Coronary slow flow: role of systemic inflammation and biomarkers in its pathophysiology.

BACKGROUND

Coronary slow flow (CSF) is characterized by reduced coronary blood flow velocity in the absence of significant obstruction, and it has been associated with systemic inflammation and endothelial dysfunction. This study aimed to evaluate the association between inflammatory indices and the presence of CSF in patients undergoing coronary angiography.

METHODS

An analytical cross-sectional study with an exploratory design was conducted in 77 patients undergoing coronary angiography, including those with CSF (n = 43) and controls with angiographically normal coronary arteries (n = 34). Clinical, biochemical, and hematological variables, TNF-α levels, and inflammatory indices (TyG, NLR, LMR, NPR, PIV, and SIRI) were assessed. Appropriate statistical tests and an exploratory multivariate logistic regression model were performed to evaluate associations with CSF.

RESULTS

The prevalence of CSF was 2.6%, with hypertension and dyslipidemia being the most frequent comorbidities. Patients with CSF exhibited significantly higher levels of total cholesterol (p = 0.024), LDL cholesterol (p = 0.016), monocytes (p = 0.017), and neutrophils (p = 0.015). Inflammatory indices TyG, NLR, NPR, PIV, and SIRI were significantly elevated in the CSF group (p < 0.05), whereas LMR was lower. No significant differences were found in TNF-α levels, although elevated values were observed in both groups. Multivariate logistic regression analysis did not identify statistically significant independent predictors of coronary slow flow.

CONCLUSIONS

CSF appears to represent a systemic inflammatory and microvascular phenotype rather than an isolated angiographic finding. Patients with CSF exhibited higher values of integrated inflammatory indices, suggesting a coordinated cardiometabolic inflammatory profile. These indices may serve as practical and accessible complementary markers associated with CSF; however, they should be considered hypothesis-generating rather than validated diagnostic tools. Larger prospective multicenter studies are required to confirm these associations and their clinical implications.