Daily Anesthesiology Research Analysis

OBJECTIVE: The aim of this study was to examine the association between peri-operative myocardial injury (MIn) and the occurrence of adverse cardiovascular events and or death 1 year after carotid revascularisation. METHODS: In this prospective, multicentre cohort study, 527 consecutive patients undergoing elective carotid endarterectomy (CEA) or carotid artery stenting (CAS) (June - October 2023) were enrolled across five tertiary centres. High sensitivity cardiac troponin was measured pre- and post-operatively, and patients were followed for 1 year. The primary endpoint was myocardial infarction (MI). Secondary endpoints were stroke, cardiac related death, and all cause death 1 year following CEA or CAS. Survival analysis was used to assess the impact of MIn on time dependent outcomes of interest. RESULTS: One year follow up was completed in 505 patients (95.8%), predominantly males (n = 349, 69.1%), asymptomatic (n = 339, 67.3%), with a mean age of 71.6 ± 8.6 years (range 41 - 90 years). During follow up, eight lethal outcomes were documented, of which one patient (0.2%) died due to cardiac related cause. One year post-operatively, the incidence of MI was 2.6% (n = 13) and the incidence of stroke was 3.8% (n = 19). Post-operative MIn and pre-operative diagnosis of malignancy independently predicted MI within 1 year after CEA or CAS (odds ratio [OR] = 6.54, 95% confidence interval [CI] 1.91 - 22.22, p = .003; OR = 6.13, 95% CI 1.67 - 22.73, p = .006, respectively). MI free survival was statistically significantly lower in patients with post-operative MIn 1 year after CEA or CAS (91.9% vs. 98.2%, log rank p = .003). CONCLUSION: Post-operative MIn independently predicted 1 year MI following CEA or CAS. Patients with post-operative MIn after carotid revascularisation represent a high risk subgroup in whom targeted strategies should be considered to reduce the risk of subsequent cardiac adverse events.

BACKGROUND: Chronic pain may involve both nociceptive pain driven by peripheral tissue damage and nociplastic pain reflecting central nervous system dysregulation, as in fibromyalgia. Electroacupuncture has been shown to modulate these pathways, but the underlying brain mechanisms remain unclear. This study investigated how electroacupuncture influences nociceptive-initiated and centrally maintained pain via changes in brain activation and functional connectivity. METHODS: In this randomized controlled trial (NCT02064296), female adults with fibromyalgia received either electroacupuncture (n = 19) or sham treatment with inactive laser stimulation (n = 25) over four weeks. Changes in brain activation and connectivity during evoked pressure-pain stimulation were assessed using functional magnetic resonance imaging before and after treatment. Here, we present a secondary analysis of data from the trial. Clinical outcomes assessed include pressure-pain tolerance and widespread pain, and analyses tested whether brain measures mediated treatment-related effects. RESULTS: Here we show that in the electroacupuncture group, reductions in widespread pain are associated with increases in pressure-pain tolerance. This relationship is mediated by greater activation of the primary somatosensory cortex and stronger connectivity between somatosensory and insular regions, consistent with a bottom-up mechanism linking peripheral nociceptive-initiated input to central nociplastic pain modulation. In contrast, the sham group shows reductions in widespread pain linked to decreased precuneus activity and precuneus-insula connectivity, consistent with a top-down process. CONCLUSIONS: Electroacupuncture and sham treatments engage distinct neural pathways to influence pain perception. These findings highlight that electroacupuncture modulates nociceptive-initiated and nociplastic pain through a bottom-up sensory pathway, whereas sham treatment engages top-down control. This mechanistic dissociation may inform patient selection and optimization of acupuncture-based therapies for chronic pain. Fibromyalgia is a long-term condition that causes widespread pain, fatigue, and increased sensitivity. Pain in fibromyalgia can come from signals in the body (nociceptive pain) and from how the brain processes those signals (nociplastic pain). This study tested how electroacupuncture, a form of acupuncture that uses gentle electrical pulses, affects these pain pathways. Adults with fibromyalgia received either four weeks of electroacupuncture or a placebo-like treatment. Brain scans and pain tests were done before and after treatment. Electroacupuncture increased people’s tolerance to pressure pain and changed activity in sensory regions of the brain that detect and interpret pain. These brain changes were linked to reduced widespread pain, suggesting that pain relief after electroacupuncture begins in the body and then leads to changes in the brain. In contrast, the placebo treatment affected only brain pathways linked to nociplastic pain. Electroacupuncture may therefore benefit people with both nociceptive and nociplastic pain.

Sepsis-induced acute lung injury (ALI) is a critical condition driven by neutrophil-dominated inflammation, lytic cell death and the subsequent DAMP release, etc. We tested whether the radical-trapping antioxidant Ferrostatin-1 (Fer-1) interrupts lipid peroxidation induced DAMP release and limits early lung injury in sepsis. We found that Fer-1 improved survival, preserved alveolar architecture, reduced lung-injury scores, and suppressed pulmonary inflammatory cytokine expression in a murine cecal ligation and puncture (CLP) model. Lung tissue RNA-sequencing showed that Fer-1 attenuated the CLP-induced inflammatory and chemotaxis transcriptome and significantly reduced neutrophil infiltration. In vitro, Fer-1 protected cells from lipid peroxidation-induced lytic death and impaired the release of large DAMPs associated with NINJ1 pathway, indicated Fer-1 acts upstream of NINJ1 to preserve membrane integrity. Fer-1 also directly lowered lipid peroxidation and reduced lipopolysaccharide (LPS)-induced IL-1β and IL-6 transcription and secretion in neutrophils, an effect reversed by pharmacological JNK/p38 activation. Together, our results indicate that Fer-1 functions as a dual-action modulator that prevents DAMP release and blunts neutrophil-driven inflammation escalation, thereby interrupting the lipid peroxidation-NINJ1-DAMP release axis, and mitigating early septic ALI.