Background: Cardiovascular diseases (CVDs) remain a leading cause of morbidity and mortality, despite advances in treatment. Early detection of vascular aging is critical, as preclinical atherosclerosis often remains undiagnosed. AI-determined vascular age, originally developed using carotid-femoral pulse wave velocity (cf-PWV), may help to identify individuals at elevated risk. This study aimed to evaluate the clinical utility of an alternative AI-determined vascular age model based on the arterial velocity pulse index (AVI) and arterial pressure volume index (API) in a Japanese hospital-based cohort. Methods: This retrospective, exploratory study analyzed electronic health records of 408 patients from Yokohama City University Hospital. This study was approved by the Clinical Research Ethics Committee (approval numbers: B180300040, F240500007), and patient consent was obtained through an opt-out process. AI-determined vascular age was estimated using a Generalized Additive Model (GAM) with backward stepwise regression, substituting cf-PWV with AVI and API. Correlations with chronological age were assessed, and comparisons of cardiovascular and renal function markers were performed across age-stratified groups. Results: AI-determined vascular age showed a strong correlation with chronological age (p < 0.05). Significant differences were observed in cardiac diastolic function parameters, B-type natriuretic peptide (BNP), and estimated glomerular filtration rate (eGFR) between the highest and lowest quintiles of AI-determined vascular age. Conclusions: AI-determined vascular age using AVI and API appears to be a feasible surrogate for cf-PWV in clinical settings. This index may aid in stratifying vascular aging and identifying individuals who could benefit from early cardiovascular risk management.

Background: The Arterial Velocity Pulse Index (AVI) and Arterial Pressure–Volume Index (API) are novel non-invasive indices of arterial stiffness derived from cuff-oscillometric measurements. Previous studies have shown that elevated AVI and API are associated with the severity of coronary artery disease and the ability to predict future cardiovascular events. However, the hemodynamic and echocardiographic characteristics of patients with concomitantly high AVI and API remain unclear. Methods: We retrospectively analyzed 112 consecutive cardiovascular outpatients (mean age 69.1 ± 12.2 years, 64.3% male) seen between January and April 2019 at Yokohama City University Hospital. The AVI and API were measured using a multifunctional sphygmomanometer (PASESA AVE1500, Shisei Datum, Japan) and averaged over a maximum of three measurements. Patients were classified into four groups according to previously established cutoff values (AVI ≥ 27, API ≥ 32). Central arterial pulse wave parameters were assessed using SphygmoCor XCEL (AtCor Medical, Sydney, Australia), and echocardiographic parameters were obtained according to standard protocols. Intergroup differences were analyzed using the Kruskal–Wallis test with Steel–Dwass post hoc comparisons. Results: Compared with the low-risk group (low AVI/low API), the high-risk group (high AVI/high API) had significantly higher brachial systolic BP (139.2 [132.8–149] vs. 128 [120–136.7] mmHg, p = 0.0011), central systolic BP (127.5 [122.3–139] vs. 117.7 [110.3–123.7] mmHg, p = 0.0018), and central pulse pressure (56.2 [51.4–60.3] vs. 37.7 [32–43] mmHg, p < 0.001). The forward and reflected wave amplitudes were significantly greater, with prolonged ejection duration and aortic T2 time. The Buckberg subendocardial viability ratio was significantly lower in the high-risk group (129.5 [119.7–145.2] vs. 148.3 [130–168.3], p = 0.040). Echocardiography revealed reduced e′ velocity (5 [4.1–5.8] vs. 6.7 [5.2–8] cm/s, p = 0.035) and increased E/e′ (13.2 [11.1–15.1] vs. 9.7 [7.9–11.3], p = 0.026) in the high-risk group, suggesting the presence of impaired diastolic function without reduced LVEF. Conclusions: Patients with high AVI and API exhibited greater central and peripheral arterial stiffness, higher systolic and pulse pressures, and impaired diastolic function compared with those with low values. These findings support the use of a cardiovascular pathophysiological model in which elevated AVI/API identify individuals at increased risk of progression to heart failure and ischemic heart disease.