The clinical impact of pectoral nerve block in an 'enhanced recovery after surgery' program in breast surgery.

Background: Pectoral nerve block (PECS) is increasingly performed in breast surgery. Aim: The study evaluated the clinical impact of these blocks in the postoperative course. Patients & methods: In this case-control study, patients undergoing breast surgery with 'enhanced recovery after surgery' pathways were divided into group 1 (57 patients) in whom PECS was performed before general anesthesia, and group 2 (57 patients) in whom only general anesthesia was effected. Results: Postoperative opioid consumption (p < 0.002), pain at 32 h after surgery (p < 0.005) and the length of stay (p < 0.003) were significantly lower in group 1. Conclusion: Reducing opioid consumption and pain after surgery, PECS could favor a faster recovery with a reduction in length of stay, ensuring a higher turnover of patients undergoing breast surgery.

'Enhanced recovery after surgery' (ERAS) protocols have been recently applied in breast cancer patients in order to improve the postoperative course. However, the incidence of moderate to severe pain after breast surgery is frequent, and a multimodal approach is recommended. In this view, the interfascial plane blocks are advocated as a valid alternative to both paravertebral and epidural blockade. In this study, we evaluated the effects of these blocks on the postoperative course in patients undergoing breast surgery with ERAS protocols. We compared two patient groups: in the first, pectoral blocks were performed before general anesthesia, while in the second no block was carried out. We found that in the patient group receiving the blocks, postoperative opioid consumption (with essentially the same pain after surgery) and length of stay were significantly lower. Therefore, although more robust studies are needed to confirm our findings, these emerging locoregional techniques could favor a faster recovery in the context of ERAS in breast surgery. These results could have important clinical implications in terms of not only reducing healthcare costs but also ensuring a higher turnover of patients undergoing breast surgery.

Interleukin-7 and interleukin-15 drive CD4+CD28null T lymphocyte expansion and function in patients with acute coronary syndrome.

AIMS: Inflammation has important roles in atherosclerosis. CD4+CD28null (CD28null) T cells are a specialized T lymphocyte subset that produce inflammatory cytokines and cytotoxic molecules. CD28null T cells expand preferentially in patients with acute coronary syndrome (ACS) rather than stable angina and are barely detectable in healthy subjects. Importantly, ACS patients with CD28null T-cell expansion have increased risk for recurrent acute coronary events and poor prognosis, compared to ACS patients in whom this cell subset does not expand. The mechanisms regulating CD28null T-cell expansion in ACS remain elusive. We therefore investigated the role of cytokines in CD28null T-cell expansion in ACS. METHODS AND RESULTS: High-purity sorted CD4+ T cells from ACS patients were treated with a panel of cytokines (TNF-α, IL-1ß, IL-6, IL-7, and IL-15), and effects on the number, phenotype, and function of CD28null T cells were analysed and compared to the control counterpart CD28+ T-cell subset. IL-7- and IL-15-induced expansion of CD28null T cells from ACS patients, while inflammatory cytokines TNF-α, IL-1ß, and IL-6 did not. The mechanisms underlying CD28null T-cell expansion by IL-7/IL-15 were preferential activation and proliferation of CD28null T cells compared to control CD28+ T cells. Additionally, IL-7/IL-15 markedly augmented CD28null T-cell cytotoxic function and interferon-γ production. Further mechanistic analyses revealed differences in baseline expression of component chains of IL-7/IL-15 receptors (CD127 and CD122) and increased baseline STAT5 phosphorylation in CD28null T cells from ACS patients compared to the control CD28+ T-cell subset. Notably, we demonstrate that CD28null T-cell expansion was significantly inhibited by Tofacitinib, a selective JAK1/JAK3 inhibitor that blocks IL-7/IL-15 signalling. CONCLUSION: Our novel data show that IL-7 and IL-15 drive the expansion and function of CD28null T cells from ACS patients suggesting that IL-7/IL-15 blockade may prevent expansion of these cells and improve patient outcomes.