Background: Obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease (COPD) are prevalent conditions with overlapping clinical features and shared consequences on autonomic function. Heart rate variability (HRV), a non-invasive biomarker of autonomic nervous system activity, may offer diagnostic, prognostic, and therapeutic insights in this patient population. Methods: A comprehensive literature review was conducted using PubMed, Google Scholar, and MEDLINE to identify peer-reviewed English-language studies published between January 2015 and December 2024. Studies were included if they evaluated HRV parameters in individuals with OSA, COPD, or overlap syndrome, explored HRV as a marker of disease severity or progression. A total of 239 studies were identified; after screening, 41 met the inclusion criteria. Results: The analysis revealed consistent evidence linking reduced HRV with both OSA and COPD severity. HRV alterations were more pronounced in overlap syndrome, reflecting synergistic autonomic dysfunction. HRV showed potential in differentiating disease stages, predicting cardiovascular risk, and evaluating treatment efficacy, particularly for CPAP therapy in OSA. Short-term HRV was particularly sensitive to autonomic changes, while long-term recordings helped track disease progression. Emerging evidence supports the use of HRV derived from wearable technologies as a viable screening tool for health and wellness. Conclusion: HRV is a valuable, non-invasive tool for assessing autonomic dysfunction in OSA, COPD, and their overlap. It offers significant potential for early diagnosis, disease monitoring, and treatment evaluation. Integrating HRV into clinical practice, could enhance diagnostic efficiency, reduce healthcare burden, and improve outcomes in high-risk respiratory populations. Furthermore, longitudinal studies are warranted to standardise HRV thresholds and validate their use in routine screening protocols.

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: Obstructive sleep apnea (OSA) is increasingly recognized as a chronic condition associated with systemic low-grade inflammation. Elevated levels of inflammatory markers such as C-reactive protein (CRP), fibrinogen, TNF-α, and IL-6 have been observed in OSA patients, independent of obesity. Tobacco use, a known pro-inflammatory factor, may further exacerbate this burden. This study aimed to evaluate whether smoking influences inflammatory markers and OSA severity in newly diagnosed patients. Methods: We conducted a retrospective, observational study on individuals newly diagnosed with OSA between 1 January 2024 and 31 December 2024 at the Clinical Hospital of Pulmonary Diseases Iași. All participants underwent overnight respiratory polygraphy using the SleepDoc Porti 9 system (Löwenstein Medical), with OSA severity classified according to the American Academy of Sleep Medicine (AASM) criteria. Inflammatory status was assessed using CRP and the erythrocyte sedimentation rate (ESR). Smokers were defined as individuals who had smoked within the past year; non-smokers had a lifetime history of fewer than 50 cigarettes. Statistical analysis was performed using IBM SPSS Statistics. Results: Smokers (n = 55) shoation Index (ODI) values, compared to non-smokers (n = 49): AHI 45.29 ± 20.94 vs. 38.40 ± 19.84 events/hour, ODI 45.69 ± 21.05 vs. 38.44 ± 19.40 events/hour (p < 0.05 for both). Mean CRP levels were approximately 3.5 times higher in smokers (10.32 ± 11.69 mg/dL) than in non-smokers (2.97 ± 2.45 mg/dL), indicating a significantly elevated inflammatory burden. Conclusions: The inflammatory burden and clinical severity of OSA may be influenced by smoking. Routine inflammatory marker screening, particularly CRP, may improve risk stratification and treatment planning in OSA patients, especially those who smoke or are obese. Routine assessment of CRP and other inflammatory markers may improve risk stratification and guide personalized treatment strategies, particularly in smokers and obese patients with OSA.

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.

Obstructive sleep apnea (OSA) is a common yet underdiagnosed condition strongly linked to the cardiovascular-kidney-metabolic (CKM) syndrome continuum, a systemic disorder characterized by interconnected metabolic, renal, and cardiovascular abnormalities. Despite overlapping risk factors, particularly obesity, current CKM staging does not formally include OSA as a potential modifier of CKM progression from early stages. Here, we conducted a narrative review revealing that OSA shares demographic and biological substrates with CKM syndrome, independently associates with cardiovascular, metabolic, and renal dysfunction through multiple shared mechanisms, and responds to intervention, including lifestyle changes, positive airway pressure, and pharmacotherapy. Integrating systematic OSA screening and management into CKM assessment, especially at early stages, may enhance risk stratification and enable personalized preventive care. This approach shows potential in mitigating disease progression and improving quality of life across the CKM spectrum. These findings support recognizing OSA as an important factor in CKM progression and highlight the potential benefits of its early identification to mitigate disease burden and improve patient outcomes.