytic turnover and differential regulation of TIMP expression in AAAs suggest that tight regulatory mechanisms are involved in the molecular regulation of MMP activation processes in the pathogenesis of AAAs.