Relationship between inflammatory markers and coronary slow flow in type 2 diabetic patients

Abstract

BackgroundDiabetes is a serious and quickly expanding global health problem. Cardiovascular disease is the leading cause of mortality in type 2 diabetes mellitus (T2DM) patients. Coronary slow flow (CSF) is characterised by delayed distal perfusion during coronary angiography with normal coronary arteries.This study aimed to investigate the correlation between CSF and inflammatory markers regarding glycemic status in T2DM.MethodsThis cross-sectional study included 120 patients who were divided equally into 4 groups according to their glycemic control and presence or absence of coronary slow flow: Group I included patients with T2DM with good glycemic control without CSF; Group II included patients with T2DM with good glycemic control and CSF; Group III included patients with T2DM with poor glycemic control without CSF; and Group IV included patients with T2DM with poor glycemic control and CSF. The neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), C-reactive protein (CRP), platelets, hematocrit, and haemoglobin were also evaluated as risk factors for coronary slow flow.ResultsThis study showed that body mass index (BMI), hematocrit level, NLR, and CRP demonstrated a moderate but significant correlation (r = 0.53) with CSF in poorly controlled T2DM. NLR cutoff > 2.1 could predict CSF in poorly controlled T2DM with a modest sensitivity and specificity. A 1.9 increase in HbA1c increases the likelihood of coronary slow flow. Dylipidemia increases the likelihood of coronary slow flow by 0.18 times. Other predictors for coronary slow flow include NLR, PLR, CRP, platelets, hematocrit, and hemoglobin. The effect of the predictors is still statistically significant after being adjusted for glycemic status, age, and sex (p < 0.001).ConclusionsPoor glycemic control increases the incidence of CSF. This supports the hypothesis that CSF is related to endothelial dysfunction as poor glycemic control causes endothelial dysfunction due to inflammation.Trial registrationZU-IRB#9419–3-4–2022 Registered 3 April 2022, email. IRB_123@medicine.zu.edu.eg.