Comparative Assessment of High-sensitive CRP and Carotid Stiffness between Patients with and without Coronary Slow Flow

Abstract Background and Aim Coronary slow flow (CSF) phenomenon represents a distinct clinical entity characterized by delayed coronary opacification despite absence of significant epicardial stenosis. The pathophysiology involves microvascular dysfunction, endothelial impairment, and systemic inflammation. This study evaluated high-sensitivity C-reactive protein (hs-CRP) levels and carotid stiffness parameters in cases with CSF and in controls with normal coronary flow (CF). Materials and Methods This case-control study included 60 participants who underwent coronary angiography for chest pain evaluation. Participants (n=30) were divided into two groups: the CSF group, defined by corrected thrombolysis in myocardial infarction frame count >27, and the control group, with normal CF. Bilateral carotid artery ultrasonography and hs-CRP measurement were performed. Carotid stiffness parameters included β-stiffness index, Peterson’s elastic modulus, distensibility coefficient, compliance coefficient, and arterial strain. Results CSF cases demonstrated significantly higher hs-CRP levels than controls (3.35±1.48 vs. 1.18±0.62 mg/L; P < 0.001). Carotid assessment revealed increased carotid intima-media thickness (0.82±0.24 vs. 0.68±0.19 mm, P = 0.012), elevated β-stiffness index (7.68±2.71 vs. 6.04±1.62, P = 0.006), and Peterson’s elastic modulus (637.33±279.7 vs. 379.67±249.81 kPa, P < 0.001). Decreased distensibility and compliance coefficients indicated reduced arterial compliance. Conclusion CSF is associated with higher hs-CRP and adverse carotid stiffness profiles. These findings support an inflammatory-vascular dysfunction axis in the CSF and justify further studies assessing their prognostic utility. Keywords: Coronary slow flow, high-sensitivity C-reactive protein, carotid stiffness, arterial compliance, microvascular dysfunction