Another Marker of Inflammation and Oxidative Stress and Its Impact on Myocardial Function, Arterial Elastance, and Vasoactive–Inotropic Score After Coronary Revascularization Surgery: A Prospective Cohort Study

CONTEXT: Inflammatory and oxidative stress responses are markedly amplified following cardiopulmonary bypass (CPB), contributing to myocardial injury, vascular dysregulation, and potential multiorgan dysfunction. AIMS: This study aimed to define how inflammatory, oxidative, and cellular stress responses quantified by tumor necrosis factor-alpha (TNF-α), hydroxyl (OH-) radical scavenging capacity, and heat shock protein-70 (HSP-70) relate to early postoperative myocardial contractility, arterial tone, and vasoactive-inotropic requirements after CPB. SETTINGS AND DESIGN: A prospective cohort study was conducted in patients undergoing coronary artery bypass grafting (CABG) with preserved preoperative ejection fraction (EF). METHODS AND MATERIALS: Postoperative biomarker levels and perioperative changes in TNF-α, OH- scavenging capacity, and HSP-70 with early myocardial contractility maximum rate of rise of left ventricular pressure (dP/dtmax), arterial elastance, and vasoactive-inotropic score were assessed. STATISTICAL ANALYSIS USED: Correlation analyses were performed using Pearson's or Spearman's correlation coefficients as appropriate. RESULTS: A total of 52 patients were included in the study. Higher postoperative HSP-70 levels were associated with reduced early myocardial contractility (r = -0.315; P = 0.025) and increased vasoactive-inotropic requirements (ρ =0.341; P = 0.014). No significant associations were observed among postoperative biomarker variables, and changes in TNF-α or OH- scavenging capacity were not related to early postoperative hemodynamic outcomes (all P > 0.05). CONCLUSIONS: Early post-CPB myocardial dysfunction appears more closely associated with cellular stress (HSP-70) than with inflammatory or oxidative responses. Elevated HSP-70 levels in the early postoperative CABG may act as damage-associated molecular patterns associated with transient myocardial depression and higher vasoactive-inotropic requirements, whereas early inflammatory and oxidative changes showed no direct hemodynamic correlation.