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The triad of vascular impairment, muscle atrophy, and cognitive decline represents critical age-related conditions that significantly impact health. Vascular impairment disrupts blood flow, precipitating the muscle mass reduction seen in sarcopenia and the decline in neuronal function characteristic of neurodegeneration. Our limited understanding of the intricate relationships within this triad hinders accurate diagnosis and effective treatment strategies. This review analyzes the interrelated mechanisms that contribute to these conditions, with a specific focus on oxidative stress, chronic inflammation, and impaired nutrient delivery. The aim is to understand the common pathways involved and to suggest comprehensive therapeutic approaches. Vascular dysfunctions hinder the circulation of blood and the transportation of nutrients, resulting in sarcopenia characterized by muscle atrophy and weakness. Vascular dysfunction and sarcopenia have a negative impact on physical function and quality of life. Neurodegenerative diseases exhibit comparable pathophysiological mechanisms that affect cognitive and motor functions. Preventive and therapeutic approaches encompass lifestyle adjustments, addressing oxidative stress, inflammation, and integrated therapies that focus on improving vascular and muscular well-being. Better understanding of these links can refine therapeutic strategies and yield better patient outcomes. This study emphasizes the complex interplay between vascular dysfunction, muscle degeneration, and cognitive decline, highlighting the necessity for multidisciplinary treatment approaches. Advances in this domain promise improved diagnostic accuracy, more effective therapeutic options, and enhanced preventive measures, all contributing to a higher quality of life for the elderly population.
The triad of vascular impairment, muscle atrophy, and cognitive decline represents critical age-related conditions that significantly impact health. Vascular impairment disrupts blood flow, precipitating the muscle mass reduction seen in sarcopenia and the decline in neuronal function characteristic of neurodegeneration. Our limited understanding of the intricate relationships within this triad hinders accurate diagnosis and effective treatment strategies. This review analyzes the interrelated mechanisms that contribute to these conditions, with a specific focus on oxidative stress, chronic inflammation, and impaired nutrient delivery. The aim is to understand the common pathways involved and to suggest comprehensive therapeutic approaches. Vascular dysfunctions hinder the circulation of blood and the transportation of nutrients, resulting in sarcopenia characterized by muscle atrophy and weakness. Vascular dysfunction and sarcopenia have a negative impact on physical function and quality of life. Neurodegenerative diseases exhibit comparable pathophysiological mechanisms that affect cognitive and motor functions. Preventive and therapeutic approaches encompass lifestyle adjustments, addressing oxidative stress, inflammation, and integrated therapies that focus on improving vascular and muscular well-being. Better understanding of these links can refine therapeutic strategies and yield better patient outcomes. This study emphasizes the complex interplay between vascular dysfunction, muscle degeneration, and cognitive decline, highlighting the necessity for multidisciplinary treatment approaches. Advances in this domain promise improved diagnostic accuracy, more effective therapeutic options, and enhanced preventive measures, all contributing to a higher quality of life for the elderly population.
Background/Objectives: Heart failure (HF) remains a leading cause of hospitalization and morbidity. Arterial stiffness, measured by pulse wave velocity (PWV) and the augmentation index (AIx), has been linked to HF severity and prognosis. This study investigates the relationship between clinical parameters, biochemical indicators, and arterial stiffness in hospitalized patients with HF, aiming to identify predictors of hospitalization and improve patient management. Methods: This cross-sectional study included 98 patients admitted with HF: 53 with acutely decompensated HF (sudden worsening of symptoms) and 45 with chronic HF (stable symptoms of HF). Clinical and biochemical parameters, including ejection fraction (EF), N-terminal prohormone of brain natriuretic peptide (NT-proBNP) levels, and arterial stiffness indicators (PWV and AIx), were measured at admission. During follow-up, 59 patients required re-hospitalization due to acutely decompensated HF, while 39 remained outpatients without further hospitalization. The relationship between these parameters was analyzed using Pearson correlation coefficients, and multiple Cox regression analysis was conducted to identify independent predictors of re-hospitalization. Results: A significant negative correlation between EF and PWV was found (r = −0.853, 95% CI [−0.910, −0.764]), suggesting an association between improved heart function (higher EF) and reduced arterial stiffness (lower PWV). A moderate positive correlation between EF and AIx (r = 0.626, 95% CI [0.473, 0.805]) suggests that, while higher EF is associated with increased AIx, the relationship is weaker compared to EF and PWV. This may reflect differing contributions of vascular and myocardial factors to HF severity. Hospitalized patients exhibited significantly poorer clinical and biochemical profiles, including higher NT-proBNP levels (p < 0.001) and worse blood pressure (BP) measurements (systolic and diastolic, p < 0.01). Multiple Cox regression analysis identified PWV, Aix, and NT-proBNP as independent predictors of re-hospitalization in HF patients, with significant hazard ratios: PWV (HR = 1.15, p = 0.02), AIx (HR = 1.03, p = 0.02), and NT-proBNP (HR = 1.0001, p < 0.01). Conclusions: Arterial stiffness indices (PWV and AIx), EF, and NT-proBNP were identified as significant predictors of re-hospitalization in HF patients. These findings suggest that integrating arterial stiffness measurements into routine clinical assessments may enhance the risk stratification and inform targeted interventions to reduce hospitalizations and improve outcomes.
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