Background: Obstructive sleep apnea (OSA) is prevalent and often underdiagnosed in cardiology. Worldwide, approximately 936 million adults aged 30–69 are affected by OSA, with the highest numbers in the USA, China, Brazil, and India. In cardiovascular clinics, OSA is found in about 40–80% of patients with hypertension, heart failure, coronary artery disease, atrial fibrillation, or stroke. Meta-analyses link OSA to nearly twice the risk of cardiovascular disease, stroke, and all-cause mortality. Continuous positive airway pressure (CPAP) therapy addresses the underlying mechanisms of OSA and enhances intermediate cardiovascular indicators. Materials and Methods: We conducted a narrative review using major medical search engines (PubMed, Embase, Cochrane) to examine recent statements, meta-analyses, large cohorts, and key trials. The review focused on the cardiovascular burden of sleep apnea and its pathophysiology—including arrhythmic, hemodynamic, vascular, and coagulation aspects—as well as the effects of CPAP on intermediate cardiovascular outcomes. We aimed to provide a synthesised overview of current cardiovascular evidence related to the burden and mechanisms of OSA, and to summarise the effects of continuous positive airway pressure (CPAP) on intermediate and clinical cardiovascular outcomes. Results: Intermittent hypoxia, sleep fragmentation, and major negative fluctuations in intrathoracic pressure create a clear pathway leading to adverse cardiovascular outcomes. This occurs through mechanisms like sympathetic activation, RAAS activation, endothelial dysfunction, oxidative stress, and inflammation, linking OSA to these health issues. Studies show that greater severity of OSA correlates with higher cardiovascular risk, including increased incidence and recurrence of AF, resistant hypertension, and new cases of heart failure. CPAP effectively lowers AHI and enhances nocturnal oxygen levels, as well as intermediate cardiovascular indicators such as blood pressure, sympathetic activity, and certain aspects of ventricular function, with clinical benefits most evident in adherent patients. Conclusions: OSA is a significant, modifiable risk factor for cardiovascular disease. Routine cardiovascular care should include targeted screening for OSA, especially in cases of resistant hypertension, atrial fibrillation, and heart failure, along with timely sleep testing and adherence-focused CPAP therapy, in addition to traditional risk-reduction methods.

Background: Combined Pulmonary Fibrosis and Emphysema (CPFE) is a distinct syndrome characterized by upper-lobe emphysema and lower-lobe fibrosis, predominantly in older male smokers. Despite often preserved spirometric volumes, patients exhibit severely reduced diffusing capacity and high susceptibility to complications, including pulmonary hypertension (PH), acute exacerbations, and lung cancer, contributing to poor prognosis. Purpose: This review aims to synthesize current evidence on CPFE, focusing on clinical phenotype, functional impairment, differential diagnosis, complications, and emerging management strategies, highlighting distinctions from idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD). Methods: A narrative review of observational cohorts, retrospective series, and clinical studies examining CPFE patients was performed. Data on demographics, smoking history, symptomatology, pulmonary function, radiology, comorbidities, complications, and treatment approaches were extracted and integrated. Results: CPFE affects mainly males aged 65–70, with >90% reporting > 40 pack–years smoking history. Dyspnea is the cardinal symptom (>95%), often disproportionate to preserved FVC and TLC, accompanied by chronic cough in 30–70%. Exercise-induced desaturation is frequent, correlating with PH, observed in 47–90% of patients. Pulmonary function tests reveal preserved volumes, normal or near-normal FEV1/FVC, and severely reduced DLCO (35–45%), distinguishing CPFE from COPD and IPF. HRCT confirms the combined emphysematous and fibrotic pattern, critical for differential diagnosis. Acute exacerbations occur in 20–28% of cases, lung cancer in 22–46% (mostly squamous cell), and long-term oxygen therapy is required in >70%. Five-year survival is 35–55%, lower than emphysema alone and comparable or worse than IPF. Management focuses on smoking cessation, antifibrotics, oxygen therapy, and complication-specific treatments, and selected patients may undergo lung transplantation. Conclusions: CPFE is a clinically and functionally unique entity with a high burden of pulmonary and systemic complications. Accurate recognition using HRCT and DLCO, along with early intervention and tailored management, is essential to improve patient outcomes and guide prognostic stratification.

Background: Obstructive sleep apnea (OSA) impacts daytime alertness, mood, cognition, and quality of life (QoL). Initial alterations in these patient-reported outcomes (PROs) following CPAP therapy, along with their association with adherence and residual respiratory events, are only partially understood. Materials and methods: We conducted a retrospective, observational study from January 2024 to May 2025 involving adult patients with OSA. Standardized assessments were performed at baseline and at six months following the initiation of CPAP: Epworth Sleepiness Scale (ESS), WHOQOL-BREF, MoCA, DASS-21, GAD-7, and PHQ-9. The primary endpoint was the change in Patient-Reported Outcomes (PROs) and cognitive performance. The second was to identify associations between these improvements and the degree of adherence to CPAP therapy and residual AHI. Results: Seventy-two patients (median age, 57; 65.3% male) with moderate to severe OSA had a baseline median AHI of 34.5/h, ODI of 35.5/h, and a mean nocturnal SpO₂ of 92.4%. The initial burden was high: median ESS was 14, indicating excessive daytime sleepiness (EDS), present in 68.9%; median MoCA was 24, with 98.6% scoring below 26; median PHQ-9 was 7; median GAD-7 was 5; and 56.8% and 47.9% scored below 50 in physical and psychological domains of WHOQOL-BREF, respectively. After 6 months, group averages showed improvement: ESS decreased to 8.6 ± 3.7, with a 27.0% residual EDS; PHQ-9 was 7.1 ± 4.5; GAD-7 was 6.2 ± 4.1; and MoCA increased to 25.3 ± 2.7, although 48.6% still showed impairment. WHOQOL-BREF scores improved across domains: physical 58.7 ± 14.2, psychological 61.5 ± 13.6, social 63.2 ± 15.4, and environmental 59.8 ± 14.7, with fewer scores below 50 (physical 23.0%, psychological 18.9%). CPAP adherence was high, with a mean of 87.7% and a median of 95%, predicting a greater ESS reduction (p = 0.027) and showing a trend toward improvement in PHQ-9 scores (ρ = 0.218; p = 0.066). Residual respiratory indices at 6 months (AHI, ODI, SpO₂) did not correlate with PRO or cognitive scores at the same time point (all p > 0.16), nor with their change scores. Conclusions: Over the course of six months, CPAP therapy led to notable improvements in sleepiness, mood, anxiety, cognition, and overall quality of life. Nonetheless, many patients continued to face residual problems, mainly excessive daytime sleepiness (EDS) and cognitive challenges. The positive effects were more closely associated with how well patients adhered to the treatment than with remaining levels of residual AHI or ODI.

Introduction: COPD-OSA overlap syndrome (OVS) is defined by the coexistence of chronic obstructive pulmonary disease and obstructive sleep apnea syndrome in the same patient; it affects 28.3% of patients evaluated for either condition and is associated with significantly higher mortality compared to either pathology in isolation. Current therapeutic approaches, involving PAP therapy and bronchodilation, treat this syndrome as a homogeneous entity and ignore the biological heterogeneity of this patient population. Objectives: This review proposes a systematic framework for the endotypic classification of biological interactions between COPD and OSA, integrating current literature on the pathophysiological mechanisms underlying the OVS, clinically accessible biomarkers, and emerging therapies. Methods: A narrative review based on available literature, focusing on studies published between 2010 and 2026 identified via searches in PubMed, PMC, and Dove Medical Press using the terms: COPD-OSA overlap syndrome, endotype, precision medicine, phenotype, biomarker, dupilumab, and incretin-based therapies. Results: Four clinical phenotypes (obese-metabolic, emphysematous, bronchitic-hypoxemic, and hypercapnic) and three molecular endotypes (Th2/eosinophilic, neutrophilic/oxidative, and metabolic-adipokine) are proposed, each with distinct pathophysiological mechanisms and specific therapeutic implications. The interaction between the two conditions generates a unique, pronounced hypoxemic profile. We propose the “double-hit hypoxemia” model as a conceptual framework characterized by amplified systemic inflammation and increased cardiovascular risk compared to either pathology in isolation. This proposed model has not yet been prospectively validated. Dupilumab (approved for an inflammatory phenotype in COPD patients characterized by eosinophil counts ≥ 300 cells/μL) represents a promising option, though currently unsupported in the OVS population, that could nonetheless be relevant to the Th2/eosinophilic endotype of this syndrome and tirzepatide (which reduced the AHI by up to 23.8 events/hour versus placebo in the SURMOUNT-OSA trial, conducted in patients with obesity and moderate-to-severe OSA, rather than in patients with confirmed OVS) could represent a promising therapy for the metabolic-adipokine endotype of obese patients with OVS. A minimal biomarker panel, comprising blood eosinophils, FeNO, daytime PaCO₂, BMI, and T90, allows for a practical approach to identifying the dominant endotype. Conclusions: Endotyping of OVS may provide a framework for moving beyond a uniform therapeutic approach toward more individualized management based on the dominant underlying biological mechanism. Randomized clinical trials focusing on endotypic stratification and OVS cohorts remain research priorities.