Arterial stiffness is associated with increased cardiovascular risk in chronic obstructive pulmonary disease (COPD). However, whether this increase reflects disease-specific vascular effects or is primarily driven by age and hemodynamic factors remains unclear, particularly in early disease states such as pre-COPD and preserved ratio impaired spirometry (PRISm). This study aimed to evaluate arterial stiffness across the COPD spectrum and to determine the independent predictors of pulse wave velocity (PWV). This cross-sectional study included healthy controls (n=60), a combined pre-COPD/PRISm group (n=121), and COPD patients (n=120) classified according to spirometric criteria. Arterial stiffness was assessed noninvasively using brachial oscillometric PWV. Clinical characteristics, smoking exposure, spirometric parameters, symptom scores, and hemodynamic measurements were recorded. Correlation analyses and hierarchical multivariate linear regression were performed to identify independent determinants of PWV. PWV values were significantly higher in the pre-COPD/PRISm and COPD groups than in healthy controls, with the highest levels observed in COPD patients at GOLD stage E (p<0.001). Although PWV showed significant correlations with spirometric parameters and symptom scores in unadjusted analyses, these associations lost significance after adjustment for age and smoking exposure. In contrast, mean arterial pressure and central pulse pressure remained strongly associated with PWV (p<0.001). In multivariate analysis, age was the strongest independent predictor of PWV, followed by mean arterial pressure and body surface area, while FEV1% was not a significant contributor. Arterial stiffness is increased not only in COPD but also in individuals with pre-COPD/PRISm. However, this increase appears to be primarily driven by age-related and hemodynamic factors rather than disease-specific airflow limitation. These findings highlight the importance of early cardiovascular risk assessment focusing on hemodynamic parameters.

Background: Asthma is a heterogeneous inflammatory airway disease increasingly recognised to be associated with elevated cardiovascular risk. Arterial stiffness, commonly assessed by pulse wave velocity (PWV), is a well-established predictor of cardiovascular events. However, it remains unclear whether vascular involvement in asthma reflects true arterial stiffening or predominantly altered arterial wave reflection. Objectives: To investigate arterial stiffness and wave reflection characteristics in patients with controlled and uncontrolled asthma compared with healthy controls. Design: Cross-sectional observational study. Methods: A total of 158 participants (56 healthy controls, 50 patients with controlled asthma, and 52 patients with uncontrolled asthma) underwent non-invasive arterial stiffness and hemodynamic assessments. Peripheral and central blood pressures, PWV, augmentation pressure, augmentation index and reflection magnitude were measured. Group comparisons were performed using unadjusted analyses and multivariable analysis of covariance (ANCOVA). Multivariate analysis of covariance (MANCOVA) was used to evaluate wave reflection parameters simultaneously, adjusting for age, body mass index, smoking status, heart rate and systolic blood pressure. Results: PWV differed significantly between groups in unadjusted analyses, with higher values observed in asthma groups. However, this association was no longer significant after multivariable adjustment, with age and systolic blood pressure emerging as the strongest independent determinants of PWV. In contrast, MANCOVA revealed a significant overall group effect on wave reflection parameters. Subsequent univariate analyses demonstrated that reflection magnitude remained significantly higher in both controlled and uncontrolled asthma groups compared with healthy controls after adjustment, whereas augmentation pressure and augmentation index did not show independent group effects. Conclusion: Vascular involvement in asthma appears to be characterised primarily by altered arterial wave reflection rather than overt arterial stiffening. These findings suggest that vascular alterations observed in asthma are primarily related to changes in arterial wave reflection and may be influenced by systemic hemodynamic factors (e.g. blood pressure and body composition), rather than asthma control itself.

Background and Objectives: Hypertension is highly prevalent among individuals with chronic kidney disease (CKD) and contributes substantially to both cardiovascular morbidity and progressive renal dysfunction. Ambulatory blood pressure monitoring (ABPM) provides superior diagnostic accuracy compared with office measurements and is recommended for evaluating blood pressure patterns and hypertension-mediated organ damage in CKD. Morning blood pressure, in particular, has gained increasing attention due to its association with adverse cardiovascular and renal outcomes. However, evidence regarding the independent impact of morning hypertension in CKD remains limited. This study aimed to determine the prevalence of morning and nocturnal hypertension phenotypes in hypertensive CKD patients and to evaluate their associations with renal and cardiac target organ damage. Materials and Methods: A total of 132 patients with CKD stages 1–5 underwent 24-h ABPM, transthoracic echocardiography, and comprehensive biochemical evaluation. Morning and nocturnal hypertension were defined according to ESC 2024 guidelines. Demographic, clinical, echocardiographic, and renal parameters were compared between groups. Correlation analyses were performed to explore associations between blood pressure phenotypes and markers of target organ damage. Multivariable regression models were used to assess independent predictors of renal and cardiac structural alterations. Results: Morning hypertension was present in 42.4% of patients, whereas nocturnal hypertension was detected in 78%. Patients with morning hypertension exhibited significantly lower eGFR and higher UACR levels (both p < 0.001). Morning hypertension showed positive correlations with creatinine, urea, PTH, ESR, and UACR, and negative correlations with eGFR, albumin, calcium, hemoglobin, and TAPSE. In multivariable regression, morning hypertension was independently associated with lower eGFR (β = −0.26; p = 0.002). Nocturnal hypertension was positively associated with IVSd (β = 0.19; p = 0.024) and UACR, supporting its role in cardiac remodeling and renal injury. Conclusions: Morning hypertension may represent a clinically relevant blood pressure phenotype in CKD and may be associated with markers of renal dysfunction; however, longitudinal studies are needed to determine its prognostic significance. The strong associations of nocturnal hypertension with IVSd and albuminuria further highlight the importance of evaluating 24-h blood pressure patterns. Incorporating ABPM into routine clinical practice may enhance risk stratification and guide individualized treatment strategies in CKD.