Aortic Stiffness and Neutrophil-to-Lymphocyte Ratio in Coronary Artery Disease: Pathophysiological Links and Clinical Implications

Abstract

Background: Aortic stiffness (AoS) is one of the first obvious signs of detrimental structural and functional alterations in the arterial wall. It is a promising indicator of subclinical disease and a non-invasive way to measure maladaptive alteration and remodeling of aortic characteristics. Pathologically elevated AoS increases hemodynamic strain on the left ventricle and central systolic pressure. Furthermore, processes linked to AoS, such as inflammation and oxidative stress pathway activation, may be indicative of underlying vascular risk. The neutrophil-to-lymphocyte ratio (NLR) represents systemic inflammatory activity and has been associated with atherosclerosis and arterial stiffness. Coronary artery disease (CAD) is characterized by the development of atherosclerosis in the coronary arteries, and inflammatory processes have an important role in its underlying vascular pathology.

Aim: This review aims to highlight the pathophysiological links between aortic stiffness, systemic inflammation represented by the neutrophil-to-lymphocyte ratio, and coronary artery disease, with emphasis on vascular remodeling mechanisms and their potential clinical implications.

Conclusion: Aortic stiffness, systemic inflammation, and coronary atherosclerosis represent interconnected components of vascular pathological remodeling. Neutrophil activation, oxidative stress, extracellular matrix degradation, altered collagen and elastin balance, and loss of lymphocytic counter-regulation provide mechanisms through which inflammatory activity may contribute to progressive arterial stiffening. Assessment of aortic stiffness together with inflammatory biomarkers such as NLR may provide complementary information regarding vascular alterations associated with coronary artery disease.