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.

Post-viral neuroinflammatory syndromes, particularly those occurring after SARS-CoV-2 infection, have received increasing attention due to their complex and persistent neurological manifestations. The aim of this narrative review is to integrate current evidence on the molecular and cellular mechanisms underlying chronic neuroinflammation following viral infections, with a focus on dysregulated innate immune responses, macrophage–microglia interactions, oxidative–mitochondrial stress, and impaired inflammation resolution pathways. Our synthesis shows that prolonged activation of macrophages and glial cells promotes the continuous release of pro-inflammatory mediators, while defective phagocytosis and inadequate clearance of cellular debris maintain an inflammatory microenvironment. Mitochondrial dysfunction further amplifies immune activation by stimulating metabolic stress and reactive oxygen species production. In parallel, deficiencies in mediators specialized in inflammation resolution impede the transition from inflammation to resolution, allowing neuroimmune imbalance and nociceptive sensitization to persist long after virus clearance. Key conclusions indicate that these interconnected mechanisms collectively contribute to the long-term neurological symptoms observed in post-viral states, including cognitive impairment, neuropathic pain, and fatigue. Emerging therapeutic strategies targeting cytokine signaling, microglial reactivity, mitochondrial function, and resolution pathways are promising, but remain insufficiently validated in clinical practice. Overall, evidence suggests that post-viral neuroinflammation results from the convergence of sustained immune activation and failure of endogenous resolution mechanisms, highlighting the need for further mechanistic studies and targeted interventions.

In recent years, gut microbiota has emerged as a central modulator of cardiovascular health and disease. This has led to a transition from the old understanding of cardiovascular pathology as a largely cardiac-centric problem to a systemic, multi-organ process. A growing body of evidence demonstrates that changes in the makeup of gut microbes, generally called dysbiosis, are significant in the development and progression of cardiovascular illnesses, including heart failure. Moreover, there are bidirectional interactions between the failing heart and the gut. In heart failure, impaired hemodynamics and venous congestion further worsen intestinal hypoperfusion and barrier dysfunction in a self-perpetuating cycle that exacerbates dysbiosis and systemic inflammation. The gut–heart axis offers a fresh paradigm for illness progression beyond classical neurohormonal and hemodynamic processes. The gut microbiota acts as an endocrine organ by producing bioactive metabolites such as TMAO (trimethylamine N-oxide), SCFA (short-chain fatty acids) and bile acids, which, via several routes, have a serious impact on host health and disease. This narrative review aims to summarize the current evidence for the gut microbiota as a new cardiovascular risk factor, focusing on biological mechanisms and clinical and epidemiological evidence.

Ischemic heart disease (IHD) remains the leading cause of chronic heart failure (HF) worldwide, yet the biological processes underlying this transition are not fully elucidated. Growing evidence indicates that chronic, low-grade inflammation acts as a pivotal link between ischemic injury and progressive myocardial dysfunction. Our review is the most up-to-date and structured synthesis on the pathophysiological pathways, biomarkers, and therapeutic implications of subclinical inflammation in patients with IHD at risk of developing HF. Following acute or repetitive ischemic episodes, persistent immune activation—mediated through interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α)—promotes endothelial dysfunction, microvascular instability, and extracellular matrix remodeling. These mechanisms culminate in ventricular stiffness, diastolic impairment, and adverse structural remodeling, even when left ventricular ejection fraction is preserved. Biomarkers such as Galectin-3, cancer antigen 125 (CA125), and high-sensitivity C-reactive protein (hsCRP) provide valuable insight into the interplay between fibrosis, congestion, and systemic inflammatory load, supporting early detection of subclinical myocardial injury. Advanced imaging modalities, including strain echocardiography and cardiac magnetic resonance imaging (MRI) mapping, enhance the phenotypic characterization of inflammatory cardiomyopathy. Understanding and targeting these inflammatory pathways may open new avenues for precision-based prevention and treatment, ultimately improving outcomes across the IHD–HF continuum.

Chronic obstructive pulmonary disease (COPD) is increasingly recognized as a systemic disease characterized by chronic inflammation and oxidative stress, with frequent cardiovascular involvement. This study investigated the associations between oxidative stress-related inflammatory markers and structural and electrical cardiac abnormalities in patients with COPD using a comprehensive multimodal cardiopulmonary assessment. A total of 100 clinically stable patients with COPD underwent inflammatory biomarker evaluation (IL-6, IL-8, IL-1β, and TNF-α), transthoracic echocardiography and 24 h Holter ECG monitoring. Advanced COPD was associated with significant differences in several structural cardiac parameters, including left atrial volume (p = 0.016), left atrial height (p = 0.027), and selected left ventricular parameters, while left ventricular ejection fraction remained preserved. Electrical abnormalities were significantly associated with systemic inflammatory markers. SII showed the highest discriminatory performance for sinus rhythm abnormalities (AUC = 0.736), whereas IL-6 showed the highest discriminatory performance for ventricular premature complexes (AUC = 0.732). Ventricular ectopic activity was also associated with significantly higher SII, SIRI, MLR, NLR, and PLR. Systemic inflammatory markers were associated with structural and electrical cardiac abnormalities in COPD, suggesting that they may provide complementary information regarding cardiovascular involvement. However, given the cross-sectional design and moderate discriminatory performance of these biomarkers, the findings should be considered exploratory and do not establish causal relationships. Prospective studies are needed to determine their potential role in cardiovascular risk stratification.

The gut microbiota is increasingly recognized as an important modulator of cardiovascular health, demonstrating complicated interactions among diet, metabolism, immunology and host physiology. Evidence is accumulating that changes in the composition and function of the gut microbiome may contribute to the pathogenesis of atherosclerosis, hypertension, heart failure, thrombosis and other cardiovascular phenotypes through mechanisms involving microbial metabolites, intestinal barrier dysfunction, inflammation and metabolic dysregulation. In this context, the key question of this narrative review is: how far can modulation of the gut microbiome and its metabolic functions be a clinically meaningful approach in the prevention and treatment of cardiovascular disease, and which of the currently available microbiome-targeted approaches have sufficient mechanistic and clinical evidence to justify translation into cardiovascular practice? To answer this question, we review the evidence linking the gut microbiome to major cardiovascular phenotypes, such as atherosclerosis, hypertension, heart failure, thrombosis and atrial fibrillation, with particular focus on the mechanisms through which microbial metabolites, intestinal barrier dysfunction, inflammation and metabolic dysregulation may affect cardiovascular risk. We then review current and emerging strategies for microbiome modulation, including dietary interventions, prebiotics, probiotics, synbiotics, postbiotics, fecal microbiota transplantation and targeted inhibition of microbial metabolic pathways such as trimethylamine (TMA)/trimethylamine N-oxide (TMAO) production. We also examine bidirectional interactions between cardiovascular drugs and gut microbiome and the role of these interactions in the development of precision methods to cardiovascular prevention and treatment. Finally, we outline the major limitations of the current evidence and highlight goals for future mechanistic, translational and clinical research.