Leucocyte activation is central to end-organ damage that occurs during cardiac surgery under cardiopulmonary bypass (CPB). Exhaled nitric oxide (NO) increases in inflammatory lung conditions and has been proposed as a marker of pulmonary inflammation during CPB. This study examined the effect of leucodepletion on leucocyte activation, pulmonary inflammation and oxygenation in patients undergoing coronary revascularisation. Fifty low-risk patients undergoing first time coronary artery bypass graft (CABG) were randomised to two groups. Twenty-five patients had an arterial line leucocyte-depleting filter and 25 controls had a standard filter. Arterial blood samples were taken before CPB, 5 and 30 min on CPB, 5 min after aortic clamp removal and 6 h post-operatively. Activated leucocytes were identified with Nitroblue Tetrazolium staining. NO was sampled via an endotracheal teflon tube 15 min after median sternotomy before CPB and 30 min after discontinuation of CPB using a real-time chemiluminescense analyser. Respiratory index (alveolar-arterial oxygenation index, AaOI) was calculated before CPB, 1, 2, 4, 8 and 18 h post-operatively. Clinical outcome end-points were also recorded. Total and activated leucocyte counts were significantly lower following leucodepletion during CPB (P < 0.0001). Exhaled NO rose significantly after CPB in the control group (3.8+/-1 ppb/s before CPB vs 5.6+/-2 ppb/s after CPB (P = 0.003) but not in the leucodepleted group (3.7+/-1 ppb/s before CPB vs 3.9+/-1 ppb/s after CPB (P = 0.051). AaOIs were consistently lower after leucodepletion (anova, P = 0.001). The duration of mechanical ventilation, the intensive care and hospital stay and the frequency of cardiac and respiratory complications were similar in the two groups. Leucodepletion reduces the numbers of circulating activated leucocytes and the pulmonary inflammation during CPB. This appears to limit lung injury and improve oxygenation in low-risk patients undergoing CABG surgery. Larger numbers of patients are required to evaluate the effect of continuous arterial line leucodepletion on the clinical outcome.

Postoperative atrial fibrillation (POAF) is the most common arrhythmia following cardiac surgery. This review critically explores the interplay between cardiopulmonary bypass (CPB) and aortic cross-clamping (ACC) times in POAF development. CPB disrupts systemic homeostasis by inducing inflammatory cascades, oxidative stress, and ischemia–reperfusion injury. Prolonged ACC times further exacerbate myocardial ischemia and structural remodeling, with durations exceeding 60–75 min consistently linked to an increased POAF risk. However, variability in outcomes across studies reveals the complex, multifactorial nature of POAF pathogenesis. Patient-specific variables, such as baseline comorbidities and myocardial protection strategies, modulate these risks, emphasizing the need for personalized surgical approaches. Despite advancements in myocardial protection techniques and anti-inflammatory strategies, the incidence of POAF remains persistently high, indicating a gap in translating mechanistic insights into effective interventions. Emerging biomarkers, including microRNAs (e.g., miR-21, miR-483-5p, etc.) and markers of myocardial injury like troponin I, offer potential for enhanced risk stratification and targeted prevention. However, their clinical applicability requires further validation in diverse patient populations. This review underscores the critical need for integrative research that combines clinical, molecular, and procedural variables to elucidate the nuanced interplay of factors driving POAF. Future directions include leveraging advanced intraoperative monitoring tools, refining thresholds for CPB and ACC times, and developing individualized perioperative protocols.