INTRODUCTION

Arterial stiffness, a hallmark of vascular aging and pathology, plays a pivotal role in the development and progression of cardiovascular disease (¹). It represents one of the earliest stages of the atherosclerotic process, a pathological condition characterized by a decrease in the artery’s ability to expand and contract in response to pressure changes (²). This condition typically increases with age, serving as an indicator of arteriosclerosis, and is exacerbated by various factors such as obesity, diabetes, smoking, and inflammation (³). In cases of vascular inflammation, stimulated white blood cells may adhere to the vascular endothelial intima, leading to capillary leukostasis, vascular damage, and increased arterial stiffness (⁴).

Several white blood cell indices, including the neutrophil-to-lymphocyte ratio (NLR) (⁵), the monocyte-to-lymphocyte ratio (LMR) (⁶), and low albumin levels (⁷,⁸), have been linked to arterial stiffness in previous studies. The Naples Prognostic Score (NPS), developed as a multifaceted assessment tool, incorporates various biomarkers to provide a comprehensive snapshot of an individual’s health status. By integrating parameters such as serum albumin, total cholesterol, neutrophil-to-lymphocyte ratio, and lymphocyte-to-monocyte ratio, this scoring system aims to capture both inflammatory and nutritional components (⁹). Previous research has correlated the NPS with the severity of coronary artery disease (¹⁰).

The Cardio-Ankle Vascular Index serves as a non-invasive measure of arterial stiffness, evaluating vascular health from the aorta to the ankle. Elevated CAVI values have been associated with increased cardiovascular risk, including hypertension, coronary artery disease, and stroke. Thus, CAVI holds promise as a valuable prognostic tool in cardiovascular risk assessment (¹¹). Studies have demonstrated that CAVI assessment in asymptomatic patients is a valuable method for assessing both arterial stiffness and the risk of subclinical coronary atherosclerosis (¹²). Our study is the first in the literature and we aimed to investigate the relationship between NPS with arterial stiffness and coronary atherosclerosis-related CAVI values, which have been shown to be associated with inflammation and coronary artery disease.

MATERIALS AND METHODS

Between January and April 2024, we consecutively enrolled non-geriatric patients into the study. Exclusion criteria comprised a history of atherosclerotic heart disease and/or myocardial infarction other than arterial hypertension, heart failure (left ventricular ejection fraction < 50 %), moderate to severe valvular disease, renal insufficiency (estimated glomerular filtration rate < 50 ml/min/1.73 m²), a history of arrhythmia, diabetes mellitus, peripheral arterial disease, severe anemia (hemoglobin < 10 g/dL), active infection, immunological disease, and malignancy potentially impacting the NPS evaluation. Patients were stratified into two groups based on their NPS values and compared in terms of arterial stiffness evaluated by CAVI and ankle brachial index (ABI).

RESULTS

The mean age of the 142 patients enrolled in the study was 54 ± 9 years. Among them, 50 (35.2 %) were male, and 92 (64.8 %) were female. Group 1 comprised 114 (80.2 %) patients, while Group 2 consisted of 28 (19 %) patients. No significant differences were observed between the two groups in terms of demographic or laboratory data, including gender, body mass index, systolic blood pressure, diastolic blood pressure, ejection fraction, plasma glucose, creatinine, estimated glomerular filtration rate, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglyceride values (p > 0.005). The mean NPS score was calculated to be 1.45 ± 0.38 for Group 1 and 2.28 ± 1.27 for Group 2. Detailed demographic, laboratory, and clinical characteristics are summarized in table I.

Table I. Demographic data and laboratory results of the study groups. 

Numerical data are expressed as mean ± standard deviation and categorical data as percentages (%). BMI: body mass index; SBP: systolic blood pressure; DBP: diastolic blood pressure; HT: hypertension; EF: ejection fraction; eGFR: estimated glomerular filtration rate; LDL: low-density lipoprotein; HDL: high-density lipoprotein; WBC: white blood cell; NPS: Naples prognostic score.

No statistically significant differences were found between Group 1 and Group 2 in terms of left CAVI (7.92 ± 1.45 vs. 8.72 ± 1.85; p = 0.295), right CAVI (7.89 ± 1.52 vs. 8.67 ± 1.34; p = 0.332), left ABI (1.08 ± 0.15 vs. 1.05 ± 0.15, p = 0.744), or right ABI (1.10 ± 0.15 vs. 1.14 ± 0.17; p = 0.858) (p > 0.005) (Table II).

Table II. Comparison of the CAVI and ABI values of the study groups. 

CAVI: cardio-ankle vascular index; ABI: ankle-brachial index; NPS: Naples prognostic score.

DISCUSSION

Our study represents the first investigation into the relationship between arterial stiffness, vascular inflammation, and NPS. We found no significant difference between patient groups with high and low NPS values in terms of CAVI, indicating that NPS did not exhibit a significant relationship with arterial stiffness.

CAVI, a parameter utilized for assessing arterial stiffness, has proven to be a valuable method for evaluating arterial stiffness in asymptomatic patients (¹¹,¹³). The NPS, on the other hand, is a novel scoring system that provides a comprehensive reflection of inflammatory and nutritional status, comprising four parameters: serum albumin, total cholesterol, NLR, and LMR (¹⁴).

Previous studies have indicated associations between cholesterol (¹⁵), serum albumin, and increased albuminuria in urine (¹⁶) with increased arterial stiffness. For instance, Cheng et al. found higher arterial stiffness in albuminuric patients (¹⁷). Similarly, increased NLR has been linked to arterial stiffness in prior research (¹⁸). The association of NPS score with different diseases has been evaluated and it has been shown that high NPS is associated with the prognosis of ST segment elevation myocardial infarction, myocardial ischemia, the prognosis of transcatheter aortic valve replacement and heart failure-related mortality (HF). Oguz et al. reported significantly higher mortality in patients with a high NPS among hospitalized heart failure patients (¹⁹). Ender et al., in a study of 499 patients with acute ST-elevation myocardial infarction, observed that the SYNTAX score increased with higher NPS at admission, indicating a relationship between NPS and the severity of coronary artery disease (¹⁰). However, Eyüp et al., in an assessment of 1,138 patients undergoing coronary computed tomographic angiography, did not find a clear benefit of NPS in predicting coronary artery severity (²⁰). According to Unkun et al., in her study, she showed that a high NPS score can be used as a predictor of ischemia in myocardial perfusion scintigraphy (²¹). Guven et al. mortality was found to be higher and significantly higher in patients with a high NPS score performed TAVR (²²).

Arterial stiffness is a component of the chronic process of atherosclerosis (²³). The lack of a significant correlation between NPS and CAVI values in our study may be attributed to the chronic nature of arterial stiffness, as seen in the study by Eyüp et al. (¹⁹). The clinical stability of our patient group and limited variability in albumin, neutrophil, lymphocyte, and monocyte counts could also contribute to this finding. Furthermore, the negative relationship between low total cholesterol levels in NPS and arterial stiffness, which develops over time, may diminish the predictive value of NPS in acute clinical conditions such as acute heart failure (¹⁹) and acute coronary syndrome (¹⁰). Nonetheless, we believe that the rapid and effective changes in the laboratory parameters comprising NPS will enhance its significance in evaluating treatment and follow-up in patient groups.

CONCLUSIONS

This study is the first to examine the relationship between NPS and arterial stiffness. We found no significant association between NPS and CAVI values in arterial stiffness.