Obstructive sleep apnea syndrome (OSA) is increasingly recognized as a common and clinically relevant comorbidity in coronary artery disease (CAD). Epidemiological studies demonstrate that OSA is highly prevalent among patients with CAD and independently increases the risk of myocardial infarction, accelerated atherosclerosis, and recurrent adverse events. The pathophysiological mechanisms underlying this association include intermittent hypoxia, sympathetic overactivation, oxidative stress, endothelial dysfunction, systemic inflammation, metabolic dysregulation, and pro-prothrombotic changes. These processes converge to promote coronary plaque formation, instability, and ischemia. Clinical evidence indicates that OSA contributes to silent nocturnal ischemia, higher rates of acute coronary syndromes, restenosis after percutaneous coronary intervention, and worse prognosis following myocardial infarction or surgical revascularization. Continuous positive airway pressure (CPAP) therapy improves blood pressure, endothelial function, and surrogate markers of ischemia, but large randomized trials have yielded neutral results on major cardiovascular events, largely due to suboptimal adherence. However, observational studies, however, suggest improved survival in patients who are adherent to CPAP therapy. Lifestyle interventions, particularly weight reduction, remain essential adjunctive strategies. This review synthesizes current evidence, evaluates therapeutic implications, and highlights the need for systematic OSA screening in CAD populations. Future research should focus on patient phenotyping, treatment adherence, and integrated care models to improve cardiovascular outcomes.

Chronic Coronary Syndrome (CCS) significantly impacts quality of life and increases the risk of adverse cardiovascular events, remaining the leading cause of mortality worldwide. The use of sensor technology in medicine is emerging as a promising approach to enhance the management and monitoring of patients across a wide range of diseases. Recent advancements in engineering and nanotechnology have enabled the development of ultra-small devices capable of collecting data on critical physiological parameters. Several sensors integrated in wearable and implantable devices, instruments for exhaled gas analysis, smart stents and tools capable of real time biochemical analysis have been developed, and some of them have demonstrated to be effective in CCS management. Their application in CCS could provide valuable insights into disease progression, ischemic events, and patient responses to therapy. Moreover, sensor technologies can support the personalization of treatment plans, enable early detection of disease exacerbations, and facilitate prompt interventions, potentially reducing the need for frequent hospital visits and unnecessary invasive diagnostic procedures such as coronary angiography. This review explores sensor integration in CCS care, highlighting technological advances, clinical potential, and implementation challenges.

Heart failure (HF) remains a leading cause of morbidity and mortality worldwide. Despite significant advances in pharmacological therapies, responses to treatment vary widely among patients. Growing evidence suggests that genetic factors play a crucial role in influencing individual responses to HF therapies. Genetic variations, including single-nucleotide polymorphisms (SNPs), gene expression profiles, and epigenetic modifications, have been shown to affect drug metabolism, receptor sensitivity, and the molecular pathways involved in HF progression. These genetic determinants may not only predict the efficacy of common therapeutic agents such as angiotensin-converting enzyme inhibitors, beta-blockers, mineralocorticoid receptor antagonists, and sodium-glucose cotransporter-2 inhibitors, but also help identify patients at risk of adverse drug reactions. As personalized medicine continues to advance, a deeper understanding of the genetic basis of drug response in HF could enable more tailored treatment strategies, improving clinical outcomes and minimizing adverse effects. This review explores the current evidence on the genetic underpinnings of response to HF treatment and discusses its potential implications in clinical practice, highlighting current knowledge gaps.

Glucagon-like peptide-1 receptor agonists (GLP1-RAs) have demonstrated significant cardiometabolic benefits, particularly in patients with type 2 diabetes and obesity. Their role in heart failure (HF) is gaining increasing attention, with growing evidence supporting their efficacy in HF with preserved ejection fraction (HFpEF). Recent trials have shown that semaglutide improves symptoms, functional capacity, and weight loss in patients with HFpEF. However, these trials did not demonstrate a reduction in HF hospitalizations or mortality. In contrast, tirzepatide has revealed a significant reduction in cardiovascular death and worsening HF events in patients with obesity-related HFpEF, suggesting broader cardioprotective effects. Concordantly, the benefit of GLP1-RAs in the setting of HF with reduced ejection fraction (HFrEF) remains uncertain. Although their mechanisms suggest potential advantages, particularly for patients with a cardiometabolic phenotype, clinical evidence supporting improvements in major clinical outcomes is lacking. Additionally, concerns regarding risk of increased HF hospitalizations, fluid retention and arrhythmic risk have led to a cautious approach in this population. As HF management continues to evolve, GLP1-RAs emerge as a promising yet complex therapeutic option. This review synthesizes the current evidence, highlights key knowledge gaps, and explores how these medications might be integrated into guideline-directed medical therapy (GDMT) to determine their optimal role across the LVEF spectrum in HF.

Inhaled medications, commonly prescribed for respiratory conditions such as asthma and exercise-induced bronchoconstriction, are increasingly scrutinized in sports medicine due to their potential performance-enhancing effects. Bronchodilators, in particular, may improve lung function, increase oxygen delivery, and influence muscle contractility, potentially enhancing athletic performance. However, supratherapeutic use raises concerns about cardiovascular risks, including tachyarrhythmias and altered autonomic balance, as well as muscle hypertrophy and sprint capacity gains. These effects blur the line between therapeutic use and doping, creating challenges for fair competition. This review explores the mechanisms by which inhaled drugs affect the cardiovascular and muscular systems, summarizes notable doping cases, and evaluates current detection methods. Despite regulatory thresholds established by the World Anti-Doping Agency, assay interpretation remains complicated by inter-individual variability, short drug half-lives, and enantiomeric differences. Addressing these gaps requires refined pharmacokinetic modeling, enantioselective assays, and metabolomic fingerprinting to safeguard both athlete health and the integrity of sport.

Regular endurance exercise is consistently associated with lower cardiovascular mortality, a favorable cardiometabolic profile, and superior cardiorespiratory fitness. However, coronary imaging studies in master endurance athletes have raised a clinically relevant paradox: despite a low burden of conventional risk factors, some athletes—particularly older men with high lifetime exercise exposure—show a greater prevalence of coronary artery calcium and subclinical coronary plaque than sedentary or less active controls. This observation has challenged the long-standing assumption that high-volume endurance exercise is uniformly protective against coronary artery disease. A binary interpretation of this literature is inadequate. Coronary flow reserve and ischemic threshold may remain adequate in some athletes, although this concept is supported by limited functional and outcome data. Based on experimental vascular biology and indirect human evidence, repetitive high-flow states during endurance exercise generate sustained laminar shear stress, cyclic wall strain, and marked increases in coronary blood flow, thereby activating endothelial mechanotransduction pathways and influencing vascular smooth muscle cell behavior, extracellular matrix remodeling, and calcification biology. These adaptations may culminate in positive arterial remodeling, luminal enlargement, and, in some individuals, a predominantly calcified plaque phenotype. Importantly, structural remodeling does not necessarily equate to functional impairment. In selected athletes, when outward remodeling and endothelial responsiveness are preserved, coronary flow reserve and ischemic threshold may remain adequate, although this concept remains supported by limited functional and outcome data. This narrative review integrates the clinical imaging literature with current concepts in vascular mechanobiology to propose that coronary remodeling in endurance athletes exists along an adaptive–maladaptive continuum shaped by cumulative exercise load, aging, sex, conventional risk factors, and biological susceptibility. This framework may help clinicians interpret CAC/CCTA findings in athletes more appropriately and avoid equating plaque burden with equivalent functional or prognostic significance.