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.

Smoking and diabetes mellitus have been recognized as significant modifying factors of the evolution of periodontitis, being considered at the moment as descriptive factors in the periodontitis grading system. The purpose of this study was to assess the consequence of smoking, type 2 diabetes, and the combination of these two factors on clinical periodontal parameters, on the levels of gingival crevicular fluid (GCF), and also on ratios of pro-inflammatory and anti-inflammatory cytokines by using a commercially available kit-based multiplex fluorescent immunoassay. The study was carried out on 124 volunteers (control (C) group = 29, diabetes mellitus (DM) group = 32, smoking (S) group = 31, and S + DM group = 32). Total mean bleeding on probing was significantly lower in the S and S + DM groups, compared to that of the other groups (p < 0.05). Total amounts of TGF-β, MIP-1α, IL-6, IL-2, and IL-17 were significantly increased in the periodontally healthy sites of diabetes patients (p < 0.05), compared to those of the controls. Systemically healthy smoking patients had higher values of GM-CSF, TGF-β, IL-4, TNF-α, IL-5, and IL-7, while diabetic smoking patients showed higher values of IL-4, TGF-β, and MIP-1α. In smoking and systemically healthy patients, IL-23, IL-7, and IL-12 showed increased concentrations, while concentrations of TGF-β, MIP-1α, IL-2, IL-7, IL-12, IL-17, IL-21, and IL-23 were higher in smoking DM patients. In conclusion, in our study, diabetes mellitus induced a general pro-inflammatory state, while smoking mainly stimulated immunosuppression in the periodontal tissues of periodontitis subjects.

Background and Objectives: Functional capacity (FC) assessed via cardiopulmonary exercise testing (CPET) is a novel, independent prognostic marker for patients with coronary artery disease (CAD). Neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ratio (PLR) are two readily available predictors of systemic inflammation and cardiovascular event risk, which could be used as cost-effective predictors of poor FC. The purpose of this study was to evaluate the utility of NLR and PLR in predicting poor FC in patients with CAD and recent elective percutaneous coronary intervention (PCI). Materials and Methods: Our cross-sectional retrospective analysis included 80 patients with stable CAD and recent elective PCI (mean age 55.51 ± 11.83 years, 71.3% male) who were referred to a cardiovascular rehabilitation center from January 2020 to June 2021. All patients underwent clinical examination, cardiopulmonary exercise testing on a cycle ergometer, transthoracic echocardiography and standard blood analysis. Results: Patients were classified according to percent predicted oxygen uptake (% VO2 max) in two groups—poor FC (≤70%, n = 35) and preserved FC (>70%, n = 45). There was no significant difference between groups regarding age, gender ratio, presence of associated comorbidities, left ventricular ejection fraction and NLR. PLR was higher in patients with poor FC (169.8 ± 59.3 vs. 137.4 ± 35.9, p = 0.003). A PLR cut-off point of 139 had 74% sensitivity and 60% specificity in predicting poor FC. After multivariate analysis, PLR remained a significant predictor of poor functional status. Conclusions: Although CPET is the gold standard test for assessing FC prior to cardiovascular rehabilitation, its availability remains limited. PLR, a cheap and simple test, could predict poor FC in patients with stable CAD and recent elective PCI and help prioritize referral for cardiovascular rehabilitation in high-risk patients.

Background and Objectives: Atherosclerosis is a multifactorial process in which inflammatory markers have both therapeutic and prognostic roles. Recent studies bring into question the importance of assessing new inflammatory markers in relation to the severity of peripheral artery disease (PAD), such as the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and lymphocyte-to-C-reactive protein ratio (LCR). Materials and Methods: We conducted a retrospective and descriptive study including 652 patients with PAD, who were divided into two groups according to the severity of the ankle–brachial index value: mild and moderate obstruction (257 patients) and severe obstruction (395 patients). We evaluated demographics, anthropometric data and clinical and paraclinical parameters in relation to the novel inflammatory biomarkers mentioned above. Results: Weight (p = 0.048), smoking (p = 0.033), the number of cardiovascular risk factors (p = 0.041), NLR (p = 0.037), LCR (p = 0.041) and PLR (p = 0.019), the presence of gangrene (p = 0.001) and the number of lesions detected via peripheral angiography (p < 0.001) were statistically significant parameters in our study. For the group of patients with severe obstruction, all three inflammatory biomarkers were statistically significantly correlated with a serum low-density lipoprotein–cholesterol level, the number of cardiovascular risk factors, rest pain, gangrene and a risk of amputation. In addition, directly proportional relationships were found between NLR, PLR and the number of stenotic lesions (p = 0.018, p = 0.016). Also, NLR (area under the curve = 0.682, p = 0.010) and PLR (AUC = 0.692, p = 0.006) were predictors associated with a high risk of amputation in patients with an ABI < 0.5. Conclusions: in our study, we demonstrated the importance of assessing inflammatory markers in relation to the presence of cardiovascular risk factors through the therapeutic and prognostic value demonstrated in PAD.

Background and Objectives: Non-alcoholic fatty liver disease is a worldwide significant public health problem, particularly in patients with type 2 diabetes mellitus. Identifying possible risk factors for the disease is mandatory for a better understandingand management of this condition. Patatin-like phospholipase domain-containing protein 3 (PNPLA3) has been linked to the development and evolution of fatty liver but not to insulin resistance. The aim of this study isto evaluate the relationships between PNPLA3 and fatty liver, metabolic syndrome and subclinical atherosclerosis. Materials and Methods: The study group consisted of patients with type 2 diabetes mellitus without insulin treatment. The degree of liver fat loading was assessed by ultrasonography, and subclinical atherosclerosis was assessed using carotid intima-media thickness (CIMT). PNPLA3 rs738409 genotype determination was performed by high-resolution melting analysis that allowed three standard genotypes: CC, CG, and GG. Results: Among the 92 patients, more than 90% showed various degrees of hepatic steatosis, almost 62% presented values over the normal limit for the CIMT. The majority of the included subjects met the criteria for metabolic syndrome. Genotyping of PNPLA3 in 68 patients showed that the difference between subjects without steatosis and subjects with hepatic steatosis was due to the higher frequency of genotype GG. The CC genotype was the most common in the group we studied and was significantly more frequent in the group of subjects with severe steatosis; the GG genotype was significantly more frequent in subjects with moderate steatosis; the frequency of the CG genotype was not significantly different among the groups.When we divided the group of subjects into two groups: those with no or mild steatosis and those with moderate or severe steatosis it was shown that the frequency of the GG genotype was significantly higher in the group of subjects with moderate or severe steatosis. PNPLA3 genotypes were not associated with metabolic syndrome, subclinical atherosclerosis, or insulin resistance. Conclusions: Our results suggest that PNPLA3 does not independently influence cardiovascular risk in patients with type 2 diabetes mellitus. The hypothesis that PNPLA3 may have a cardioprotective effect requires future confirmation.

Background: Palliative care has emerged as a key component in the management of chronic heart failure, addressing persistent physical and psychosocial symptoms that often remain insufficiently controlled by conventional cardiology. This systematic review aimed to evaluate the impact of palliative care interventions on symptom burden, quality of life (QoL) and decision-making processes in adults with chronic heart failure. Methods: A systematic search of PubMed, Scopus and Web of Science identified studies published between January 2005 and February 2025. Eligible designs included randomized controlled trials, observational cohorts and qualitative studies. The review followed PRISMA 2020 guidelines. Methodological quality was assessed using the Cochrane Risk of Bias 2.0 (RoB 2.0), Risk of Bias in Non-Randomized Studies of Interventions (ROBINS-I) and Joanna Briggs Institute (JBI) appraisal tools. Due to heterogeneity in study designs and outcomes, a narrative synthesis was conducted. Results: Nineteen studies met the inclusion criteria. Palliative care interventions consistently reduced dyspnea, fatigue, anxiety and depression and were associated with improved functional status and QoL. Integrated palliative–cardiology programs were linked to fewer hospital readmissions, shorter hospital stays and increased documentation of advance care planning. However, methodological variability, small sample sizes and non-standardized outcome measures limited comparability across studies. Conclusions: The evidence supports the early incorporation of palliative care into routine management of chronic heart failure. Early, multidisciplinary and patient-centered approaches enhance clinical and psychosocial outcomes while improving healthcare efficiency and ensuring that care aligns with patients’ goals, values and quality-of-life priorities.