Cardiovascular (CV) disease remains the leading cause of morbidity and mortality worldwide, highlighting the necessity of understanding its underlying molecular and pathophysiological pathways. Conversely, physical activity (PA) and exercise are key strategies in reducing CV event risks. Detecting latent CV conditions in apparently healthy individuals, such as athletes, presents a unique challenge. The early identification and treatment of CV disorders are vital for long-term health and patient survival. Cardiac troponin is currently the most commonly used biomarker for assessing CV changes in both athletes and the general population. However, there remains considerable debate surrounding the mechanisms underlying exercise-induced troponin elevations and its release in non-ischemic contexts. Thus, there is a pressing need to identify and implement more sensitive and specific biomarkers for CV disorders in clinical practice. Indeed, research continues to explore reliable biomarkers for evaluating the health of athletes and the effectiveness of physical exercise. It is essential to analyze current evidence on troponin release in non-ischemic conditions, post-strenuous exercise, and the complex biological pathways that influence its detection. Furthermore, this study summarizes current research on cytokines and exosomes, including their physiological roles and their relevance in various CV conditions, especially in athletes. In addition, this paper gives special attention to underlying mechanisms, potential biomarkers, and future perspectives.

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.

Cardiovascular (CV) disease remains the leading cause of morbidity and mortality worldwide, highlighting the necessity of understanding its underlying molecular and pathophysiological pathways. Conversely, physical activity (PA) and exercise are key strategies in reducing CV event risk. Detecting latent CV conditions in apparently healthy individuals, such as athletes, presents a unique challenge. Early identification and treatment of CV disorders are vital for long-term health and patient survival. Thus, there is a pressing need to identify and implement more sensitive and specific biomarkers for CV disorders in clinical practice. Similarly, research continues to explore reliable biomarkers for evaluating the health of athletes and the effectiveness of physical exercise. Cardiac troponin is currently the most commonly used biomarker for assessing CV changes in both athletes and the general population. However, there remains considerable debate surrounding the mechanisms underlying exercise-induced troponin elevations and its release in non-ischemic contexts. This has led to a new research focus on biomarkers, such as exosomes and cytokines, which may provide deeper insights. This review aims to summarize current research on cytokines and exosomes, their physiological roles, and their relevance in various CV conditions, especially in athletes. Special attention is given to underlying mechanisms, potential as biomarkers, and future perspectives. Furthermore, we review current evidence on troponin release in non-ischemic conditions, post-strenuous exercise, and the complex biological pathways that influence its detection.