Intravenous lidocaine reduces systemic inflammation but not myocardial injury following thoracic surgery for lung cancer: a randomized controlled trial

Elevated high-sensitivity troponin T levels shortly after noncardiac surgery are closely linked to myocardial injury, a key factor in 30-day postoperative mortality. Intravenous lidocaine, known for its potent anti-inflammatory and membrane-stabilizing properties, has shown cardioprotective potential in other surgical settings, but its efficacy in noncardiac thoracic surgery remains unclear. This study was a double-blind, placebo-controlled randomized trial. Participants were randomly allocated to the lidocaine or placebo group with a 1:1 ratio. Single-centre, double-blind, randomized controlled trial. Academic tertiary care medical centre. Patients scheduled for noncardiac thoracic surgery, predominantly via video-assisted thoracoscopic surgery (VATS), under general anesthesia from June 12, 2021 to June 12, 2022. Patients received intravenous lidocaine (1.5 mg kg− 1 bolus pre-induction followed by 1.5 mg kg− 1 h− 1 infusion until surgery end) or volume-matched saline. Dosing was adjusted to ideal body weight for BMI ≥ 25 kg m−². Study drugs were prepared by blinded staff and administered via standardized pumps. The primary outcome was high-sensitivity troponin T concentration at 24 h postoperatively. Secondary outcomes encompassed: (1) the absolute change from baseline to 24 h post-surgery for high-sensitivity troponin T (2) the occurrence of MINS, identified by high-sensitivity troponin T levels of 14 ng l− 1 or higher within 48 h after surgery; (3) levels of NT-proBNP, CK-MB, myoglobin, hs-CRP, and inflammatory markers on the first and second postoperative days; (4) overall opioid use during surgery; and (5) hemodynamic parameters during the operation. Between June 12, 2021, and June 12, 2022, we enrolled 119 patients who underwent thoracic surgery for lung cancer (mean age 59.41 years [SD 11.085], 58 [48.7%] male). The median [IQR] 24-hour high-sensitivity troponin T level did not differ between the lidocaine and control groups (8.00 [6.00–15.00] ng l− 1 vs. 8.00 [5.00–10.00] ng l− 1, P = 0.34). Additionally, the absolute change in hs-TnT from baseline showed no significant difference (3.21 ± 5.93 ng l⁻¹ vs. 3.00 ± 8.56 ng l⁻¹, P = 0.88).The incidence of MINS was similar between the groups (23.3% vs. 23.7%, P = 0.96). Lidocaine exhibited significant anti-inflammatory properties, resulting in an 84.8% reduction in 48-hour IL-6 levels (46.5 ± 33.6 pg ml− 1 vs. 307.0 ± 312.2 pg ml− 1, P = 0.04). In a post-hoc analysis, age was identified as a significant independent predictor of myocardial injury (OR 0.259 for age < 65 vs. ≥ 65 years; 95% CI 0.107 to 0.627; P = 0.003), but no evidence of an interaction with the treatment allocation was found. Perioperative lidocaine infusion significantly suppressed systemic inflammation, but did not reduce early myocardial biomarker release in the overall cohort. The finding that younger age was associated with a lower risk of myocardial injury, irrespective of treatment group, suggests that age is a key prognostic factor. Further studies are warranted to explore age-specific cardioprotective strategies and the underlying mechanisms of inflammatory-myocardial coupling. ChiCTR2100047336. Registered on June 12, 2021. • Intravenous lidocaine reduced IL-6 but showed no myocardial protection, challenging inflammation-driven injury models and implicating ischemia-reperfusion pathways in thoracic surgery. • Patients aged <65 years had lower myocardial injury risk, highlighting precision anesthesia opportunities for younger cohorts. • IL-6 suppression despite neutral cardiac outcomes underscores the need for multimodal strategies (e.g., combined anti-inflammatory and anti-ischemic agents) tailored to elderly high-risk patients.