Abdominal aortic aneurysm is a vascular disease which, despite the fact that it shares common risk factors with atherosclerosis, develops in parallel but as a partly independent process, through different pathogenic mechanisms. The pathogenic mechanisms involve metalloproteinase and collagenase activation, median and adventitial degradation, elastin lysis, vascular smooth cells transformation and apoptosis, collagen production and lysis imbalance combined with excessive inflammatory infiltration. Endothelial cells respond to a number of stimulating factors, including smoking, hypertension and AT1 receptor stimulation and non-uniform distribution of wall stress. Their ability to produce NO is crucial in order to adapt. Endothelial cells contribute to AAA development due to increased oxidative stress which is partly mediated by impaired NO bioavailability due to endothelial dysfunction and NADPH oxidase overexpression. In addition, they express several molecules among which adherence molecules, selectins, endothelin-1, regulating inflammatory infiltration and oxidative stress. Inflammatory cells consist of monocytes, polymorphonuclear neutrophils and lymphocytes and they are involved in the degrading process in the aortic wall by secreting proteolytic enzymes or by releasing interleukins which mediate the inflammation response. Endothelial dysfunction and arterial stiffness reflect on indices like FMD, carotid-femoral PWV and augmentation index, sometimes with controversial results. At present, surgical treatment is the only option provided in patients with large AAA, in particular. Focusing on the emerging role of endothelial cells in AAA pathology may contribute in creating new therapeutic options in a disease which has not yet a well-accepted, implemented pharmaceutical treatment.

Objectives: Whilst physical activity is linked to cardiovascular health, it has lately been recognized that different types of exercise exert diverse effects on the cardiovascular system. Therefore, we investigated the acute effects of continuous moderate-intensity aerobic exercise (CAE) and high-intensity interval aerobic exercise (hIAE) on arterial function and inflammation. Methods: Twenty healthy men (mean age 22.6 ± 3.3 years) were recruited in this crossover study. Each of the 20 volunteers participated in two separate sessions (hIAE and CAE). The augmentation index (AIx) of aortic pressure waveforms and serum levels of interleukin-17 (IL-17) were measured before and after each exercise session. Results: There were no significant differences in baseline hemodynamic and inflammatory measurements before CAE and hIAE. Compared to baseline, AIx was significantly improved after CAE (p = 0.04), while there was no significant change after hIAE (p = 0.65). Serum levels of IL-17 were significantly elevated after CAE (p = 0.042), while hIAE had no significant effect on IL-17 levels (p = 0.47). Interestingly, there was an inverse association between the elevation of IL-17 levels and the AIx improvement after CAE (p = 0.05). Conclusion: These findings provide additional evidence concerning the cardiovascular effects of different types of exercise training through modification of peripheral hemodynamics and the inflammatory process.

Soluble suppression of tumorigenesis-2 (sST2) has been introduced as a marker associated with heart failure (HF) pathophysiology and status. Endothelial dysfunction is a component underlying HF pathophysiology. Therefore, we examined the association of arterial wall properties with sST2 levels in patients with HF of ischemic etiology. We enrolled 143 patients with stable HF of ischemic etiology and reduced left ventricular ejection fraction (LVEF) and 77 control subjects. Flow-mediated dilation (FMD) was used to evaluate endothelial function and pulse wave velocity (PWV) to assess arterial stiffness. Although there was no significant difference in baseline demographic characteristics, levels of sST2 were increased in HF compared to the control (15.8 (11.0, 21.8) ng/mL vs. 12.5 (10.4, 16.3) ng/mL; p < 0.001). In the HF group, there was a positive correlation of sST2 levels with age (rho = 0.22; p = 0.007) while there was no association of LVEF with sST2 (rho = −0.119; p = 0.17) nor with PWV (rho = 0.1; p = 0.23). Interestingly, sST2 was increased in NYHA III [20.0 (12.3, 25.7) ng/mL] compared to patients with NYHA II (15.0 (10.4, 18.2) ng/mL; p = 0.003) and inversely associated with FMD (rho = −0.44; p < 0.001) even after adjustment for possible confounders. In patients with chronic HF of ischemic etiology, sST2 levels are increased and are associated with functional capacity. There is an inverse association between FMD and sST2 levels, highlighting the interplay between the dysfunctional endothelium and HF pathophysiologic mechanisms.

Aim: The NGAL is a biomarker of renal injury associated with the progression of heart failure (HF). We examine the association of NGAL with galectin-3 in patients with chronic HF. Methods: We consecutively enrolled 115 subjects with stable ischemic HF of reduced ejection fraction. Serum levels of galectin-3, b-type natriuretic peptide and NGAL were measured. Results: NGAL levels were positively correlated with galectin-3 (rho = 0.26; p = 0.04) and b-type natriuretic peptide levels (rho = 0.30; p = 0.005) and inversely correlated with ejection fraction (rho = -0.31; p = 0.02) and creatinine clearance levels. The NGAL was independently associated with galectin-3 levels. Conclusion: A positive correlation between NGAL and galectin-3 in HF patients was found, revealing a potential association between renal injury and myocardial fibrosis and remodeling in HF.

Background: Cardiac performance depends on optimum ventriculoarterial coupling which is impaired in patients with heart failure (HF). Galectin-3 is a mediator of myocardial fibrosis and remodeling, and is associated with clinical status in patients with chronic HF. We examined the association of arterial stiffness with galectin-3 levels in patients with HF of ischemic etiology. Methods: We consecutively enrolled 40 patients with stable ischemic HF and reduced ejection fraction. Central aortic stiffness was evaluated non-invasively by measuring carotid femoral pulse wave velocity (PWV). Among other factors, serum levels of galectin-3 and b-type natriuretic peptide (BNP) were measured. Results: The median galectin-3 levels in our study population were 12.9 (10.8-18.7) ng/ml and the mean PWV was 9.31±2.79 m/sec. There was significant association of galectin-3 levels with age (r=0.48, p=0.003), creatinine clearance (r=-0.66, p<0.001) and BNP levels (r=0.36, p=0.05). There was a significant association of galectin-3 levels with PWV (r=0.37, p=0.03) and patients with PWV above median also had significantly increased levels of galectin-3 compared with patients with lower values of PWV [16.1(11.8-25.2) vs. 12.1(10.5-14) ng/ml, p=0.03]. Conclusion: We found an association of arterial stiffness and PWV with galectin-3 levels in patients with chronic HF of ischemic etiology. These findings suggest a pathway driving arterial stiffening and myocardial remodelling in HF. This may provide insight into the mechanism determining prognosis and clinical status of patients with HF.