Post-PCI Inflammation and Diastolic Dysfunction in Patients with Metabolic Risk Factors: A Retrospective Observational Study

<i>Background and Objectives:</i> Left ventricular diastolic dysfunction (LVDD) is a known precursor of heart failure with preserved ejection fraction (HFpEF), particularly in patients with metabolic comorbidities. Acute coronary syndrome (ACS) and percutaneous coronary interventions (PCI) may exacerbate LVDD via systemic inflammation. This study aimed to explore the association between post-procedural systemic inflammation and the severity of diastolic dysfunction in patients with ACS and metabolic comorbidities. <i>Materials and Methods:</i> A retrospective observational study was conducted in 181 patients with ACS who underwent PCI. Inflammatory markers (leukocytes, neutrophils, and C-reactive protein [CRP]) measured at 24-48 h post-intervention were analyzed in relation to diastolic dysfunction, assessed by echocardiography. Multivariable ordinal logistic regression and correlation analyses were performed. <i>Results:</i> CRP showed a non-significant trend toward association with more advanced diastolic dysfunction (<i>p</i> = 0.081). Hypertension had a positive but nonsignificant coefficient. Other metabolic comorbidities (diabetes, dyslipidemia, and obesity) were not significantly associated. The correlation between N-terminal pro-B-type natriuretic peptide (NT-proBNP) and troponin was exploratory. NT-proBNP was the only marker significantly correlated with high-sensitivity troponin (TrHS) at 48 h, indicating a link between myocardial injury and wall stress. <i>Conclusions:</i> CRP may be weakly associated with the severity of diastolic dysfunction post-PCI. However, classical metabolic comorbidities were not independently predictive. Post-PCI inflammation showed only modest, non-significant trends toward diastolic impairment, warranting confirmation in larger prospective studies.