Abstract
BackgroundArterial stiffness is strongly linked to the pathogenesis of heart failure and the development of acute decompensation in patients with stable chronic heart failure. This study aimed to compare arterial stiffness indices in patients with heart failure with reduced ejection fraction (HFrEF) during the acute decompensated state, and three months later after hospital discharge during the compensated state.ResultsOne hundred patients with acute decompensated HFrEF (NYHA class III and IV) and left ventricular ejection fraction ≤ 35% were included in the study. During the initial and follow-up visits, all patients underwent full medical history taking, clinical examination, transthoracic echocardiography, and non-invasive pulse wave analysis by the Mobil-O-Graph 24-h device for measurement of arterial stiffness. The mean age was 51.6 ± 6.1 years and 80% of the participants were males. There was a significant reduction of the central arterial stiffness indices in patients with HFrEF during the compensated state compared to the decompensated state. During the decompensated state, patients presented with NYHA FC IV (n = 64) showed higher AI (24.5 ± 10.0 vs. 16.8 ± 8.6, p < 0.001) and pulse wave velocity (9.2 ± 1.3 vs. 8.5 ± 1.2, p = 0.021) than patients with NYHA FC III, and despite the relatively smaller number of females, they showed higher stiffness indices than males.ConclusionsCentral arterial stiffness indices in patients with HFrEF were significantly lower in the compensated state than in the decompensated state. Patients with NYHA FC IV and female patients showed higher stiffness indices in their decompensated state of heart failure.
Highlights
Arterial stiffness is strongly linked to the pathogenesis of heart failure and the development of acute decompensation in patients with stable chronic heart failure
This may be explained by the neurohormonal activation that occurs in decompensated heart failure (HF), which leads to increased sympathetic tone and peripheral vasoconstriction, resulting in an increased magnitude of wave reflections and pulse wave velocity (PWV) [18, 19]
Increased PWV will lead to the early arrival of the reflected waves to the proximal aorta during systole leading to increased augmentation pressure (AP), central systolic blood pressure (cSBP), decreased central diastolic blood pressure (cDBP), and, increased central pulse pressure (cPP)
Summary
Arterial stiffness is strongly linked to the pathogenesis of heart failure and the development of acute decompensation in patients with stable chronic heart failure. Many factors other than age contribute to the development and/or acceleration of arterial stiffness, including genetic abnormalities, diabetes mellitus, arterial hypertension, obesity, chronic kidney disease, the accumulation of advanced glycation end products (AGEs), increased production of reactive oxygen species (ROS), endothelial dysfunction, and endocrinal abnormalities such as increased activity of the renin-angiotensinaldosterone system (RAAS) and insulin resistance [4,5,6,7]. These factors affect arterial stiffness by either ECM modification and/or increasing vascular smooth muscle cell (VSMC) tone [8, 9]. As measured by PWV and parameters derived from pulse wave analysis (PWA), was higher in patients with HF than in healthy subjects, and was an independent risk factor for the development of new HF either in normal people or in patients with traditional cardiovascular (CV) risk factors, and was implicated in the development of acute decompensation of stable patients with chronic HF [10].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
