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.

Exhaled breath temperature (EBT) is a known biomarker of inflammation and airways blood flow. As opposed to previous studies, we were able to measure temperature of separate fractions of exhaled breath (fEBT) (those from the peripheral and central airways). The aim was to validate the fEBT measurement method to determine the reference values and the influence of endogenous and exogenous factors on fEBT in healthy subjects. This cross-sectional study included 55 healthy adults in whom fEBT was repeatedly measured, two days in a row, using a FractAir ^® device. Also, basal metabolic rate, level of physical activity, distance from the main road, outdoor and ambient temperature, air pressure and humidity, haematology and inflammation markers, lung function, cumulative EBT and body temperature at characteristic points on the body were measured. The results showed that fEBT from central airways was lower compared to fEBT from the periphery and that fEBTs were not related to body temperature ( p > 0.05 for all). We also showed repeatability of fEBT measurements for two consecutive days. All EBT fractions correlated significantly with ambient temperature (<0.01). No associations of fEBT with other personal and external factors were found using multivariate analysis. At room temperature of 22 °C, the physiological temperature values of the first fraction were 23.481 ± 3.150 °C, the second fraction 26.114 ± 4.024 °C and the third fraction 28.216 ± 3.321 °C. The proposed reference values represent the first part of validation of fEBT as the method for the use in clinical practice.

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.

Epicardial adipose tissue (EAT) is a distinct form of visceral adipose tissue that lies within the pericardium and directly adjacent to the myocardium. Individuals with type 2 diabetes mellitus (T2DM) exhibit excessive and metabolically active EAT, which contributes to the development of early diabetic myocardial disease, formerly referred to as diabetic cardiomyopathy. Recent studies have demonstrated that excess EAT is characterized by a proinflammatory profile that may adversely affect the underlying myocardium, leading to impaired diastolic and systolic function. In this review, we discuss the role of excessive EAT as a source of proinflammatory and profibrotic cytokines that influence adjacent ventricular and atrial myocardium through local tissue crosstalk. In addition to metabolic alterations, enlarged EAT induces hemodynamic changes that result in pericardial constraint and enhanced ventricular interdependence, both of which are hallmarks of diabetic pericardial disease. We further analyze the interplay among T2DM, inflammation, obesity, and increased EAT on the one hand, and myocardial dysfunction characterized by myocardial stiffness, elevated filling pressures, and diastolic and systolic dysfunction on the other. We emphasize that the distinct immunometabolic activity of perivascular adipose tissue may lead to a paradigm shift in the understanding of coronary artery disease, moving from a predominantly endoluminal to an exoluminal perspective. A wide range of dietary, lifestyle, and pharmacological interventions are available within this emerging diabeto-cardiometabolic continuum, each with a potential role; however, the timing of intervention is crucial. This review also explores the potential effects of antidiabetic and other pharmacological agents that modulate EAT thickness, volume, and/or activity, and discusses directions for future mechanistic and clinical research.