Aim This study aimed to analyze laboratory predictors, angiographic profile, clinical profile, and risk factors for coronary slow flow (CSF) phenomenon without coronary obstructive lesion in patients who came for a coronary angiogram.
Materials and Methods The case-control study consisted of patients who underwent coronary angiography and were divided into two groups: patients with coronary slow flow (case group, n = 100) and patients with the normal coronary flow (control group, n = 100). Coronary flow was studied using corrected thrombolysis in myocardial infarction frame count (CTFC). The slow flow was defined as CTFC beyond 2 standard deviations from the normal published range. Risk factors including age, sex, diabetes mellitus (DM), hypertension, dyslipidemia, smoking, body mass index (BMI), hematological and biochemical parameters (complete blood picture, platelet count, total and differential leucocyte count, platelet-to-lymphocyte ratio [PLR], neutrophil-to-lymphocyte ratio [NLR] and lipid profile) were assessed. In both groups, clinical information was collected, and laboratory parameters were measured and compared.
Results Patients with CSF were more likely to be male and active smokers. Total cholesterol, triglyceride, BMI, and DM were more commonly seen in the CSF group compared with the control group. Inflammatory markers like uric acid (p = 0.03) and high-sensitivity C-reactive protein (Hs-CRP) (p = 0.000) were found to be statistically significant. Hematocrit (p = 0.023), NLR (p = 0.001), total cholesterol (p = 0.000), triglycerides (p = 0.000), and BMI (p = 0.000) were statistically significant. PLR has the tendency of statistically significance (p = 0.059) BMI, total cholesterol, triglycerides, and Hs-CRP were strong predictors for CSF.
Conclusion CSF was common in males, smokers, DM patients, and it was associated with high NLR, uric acid, and Hs-CRP levels. The independent predictor of CSF was BMI, total cholesterol, triglycerides, and Hs-CRP levels. These findings provide an impetus for additional studies to confirm the role of other inflammatory markers in CSF patients and treatment strategies depending on that.