The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the ongoing global coronavirus (COVID-19) pandemic. Although initially viewed as an acute respiratory illness, COVID-19 is clearly a complex multisystemic disease with extensive cardiovascular involvement. Emerging evidence shows that the endothelium plays multiple roles in COVID-19 physiopathology, as both a target organ that can be directly infected by SARS-CoV-2 and a mediator in the subsequent inflammatory and thrombotic cascades. Arterial stiffness is an established marker of cardiovascular disease. The scope of this review is to summarize available data on the acute and long-term consequences of COVID-19 on vascular function. COVID-19 causes early vascular aging and arterial stiffness. Fast, noninvasive bedside assessment of arterial stiffness could optimize risk stratification in acute COVID-19, allowing for early escalation of treatment. Vascular physiology remains impaired at least 12 months after infection with SARS-CoV-2, even in otherwise healthy adults. This raises concerns regarding the extent of arterial remodeling in patients with preexisting vascular disease and the potential development of a persistent, chronic COVID-19 vasculopathy. Long-term follow up on larger cohorts is required to investigate the reversibility of COVID-19-induced vascular changes and their associated prognostic implications.

Obstructive sleep apnea (OSA) is characterized by repetitive upper airway collapse, chronic hypoxia and a proinflammatory phenotype. The purpose of our study was to evaluate readily available inflammatory biomarkers (C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), white blood cell count (WBC), red cell distribution width (RDW), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), mean platelet volume (MPV), WBC-to-MPV ratio (WMR) and lymphocyte-to-C-reactive protein ratio (LCR)) before and after CPAP in patients with moderate–severe OSA. We performed a prospective study that included patients with newly-diagnosed moderate–severe OSA. The control groups (patients without OSA and with mild OSA) were selected from the hospital polygraphy database. All subjects underwent routine blood panel, which was repeated in moderate–severe OSA patients after 8 weeks of CPAP. Our final study group included 31 controls, 33 patients with mild, 22 patients with moderate and 37 patients with severe OSA. CRP, ESR, NLR and WMR were correlated with OSA severity. After 8-week CPAP therapy, we documented a decrease in weight status, which remained statistically significant in both CPAP-adherent and non-adherent subgroups. Readily available, inexpensive inflammatory parameters can predict the presence of moderate–severe OSA, but are not influenced by short-term CPAP.

Background: Both obstructive sleep apnea (OSA) and metabolic syndrome (MS) promote arterial stiffening. As a basis for this study, we presumed that arterial stiffness could be assessed using the Arteriograph (TensioMed, Budapest, Hungary) to detect early modifications induced by continuous positive airway therapy (CPAP) in reversing this detrimental vascular remodeling. Arterial stiffness is increasingly acknowledged as a major cardiovascular risk factor and a marker of subclinical hypertension-mediated organ damage. The aim of this pilot study was to evaluate the arterial stiffness changes in patients with moderate–severe OSA and MS after short-term CPAP use. Methods: We performed a prospective study that included patients with moderate–severe OSA and MS who had not undergone previous CPAP therapy. All subjects underwent clinical examination and arterial stiffness assessment using the oscillometric technique with Arteriograph (TensioMed, Budapest, Hungary) detection before and after 8-week CPAP therapy. Results: 39 patients with moderate–severe OSA were included. Eight weeks of CPAP therapy significantly improved central systolic blood pressure (Δ = −11.4 mmHg, p = 0.009), aortic pulse wave velocity (aoPWV: Δ = −0.66 m/s, p = 0.03), and aortic augmentation index (aoAix: Δ = −8.25%, p = 0.01) only in patients who used the device for a minimum of 4 h/night (n = 20). Conclusions: Arterial stiffness was improved only among CPAP adherent patients and could be detected using the Arteriograph (TensioMed, Budapest, Hungary), which involves a noninvasive procedure that is easy to implement for the clinical evaluation of arterial stiffness.

Arterial stiffness naturally increases with age and is a known predictor of cardiovascular morbimortality. Blood flow restriction (BFR) training involves decreasing muscle blood flow by applying a strap or a pneumatic cuff during exercise. BFR induces muscle hypertrophy even at low intensities, making it an appealing option for older, untrained individuals. However, BFR use in patients with cardiovascular comorbidities is limited by the increased pressor and chronotropic response observed in hypertensive elderly patients. Furthermore, the impact of BFR on vascular function remains unclear. We conducted a comprehensive literature review according to PRISMA guidelines, summarizing available data on the acute and long-term consequences of BFR training on vascular function. Although evidence is still scarce, it seems that BFR has a mild or neutral long-term impact on arterial stiffness. However, current research shows that BFR can cause an abrupt, albeit transient, increase in PWV and central blood pressure. BFR and, preferably, lower-body BFR, should be prescribed with caution in older populations, especially in hypertensive patients who have an exacerbated muscle metaboreflex pressor response. Longer follow-up studies are required to assess the chronic effect of BFR training on arterial stiffness, especially in elderly patients who are usually unable to tolerate high-intensity resistance exercises.

Obstructive sleep apnea (OSA) is associated with increased cardiovascular risk, sedentarism, depression, anxiety and impaired quality of life. The long-term effectiveness of positive airway pressure (PAP) is insufficiently studied and limited by poor patient compliance. The aim of this pilot prospective cohort study was to evaluate long-term adherence in overweight patients with moderate–severe OSA and hypertension and to analyze changes in weight, sleepiness and quality of life. We performed a prospective study that included overweight patients with moderate–severe OSA and hypertension who had not undergone previous PAP therapy. All subjects received a standard physical examination, education regarding lifestyle changes and free PAP therapy for 2 months. After five years, the patients were invited to participate in a telephone-based interview regarding PAP compliance and completed standard questionnaires assessing adherence to medication, physical activity, diet, anxiety and quality of life (QoL). Only 39.58% of the patients were adherent to PAP 5 years (58.42 ± 3.70 months) after being diagnosed with moderate–severe OSA. Long-term PAP use results in sustained weight loss; improved blood pressure control, sleepiness and QOL; and lower anxiety and depression scores. PAP compliance was not associated with a higher level of daily physical activity or a healthier diet.

Background: With a steady increase in prevalence, chronic obstructive pulmonary disease (COPD) is recognized as a leading contributor to global mortality, which underscores the need to identify prognostic biomarkers that are easy to use in everyday practice. As both local and systemic inflammation play a pivotal part in the development and progression of COPD, the purpose of our study was to assess the role of inflammatory markers in estimating disease severity (GOLD 1 to 4) to guide the management and treatment of patients with COPD, thus helping to reduce episodes of decompensation and fatal outcomes in both immediate and long-term contexts. Methods: We performed a descriptive observational analysis with a cross-sectional design including 100 patients with stable COPD. All subjects underwent standard clinical examination, lung function tests and a comprehensive inflammation blood panel. Results: We included 55 patients with mild–moderate COPD (GOLD 1–2), 33 patients with advanced stages of COPD (GOLD 3) and 12 patients with very severe forms of the disease (GOLD 4). Male sex, smoking status, BMI, IL-1 beta, NLR, and nocturnal heart rate were parameters with significant value for assessing COPD severity (p < 0.05 for all). NLR correlates significantly with the predicted distance in the 6 MWT (p = 0.039). Significant associations were identified between IL-8 and duration of exposure of biomass fuel (p = 0.045) as well as between IL-6 and pack-years (p = 0.024), with both prognostic and therapeutic impact. Furthermore, the analysis of the total cohort revealed positive correlations between serum IL-6 and FVC (%) (p = 0.033) or NLR and the ratio between FEV1 and FVC (p = 0.048). The neutrophil-to-lymphocyte ratio (NLR) proved to be a reliable indicator of stages 3–4 GOLD (AUC 0.66, threshold value 2.3045, p = 0.004—a one-point increase in NLR corresponded to a 2.148 increase in FEV1). Conclusions: NLR emerged as a simple, accessible and highly informative biomarker in COPD, linked to disease severity and functional decline. Its integration into routine assessment could enhance prognosis and guide clinical decisions, a finding that warrants confirmation in future multicenter studies.