Arterial stiffness is an important and independent risk factor for CV diseases . It is strongly linked to the pathogenesis of HF and implicated in the acute decompensation of stable patients with chronic HF . However, there is little data describing the changes in arterial stiffness parameters during the transition from the acute decompensated state of HF to the compensated state. Our study aimed to compare arterial stiffness parameters derived from non-invasive PWA by the Mobil-O-Graph 24 h PWA device in patients with HFrEF during the decompensated state and three months later during the compensated state. The main finding in our study was the significant decrease in arterial stiffness parameters in patients with the compensated state of HFrEF compared to their initial values during the decompensated state. This may be explained by the neurohormonal activation that occurs in decompensated HF, which leads to increased sympathetic tone and peripheral vasoconstriction, resulting in an increased magnitude of wave reflections and PWV [18, 19]. Increased PWV will lead to the early arrival of the reflected waves to the proximal aorta during systole leading to increased AP, cSBP, decreased cDBP, and, finally, increased cPP.
Similar results were reported by Demir et al.  who recruited 98 patients (76 males, mean age 59.4 ± 11.6 years) with acute decompensated HFrEF (NYHA class III and IV) and measured the PWV and AIx during the hospitalization then followed the patients up to 18 months with repeated measurements. All patients had ICM with LVEF values of ≤ 35%. They used the Arteriograph for their measurements. During the follow-up period, 70 patients were re-hospitalized for recurrent decompensated HF; of them, 12 patients died during hospitalization. The authors reported that both PWV and AIx were significantly higher in all the 70 patients who were re-hospitalized in comparison with the values obtained when these patients were adequately treated after their initial admission. In addition, they reported that both PWV and AIx were significantly higher in patients who died compared to survivors, and that both were predictors of mortality.
Another previous study, in which 80 patients with acute decompensated HF (NYHA class III and IV), was carried out by Sung et al. . The authors measured cfPWV using applanation tonometry and conducted PWA on the carotid pulse wave for the measurement of carotid AP and AIx (which are considered as surrogates for aortic AP and AIx, respectively, in the absence of significant carotid stenosis). The measurements were taken on admission, one day before discharge, and two weeks after discharge, and then, patients were followed up monthly for up to six months. The study endpoints included four CV events (rehospitalization due to decompensation, myocardial infarction, stroke, and death). During the follow-up period, 29 patients experienced CV events. Of the remaining 51 patients that did not experience CV events (42 males, mean age 72.2 ± 14.9 years), 26 patients had HFrEF. However, the authors did not specifically mention the data of the patients with HFrEF but they mentioned the data of the 51 patients, including those with HFpEF. They found that the brachial and central SBP and PP and cfPWV measured two weeks after discharge were less than the admission values in these 51 patients without events but not in those with events who were found to still have high measurements.
On the other hand, Kim et al.  studied patients with acute decompensated HF (NYHA class III and IV) during hospitalization and then three months later after discharge while being in the compensated state. The study included 55 patients (25 males, mean age 65.4 ± 12.6 years). During follow-up, seven patients were excluded because they were re-hospitalized within three months after discharge due to recurrent decompensated HF (according to the study’s exclusion criteria), and three patients were lost to follow-up. Of the remaining 45 patients, only 19 had HFrEF (mean EF was 31.8 ± 5.8%). They used applanation tonometry for pressure waves recording at the carotid, radial, femoral, and dorsalis pedis arteries for measurement of the carotid-femoral (central), carotid-radial (upper extremity), and femoral-dorsalis (lower extremity) pulse wave velocities. They reported that the PWV measured at different sites showed no significant changes between the decompensated and compensated states in HFrEF patients. The results of the study by Kim et al. were different from our findings that PWV decreased significantly in transition from the decompensated state to the compensated state. This may be due to the small number of patients included in their study (19 patients), which prevented them from attaining statistical significance during comparative statistics. Also, their patients were obviously older than ours (mean age was 65.4 ± 12.6 vs. 51.6 ± 6.1 years) and had a higher prevalence of hypertension (71% vs. 46%), which may have influenced the PWV values and the degree of improvement with the transition to the compensated state.
In our study, patients with decompensated HF NYHA class IV had higher cPP, AP, AIx@75, and PWV as compared to those with NYHA class III. This may be explained by the excess neurohormonal activation in NYHA class IV patients, which leads to multiple pathophysiological changes that become more evident with more severe HF. This was supported by data from previous studies by Denardo et al.  and Sung et al.  that reported increased arterial wave reflection and PWV in patients with acute decompensated HF and their significant increase with more severe HF. Also, as previously mentioned, Sung et al.  reported that brachial and central SBP and PP and cfPWV measured 2 weeks after hospital discharge in patients treated for acute decompensated HF decreased progressively in patients without events but not in those with events (including recurrent decompensation) who were still having high measurements. In addition, PWV was shown to have a significant positive correlation with the NT-proBNP level in patients with decompensated HF, which is known to increase with more severe HF . Moreover, Giannattasio et al.  showed that arterial stiffness increased with more severe HF and had a positive correlation with impaired cardiac diastolic function.
In our study, male patients, as compared to females, had a significantly lower heart rate, central PP, and AIx@75 in the decompensated state. The higher heart rate in female patients may be due to a higher prevalence of more severe heart failure (NYHA class IV HF) and significantly lower blood hemoglobin levels in comparison with male patients. The higher AIx@75 during the compensated state can be explained by the fact that females generally have higher AP and AIx values than males, partly due to their shorter stature, which makes the reflection sites in the arterial tree closer to the heart and proximal aorta; so, the reflected waves return to the proximal aorta in systole rather than diastole . Previous studies showed gender differences in HF pathophysiology with higher wave reflection, greater pulsatile load, and higher cPP in females than in males [28, 29].
In the current study, we found that patients with ICM had a significantly higher central and peripheral SBP, central and peripheral DBP, and PWV than those with DCM both in the decompensated state and in the compensated state of HF. This may be due to the higher cardiovascular risk profile in ischemic patients. A previous study demonstrated that patients with coronary heart disease have demonstrated increased arterial stiffness, as indicated by higher PWV and AIx values than are found in healthy individuals . Similar to our results, Osmolo vs. kaya et al.  found that cfPWV was higher in patients with ICM compared to patients with DCM, while the cPP and AIx did not differ significantly between the two groups. A recent meta-analysis demonstrated that statin therapy could reduce the aortic augmentation index irrespective of the low-density lipoprotein level . Our results showed similar findings where patients who were on regular statin therapy (patients with ICM) demonstrated lower augmentation indexes than patients on no statin therapy (patients with DCM); however, the difference was not statistically significant.
A moderate significant positive correlation was found between age and PWV. Previous studies examined the relationship between age and arterial stiffness as measured by cfPWV, which is the gold standard for measuring arterial stiffness. One of the largest studies is the one by Mattace-Raso et al., which included approximately 18,000 subjects and showed a strong positive correlation with age . Aging leads to the breakdown of elastic fibers in the walls of large elastic arteries and increases the production of stiffer proteins like collagen and proteoglycans. Also, atherosclerosis, endothelial dysfunction, and arterial wall calcification increase with aging. All these factors lead to increased arterial stiffness with increasing age .
Similarly, our patients had a significant weak positive correlation between BMI and all parameters of arterial stiffness, except the PWV. In agreement with our results, Rodrigues et al.  and Desamericq et al.  reported no correlation between the PWV and the BMI, also Biwen et al.  reported a significant negative correlation between the brachial-ankle PWV (baPWV) and the BMI. Regarding the AIx, Niruba et al.  reported a significant positive correlation with the BMI, while Logan et al.  reported a negative correlation between the same two parameters. Some of the mechanisms of increased arterial stiffness in subjects with higher BMI are insulin resistance, the accumulation of AGEs, and increased circulating leptin level. Leptin increases vessel tone, stimulates vascular smooth muscle proliferation, and induces the production of ROS [40, 41].