Mitochondrial Bioenergetic Dysfunction as a Driver in Postoperative Low Cardiac Output Syndrome: Mechanistic Insights and Clinical Implications After Cardiac Surgery

Background: Low Cardiac Output Syndrome (LCOS) remains a common and clinically significant complication after cardiac surgery, characterized by impaired myocardial performance and inadequate systemic oxygen delivery despite optimized preload, afterload, and rhythm control. Although LCOS has traditionally been attributed to ischemia–reperfusion injury, myocardial stunning, inflammation, and neurohormonal dysregulation, accumulating evidence suggests that subcellular energetic impairment may contribute to postoperative myocardial dysfunction. Objective: This review evaluates mitochondrial dysfunction as a potential pathophysiological substrate that may underlie or exacerbate postoperative LCOS, integrating experimental, translational, and clinical findings relevant to adult cardiac surgery. Methods: A focused narrative review of preclinical and clinical literature was performed, emphasizing mitochondrial bioenergetics, calcium handling, redox signaling, and mitochondrial quality control in the context of cardiopulmonary bypass, ischemia–reperfusion, and postoperative myocardial injury. Results: Cardiomyocytes rely predominantly on mitochondrial oxidative phosphorylation, which supplies approximately 95% of myocardial ATP under physiological conditions. Surgical ischemia–reperfusion, cardioplegia, and systemic inflammatory activation are associated with transient mitochondrial disturbances, including impaired electron transport, increased reactive oxygen species generation, calcium overload, and mitochondrial permeability transition pore opening. These changes may contribute to reduced ATP availability, delayed myocardial recovery, contractile inefficiency, and increased susceptibility to arrhythmias. Emerging evidence suggests that circulating mitochondrial biomarkers, such as cell-free mitochondrial DNA, correlate with postoperative organ dysfunction, supporting the presence of systemic mitochondrial stress after cardiac surgery. Conclusions: Postoperative LCOS may partially reflect a reversible state of myocardial energetic failure. Recognition of mitochondrial involvement complements established hemodynamic and inflammatory models and offers a biologically plausible framework for variability in postoperative cardiac recovery.