The proportion of adults aged ≥65 years worldwide is projected to double from approximately 10% in 2010 to 20% by 2040 (1). With advancing age, the vasculature undergoes structural and functional degeneration, collectively termed “vascular aging,” which has become the leading contributor to disability and mortality in older adults (2). Arteriosclerosis, the hallmark structural manifestation of vascular aging, reflects intrinsic alterations in the arterial wall that increase vascular stiffness and strongly predispose individuals to cardiovascular disease (CVD) (3). In community-dwelling Chinese aged 70–79 years, the rate of prevalence of carotid atherosclerosis has been reported to reach 60%–80% (4). Although carotid-femoral pulse wave velocity (cfPWV) is widely recognized as the gold standard for assessing arterial stiffness, its measurement is time-consuming (5). In contrast, brachial-ankle pulse wave velocity (baPWV) provides a simpler and more efficient alternative (6).

The fibrinogen-to-albumin ratio (FAR) is calculated as the ratio of fibrinogen to albumin in peripheral blood. Fibrinogen and albumin are circulating proteins that exert distinct physiological functions. Fibrinogen is an indicator of a procoagulant state and a biomarker for chronic inflammation (7, 8). Elevated plasma fibrinogen levels are closely associated with an increased risk of major adverse cardiovascular events (MACEs) (9, 10). In contrast, albumin possesses anti-inflammatory, antioxidant, and anticoagulant properties (10–13). Hypoalbuminemia is associated with an elevated risk of MACEs (14, 15). Recent studies have demonstrated that the FAR, a readily available and cost-effective marker, may predict MACEs more accurately than fibrinogen or albumin alone (16, 17). However, the association between FAR and arteriosclerosis has not yet been clearly elucidated.

The present study was designed to investigate the association between FAR and baPWV and to clarify the role of the FAR in evaluating cardiovascular aging.

This study aimed to explore the association between FAR and arterial stiffness. BaPWV is a validated and convenient clinical indicator for assessing arterial stiffness. FAR was independently associated with both baPWV and arteriosclerosis, and these associations remained statistically significant after adjusting for potential confounding factors. A linear dose–response relationship between FAR and arteriosclerosis was further confirmed. A significant difference in the FAR was observed between participants with and without arteriosclerosis. The arteriosclerosis group exhibited a higher mean FAR compared with the non-arteriosclerosis group (10.1 ± 4.3% vs. 8.3 ± 2.8%). Participants with arteriosclerosis were older and more likely to have comorbid cardiovascular risk factors such as diabetes and hypertension. This finding aligns with established clinical patterns, as arterial stiffness increases with age and is often accompanied by metabolic risk factors.

Atherosclerosis is characterized by arterial lumen narrowing and the formation, erosion, and rupture of atherosclerotic plaques (20). These pathological processes directly induce ischemia or thrombosis, thereby contributing to CVD, including peripheral vascular disease, cerebrovascular disease, and coronary heart disease. In severe cases, inadequate collateral circulation may lead to myocardial infarction or cerebral infarction. As a chronic, highly deleterious vascular disorder, atherosclerosis has shown an increasing incidence. Identifying individuals at risk of cardiovascular events remains a key focus of preventive strategies, emphasizing the critical role of early detection and intervention in mitigating disease progression at its initial stages. Arteriosclerosis, characterized by increased arterial stiffness, represents an early marker of atherosclerosis (21). BaPWV is validated and convenient for assessing arterial stiffness, but it is not routinely available in many hospitals and primary-care settings, highlighting the need for a simpler alternative.

Existing evidence supports the relevance of FAR to cardiovascular pathophysiology. For instance, Ozdemir et al. identified FAR as a predictor of exaggerated morning blood pressure surges, a well-recognized CVD risk factor (22). FAR has also been independently associated with coronary artery disease (CAD) severity in patients with ST-segment elevation myocardial infarction (23). Similar associations have been reported in patients with non-ST-segment elevation myocardial infarction (24, 25). Moreover, FAR robustly predicts MACEs in CAD patients undergoing percutaneous coronary intervention (26). Zheng et al. linked FAR to adverse outcomes after lacunar stroke (27). Collectively, these studies position FAR as a risk factor for adverse cardiovascular events.

Notably, the association between FAR and baPWV remains insufficiently explored. In the present study, when FAR and baPWV were analyzed as continuous variables in univariable analyses, FAR was positively correlated with baPWV. Furthermore, when arteriosclerosis was defined as baPWV ≥1,800 cm/s, the prevalence of arteriosclerosis increased progressively across ascending FAR quartiles. These findings indicate that elevated FAR is independently associated with greater baPWV.

The potential mechanisms underlying the association between FAR and arteriosclerosis require further exploration. Arteriosclerosis, an early hallmark of vascular aging, is characterized by reduced vascular wall elasticity and increased stiffness (2). A growing body of evidence supports the concept of “inflammaging,” which links chronic, low-grade inflammation to progressive arterial stiffening (28). Aminuddin et al. reported an association between inflammation and elevated PWV (29). In addition, abnormal hemodynamic changes, including increased blood viscosity and coagulation activation, contribute to arteriosclerotic progression (30). FAR, influenced by both fibrinogen and albumin, may be involved in the interplay of these processes (inflammatory and hemodynamic pathways) that are associated with arteriosclerosis, although the direction of this relationship remains unclear. Fibrinogen, a key inflammatory marker, enhances inflammatory cell adhesion and upregulates proinflammatory cytokine synthesis (31). Elevated fibrinogen levels may increase blood viscosity, potentially inducing shear stress–mediated endothelial damage and coagulation activation (32). Conversely, lower albumin levels correlate with heightened inflammation (11). Inflammation increases vascular permeability and disrupts fluid homeostasis, leading to rapid changes in plasma albumin concentrations (32, 33). Observational data further show an inverse correlation between plasma albumin and C-reactive protein (CRP), a classic inflammatory marker (34). Beyond its role in inflammation, albumin exerts antioxidant effects by scavenging reactive oxygen species (ROS) and limiting oxidative stress (12, 35). Albumin also has anticoagulant properties that help maintain hemostatic balance. Therefore, hypoalbuminemia is associated with a prothrombotic state (36–38). Fibrinogen and albumin may jointly promote systemic inflammation and hemodynamic disturbances, and their alterations may together contribute to the pathophysiological processes underlying arteriosclerosis. As an integrated index, FAR captures the concurrent pattern of elevated fibrinogen and reduced albumin and may therefore be more sensitive than either marker alone in reflecting inflammatory activity and hemodynamic perturbations. In the present study, a higher FAR was associated with an increased risk of arteriosclerosis, suggesting that chronic inflammation and hemodynamic dysregulation may represent key potential pathways linking FAR to arterial stiffening.

Interaction analyses showed that the association between FAR and arteriosclerosis was not significantly modified by gender, smoking status, diabetes, hypertension, dyslipidemia, or high BMI, suggesting that the predictive value of FAR may be broadly applicable in older adults. Even among elderly individuals without overt traditional cardiovascular risk factors, an elevated FAR remained associated with a higher risk of arteriosclerosis, indicating that FAR may serve as a potential early warning marker of vascular aging.

Several limitations in this study should be noted. First, the retrospective cross-sectional design precludes causal inference between FAR and baPWV. Arterial stiffness itself may induce chronic inflammation or disrupt hemodynamic homeostasis, thereby increasing FAR, and reverse causation cannot be excluded. Prospective cohort studies or interventional trials are needed to determine directionality. Second, the generalizability of our findings is limited. The study included older adults aged 65 years or older, and the distribution of FAR and its association with baPWV may differ in adults younger than 65 years who typically have better vascular elasticity and lower baseline inflammation. In addition, only older Chinese participants were included, and differences in genetic background, lifestyle, and disease spectrum may limit extrapolation to other age groups and ethnic populations. Third, the sample size of 389 was adequate for primary correlation and regression analyses, but statistical power for subgroup analyses was limited. Fourth, residual confounding remains possible in this single-center retrospective study. Although we adjusted for routine covariates, we did not account for chronic inflammatory diseases such as rheumatoid arthritis and systemic lupus erythematosus, liver dysfunction, nutritional indicators such as prealbumin and dietary protein intake, inflammatory markers including CRP and IL-6, or relevant medication history, all of which may affect the precision of association estimates. Overall, large-scale, multicenter, multiethnic prospective studies are warranted to further validate the clinical value of FAR as a marker of vascular aging.

This study provides evidence in older adults that FAR is independently and linearly associated with arterial stiffness, offering a simple and readily available indicator for vascular aging assessment.