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Background:. The National Surgical Quality Improvement Program (NSQIP) database provides an important resource for determining complication rates and risk factors for surgical procedures. However, NSQIP is limited to 30-day follow-up, and it is unclear whether this is reliable for evaluating prosthetic breast reconstruction outcomes. Methods:. A single-institution, cross-sectional, retrospective review was performed for patients undergoing mastectomy with immediate, prepectoral tissue expander reconstruction. Timing of complications was stratified as early (within 30 days of operation) versus late (after 30 days). Categorical variables were compared using χ2 (or Fisher exact) tests, and continuous variables were analyzed using Kruskal-Wallis or Wilcoxon rank-sum tests. Results:. There were 301 patients (509 reconstructed breasts) included with a median follow-up time of 11 months. Of them, 176 patients (58%) experienced a postoperative complication—140 patients (47%) experienced an early complication and 36 patients (12%) experienced a late complication. Patients with late complications had a significantly higher rate of reconstructive failure compared with the early complication group (17% versus 10%; P = 0.001) and were more likely to require a flap (28% versus 7%; P = 0.001) for final reconstruction. Revision surgery rates after final implant placement were higher in the late complication group (36% versus 64%; P = 0.285). Conclusions:. Late complications after prepectoral breast reconstruction have a more prominent impact on reconstructive failure and revisions than early complications. This finding may inform strategies to revise national databases such as NSQIP to include more detailed information and longer capture periods.

Purpose: Our laboratory studies contributions of breast adipose stromal cells (bASCs) to breast cancer initiation and progression. To date, most studies of ASC biology have focused on abdominal ASCs. We hypothesize that bASC biology impacts the breast microenvironment in a manner that influences a woman’s risk of developing breast cancer. Methods: In order to better understand how aberrant bASC biology contributes to breast cancer, we built a bASC cell repository from women undergoing mastectomies at Duke University Hospital (Duke IRB Pro00100739). Some of these women are at high risk for developing breast cancer. High risk biology includes women with genetic predispositions to cancer, as well as obese and post-menopausal women. bASCs were isolated from the stromal vascular fraction of breast adipose tissue from patients. Additionally, commercially-available ASCs isolated from the abdomen were obtained from Zenbio. Senescence was measured in bASCs using the SPiDER beta gal senescence detection kit (Dojingo). Senescence-associated cytokines were measured in conditioned media collected from these bASCs by ELISA (R&D Systems). The ability of bASCs to differentiate into adipocytes was measured using the Adipo-Red adipocyte differentiation assay (Lonza). Results: To date, we have isolated bASCs from 16 patients undergoing mastectomies at Duke University Hospital. We have studied differences in the biology of these bASCs that may be associated with increased breast cancer risk. A commonality observed in high risk patients was senescence, demonstrated by bASCs undergoing growth arrest and secretion of beta-galactosidase. Similarly, bASCs from high risk patients demonstrated secretion of inflammatory cytokines such as Interleukin-6 (IL-6), Interleukin-8 (IL-8), and Interleukin-1beta (IL-1 beta) that are associated with the senescence-associated secretory phenotype. We hypothesize that the secretion by these bASCs of such cytokines creates an inflammatory breast microenvironment that increases breast cancer risk. Our data also indicate that bASCs from high risk patients exhibit a defect in their ability to differentiate into adipocytes. Conclusion: Our studies are the first to report on a repository of breast ASCs (bASCs) from patients undergoing mastectomies. Results indicate that bASC biology differs significantly amongst patients, with a subset exhibiting a senescent secretory phenotype associated with a block in their ability to differentiate into adipocytes. We hypothesize bASC senescence, associated with a senescence secretory phenotype, results in: 1) the inability of these bASCs to differentiate into adipocytes, and 2) a senescence-associated secretory phenotype that impacts the breast tumor microenvironment. As we continue to build the repository, studies are in progress to test if inflammatory cytokines secreted by senescent bASCs work in a paracrine fashion on breast epithelium to drive breast cancer initiation/ progression.