Diabetes-Associated Heart Failure After Percutaneous Coronary Intervention: Molecular Mechanisms and Prospects for...

Diabetes mellitus (DM) is a major independent risk factor for heart failure (HF) following percutaneous coronary intervention (PCI). Metabolic disturbances associated with DM, including insulin resistance, hyperglycemia, and altered substrate utilization, contribute to myocardial injury and adverse ventricular remodeling through multiple interconnected molecular pathways. This review systematically examines the pathophysiological mechanisms underlying post-PCI HF in patients with DM and coronary artery disease, with particular emphasis on cardiomyocyte metabolic dysfunction, inflammatory signaling, cell death pathways, and microvascular injury. The diabetic myocardium is characterized as being predisposed to maladaptive responses to PCI-related stressors, including ischemia-reperfusion injury, contrast-induced nephropathy, and stent-associated inflammation, thereby increasing the risk of HF. Building on these mechanistic insights, emerging biomarkers for early risk stratification and predictive modeling, together with multi-targeted therapeutic strategies, are reviewed. These include cardioprotective glucose-lowering agents such as sodium-glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 receptor agonists (GLP-1RAs), myocardial metabolic modulators, and integrated multidisciplinary management approaches. The integration of clinical, molecular, and imaging biomarkers may facilitate the early identification of high-risk patients and support the implementation of personalized therapeutic interventions. Collectively, the available evidence provides a mechanistic and clinically relevant framework for preventing the progression of HF and improving cardiovascular outcomes in patients with DM undergoing PCI.