Background/Objectives: Hospitalizations for acute exacerbations in patients with chronic obstructive pulmonary disease (AECOPD) are connected with considerable mortality and morbidity and have a great impact on healthcare costs. We aimed to identify potentially important characteristics that distinguish patients with AECOPD that required hospitalization between those that did not. Methods: We performed a post hoc study of a previously conducted observational study assessing the discharge records of AECOPD patients who were either hospitalized or discharged directly from the emergency department (ED). Results: A total of N = 593 AECOPD patients (37.4% female) were included: N = 225 (37.9%) were hospitalized, while 368 (62.1%) were discharged from the ED. Patients had a mean age of 71 (±9.14) years. Further, 64.7% had arterial hypertension, and 60.4% of hospitalized and 42.1% of discharged patients had cardiovascular disease (excluding hypertension) (p < 0.001). In addition, 24% of hospitalized patients suffered from diabetes mellitus (vs. 16.8% of those discharged, p = 0.042). Patients that were discharged had a higher median eosinophil count than hospitalized patients (p < 0.001). Among the 368 patients discharged from the ED, 23.6% visited the ED due to AECOPD, and 50.6% were hospitalized in the subsequent three months. Patients that had at least one AECOPD in the subsequent three months had significantly lower initial eosinophil counts than those that did not (p = 0.015). Conclusions: Hospitalized AECOPD patients had a higher prevalence of pre-existing cardiovascular disease, diabetes mellitus and lower blood eosinophil counts. Patients that had subsequently visited ED in the following three months initially had lower blood eosinophil counts than those that did not make subsequent visits.

Background: Initiation criteria for biologic therapies for severe asthma are well established, but guidance on dose reduction or discontinuation remains limited. Sustained clinical remission presents an opportunity to evaluate biologic dose tapering strategies. Objective: To validate a down-titration algorithm by assessing the feasibility and safety of extending the dosing interval of anti–IL-5 biologics (mepolizumab, benralizumab) by 50% in patients with severe asthma in clinical remission. Methods: In this single-center, real-world, longitudinal study, 31 patients with severe asthma and sustained four-component remission for > 12 months were enrolled. The biologic dosing interval was extended by 25% at baseline and by 50% at 6 months if four-component remission was maintained. Remission was assessed at 26 and 52 weeks using established three- and four-component criteria. Bayesian logistic and mixed-effects models were used to evaluate clinical and biomarker outcomes. Results: Over the 12-month study period, a 50% dose interval extension was successfully achieved in 28 out of 31 patients (90%). At study end, 18 patients (58%) remained in four-component remission, while 25 (81%) met three-component remission criteria. Acute exacerbations occurred in 3 patients (10%). Comparison between benralizumab and mepolizumab showed no significant differences. While peripheral eosinophil counts increased slightly, mean levels remained below 300 cells/μL. FeNO levels showed no significant change. Conclusion: Following a 50% extension of anti–IL-5 biologic dosing intervals, full four-component clinical remission was maintained in 58% of patients, while 81% preserved three-component remission with a low exacerbation rate. These findings indicate that a uniform 50% interval extension cannot be applied universally without risk of partial loss of disease control. However, the high proportion of patients maintaining clinically meaningful 3-component remission supports the feasibility of a structured, stepwise dosing-interval extension strategy in selected patients with severe asthma, emphasizing the need for individualized implementation.

Sleep-disordered breathing (SDB)—including obstructive sleep apnea (OSA) and central sleep apnea (CSA)—is highly prevalent among individuals with heart failure (HF), yet frequently underdiagnosed. Increasing evidence shows that SDB and HF interact in a vicious cycle: recurrent hypoxic episodes, fluctuations in intrathoracic pressure, and autonomic dysregulation further strain cardiac function, while HF itself predisposes to the development of apnea. This interplay worsens arrhythmia burden, symptom severity, and long-term prognosis. This review will explore how OSA and CSA influence HF progression and outcomes, elucidate the underlying mechanisms linking these conditions, and discuss diagnostic challenges—from simple screening questionnaires to advanced telemonitoring approaches. We will critically evaluate current therapeutic options, including continuous positive airway pressure (CPAP), adaptive servo-ventilation (ASV), and emerging technologies, in light of major clinical trials and guideline recommendations. Finally, we will highlight the importance of a multidisciplinary, patient-centered approach to improve outcomes in this complex patient population.

Sleep-disordered breathing (SDB) — including obstructive sleep apnea (OSA) and central sleep apnea (CSA) — is highly prevalent among individuals with heart failure (HF), yet frequently underdiagnosed. Increasing evidence shows that SDB and HF interact in a vicious cycle: recurrent hypoxic episodes, fluctuations in intrathoracic pressure, and autonomic dysregulation further strain cardiac function, while HF itself predisposes to the development of apnea. This interplay worsens arrhythmia burden, symptom severity, and long-term prognosis. This review will explore how OSA and CSA influence HF progression and outcomes, elucidate the underlying mechanisms linking these conditions, and discuss diagnostic challenges — from simple screening questionnaires to advanced telemonitoring approaches. We will critically evaluate current therapeutic options, including continuous positive airway pressure (CPAP), adaptive servo-ventilation (ASV), and emerging technologies, in light of major clinical trials and guideline recommendations. Finally, we will highlight the importance of a multidisciplinary, patient-centered approach to improve outcomes in this complex patient population.

Background: The apnea–hypopnea index (AHI) is the conventional metric for grading obstructive sleep apnea (OSA) severity; however, it poorly reflects the true physiological impact of the disorder. The recently introduced hypoxic burden (HB) quantifies total exposure to intermittent hypoxia by integrating the duration and depth of oxygen desaturations associated with respiratory events. HB has emerged as a more biologically relevant and prognostically powerful biomarker than AHI. Methods: This narrative review summarizes the concept, methodology, and clinical significance of HB. Theoretical foundations, algorithmic approaches, and standardization challenges are discussed, along with evidence from major cohort studies evaluating the relationship between HB, cardiovascular outcomes, and treatment response. Results: HB integrates frequency, duration, and amplitude of desaturations into a continuous measure of nocturnal hypoxemia. Multiple independent cohorts (e.g., MrOS, Sleep Heart Health Study) have demonstrated that HB predicts cardiovascular morbidity and mortality more strongly than AHI. Elevated HB is associated with oxidative stress, endothelial dysfunction, sympathetic activation, and systemic inflammation. Reductions in HB during therapy with continuous positive airway pressure (CPAP), noninvasive ventilation (NIV), or oxygen supplementation correlate with improvements in hemodynamic and inflammatory markers, suggesting its potential as a dynamic therapeutic target. Conclusions: HB represents a major advance in the physiological assessment of OSA, linking sleep-related hypoxemia to biological stress and clinical outcomes. Its clinical integration—through standardized computation and incorporation into digital and AI-driven platforms—may enable personalized, physiology-based sleep medicine and establish HB as a key prognostic and therapeutic biomarker comparable to HbA1c in diabetes.