Search Results (2,385)

Background: Near-infrared spectroscopy (NIRS)-based wearable devices offer non-invasive, continuous monitoring of muscle oxygenation, providing direct microvascular and metabolic information that complements indirect indices of intensity such as heart rate and accelerometry. Their clinical applicability in chronic non-communicable diseases (NCDs) remains under active development. Methods: A structured narrative review was conducted in PubMed, Scopus, Web of Science, and IEEE Xplore (January 2010–January 2026) using pre-specified search strings combining NIRS, muscle oxygenation, SmO₂, StO₂, wearable, exercise intensity, ventilatory/lactate threshold, and individual chronic disease terms. Eligible studies addressed technical validation of wearable NIRS, NIRS-derived exercise intensity estimation, clinical applications in NCDs, or rehabilitation implementation. Evidence was synthesized thematically; quality of validation studies was appraised against AMSTAR-2-informed, COSMIN-informed, or Cochrane RoB-2 criteria. Results: Wearable continuous-wave NIRS shows acceptable concurrent validity with frequency-domain laboratory systems (r = 0.79; range 0.69–0.88; ±8% SmO₂ agreement in 95% of measurements) and good test–retest reliability for moderate-to-severe domains (ICC 0.72–0.91). NIRS-derived breakpoints align more reliably with the second ventilatory/lactate threshold (ICC = 0.80) than with the first (ICC = 0.53), constraining its use for prescribing lower-intensity domains. In chronic obstructive pulmonary disease, peripheral arterial disease, chronic respiratory failure and selected cardiovascular conditions, wearable NIRS detects disease-specific patterns of muscle deoxygenation and post-exercise reoxygenation that track responses to rehabilitation. Conclusions: Current evidence supports wearable NIRS as a complementary, intensity-aware monitoring tool—particularly for delineating the heavy/severe-intensity boundary and detecting peripheral metabolic limitations—rather than as a stand-alone replacement for ventilatory or lactate thresholds. Because much of the evidence derives from small, single-sex or athlete-only cohorts, these findings should be regarded as a promising basis requiring further validation in broader NCD populations. Implementation in NCDs requires standardized placement and calibration protocols, sex- and body composition-stratified reference values, motion-artifact mitigation, and adequately powered longitudinal trials in clinical populations. Full article

Remote patient monitoring (RPM) is widely framed as a foundational technology for the next generation of chronic-disease care. Specific applications—pacemaker follow-up, hypertension cohorts, structured heart-failure programmes, post-surgical biosensor protocols, and virtual wards—now generate measurable clinical and economic value. Yet a decade of evaluations and implementation studies suggests that the surrounding ecosystem has matured unevenly: working applications coexist with persistent cross-cutting fragility. In this Perspective we argue that four structural gaps continue to constrain RPM’s promise at scale: (i) economic models that do not credibly compensate the asynchronous clinical work that RPM generates; (ii) ambiguous frameworks for professional liability and accountability for continuous data streams, intensified by artificial-intelligence (AI)-mediated decision support; (iii) privacy, equity, and benefit-sharing arrangements that do not yet make patients unambiguous net beneficiaries—a gap visible across very different health systems internationally; and (iv) engagement and adherence dynamics that determine whether programmes deliver value at all, but are still treated as secondary outcomes. The COVID-19 emergency briefly suspended much of the friction in this ecosystem and produced a useful natural experiment: what scaled rapidly under emergency conditions, and what subsequently atrophied, illuminates which gaps are technical, which are economic, and which are institutional. We close with a six-point research and policy agenda intended to move RPM from localised successes to a trustworthy, generalisable standard of care. Full article

Cardiorenal Syndrome (CRS) types depend on the primary impaired organ, Heart (Types I/II) or Kidney (Types III/IV), and are chronic (Types II/IV) or acute (Types I/III). Type V associates to a systemic disease. Diagnosis of CRS type via biochemical indices (e.g., B-type-natriuretic-peptide (BNP), neutrophil-gelatinase-associated-lipocalin (NGAL)) has not been documented absolutely, until now. Here we used advanced imaging facilities, atomic force microscope (AFM) and scanning electron microscope (SEM) for the biopsy of peripheral blood smears coming from CRS patients, aiming to investigate the possible existence of cellular indices associated with CRS pathology. Standard biochemical and hematological indices were comparatively recorded. Cylindrical micro/nano-metric Vesicles (mnVs) were observed in all CRS patients. In CRS patients with Types III/IV, the AFM/SEM data revealed an increased mnVs population and activated platelets that may represent their potential parent cells. In these patients, increased basic uraemic indices and BNP and NGAL levels were also observed. On the contrary, in patients with CRS Types I/II/V, the AFM/SEM data showed a comparatively smaller mnVs population, accompanied by lower levels of BNP and NGAL. According to our results, a higher mnVs population was observed in CRS Types III/IV, possibly released from platelets. The mnVs population may be associated with basic uraemic indices and increased BNP and NGAL levels. Full article

Background and objective: Hypoxemia and respiratory failure (RF) in chronic obstructive pulmonary disease (COPD) are associated with exacerbations, comorbidities and increased mortality. However, the prevalence of hypoxemia and RF in stable COPD is unknown. We aimed at investigating the prevalence and determining predictive factors for chronic gas exchange abnormalities in COPD patients. Methods: A retrospective cohort study that enrolled clinically stable COPD patients referring to a pulmonary outpatient clinic. Anthropometrics, clinical characteristics, blood gas analysis and lung function were analyzed. Patients were grouped according to hypoxemia (PaO₂ <80 and ≥60 mmHg), type 1 (PaO₂ < 60 mmHg) or type II (PaO₂ < 60 and PaCO₂ > 45 mmHg) RF. A sensitivity analysis adopting an age-adjusted definition of hypoxemia was performed. Predictive factors for hypoxemia or RF were assessed with multifactorial analysis. Results: We analyzed data from 515 patients. Fixed-ratio hypoxemia, RF type 1 and type 2 were observed in 352 (68.3%), 27 (5.2%) and 43 (8.3%) patients, respectively. Risk of hypoxemia was associated with preserved alveolar volume, residual volume/total lung capacity, and lung diffusion capacity. Heart failure, ischemic heart disease, atrial fibrillation, and metabolic syndrome were predictive factors for RF. Patients with age-adjusted hypoxemia (n = 321 patients, 62.3%) showed no difference in terms of anthropometrics, lung function, and clinical characteristics as compared with fixed-threshold hypoxemia. Conclusions: Hypoxemia is frequent in stable COPD. Lung function parameters and comorbidities can support the identification of patients at risk of RF. Blood gas analysis should be always performed in patients with COPD to allow for personalized therapy and management. Full article

Background/Objectives: Patients with chronic kidney disease (CKD) have an increased risk of ischemic heart disease (IHD). Some discrepancies exist between cardiological and nephrological guidelines regarding the extent of diagnostic procedures in CKD patients who are candidates for kidney transplantation. The aim of this study was to assess the cardiac status of these patients after cardiological checkup. Methods: The present study included all kidney transplant candidates referred to the Regional Qualification Center between January 2021 and February 2024. We characterized the group of patients in whom IHD was diagnosed during the cardiological checkup. Results: Among 346 patients, IHD was newly identified in 44 (12.7%) subjects. These patients were significantly older [median 62.9 (51.9–65.4) vs. 47.2 (36.8–57.9) years; p < 0.001], had longer dialysis vintage [median 20 (12.5–42) vs. 14 (6–31) months; p < 0.05] and were more frequently diabetic (29.6 vs. 16.9%, p < 0.05) than the rest of the study cohort. Of note, they were also characterized by significantly more frequent manifestation of atherosclerosis lesions visualized using routine imaging methods (i.e., chest X-ray and abdominal aorta and iliac artery visualization). The stepwise logistic regression analysis revealed that age [OR 1.05 (1.02–1.09); p <0.01] and the ad hoc atherosclerotic score [OR 1.88 (1.27–2.77); p < 0.001] independently predicted the diagnosis of IHD during the cardiological qualification of potential kidney transplant candidates. Conclusions: During the cardiological examination, IHD was diagnosed in a substantial number of kidney transplant candidates. The presence of atherosclerotic lesions detected by routine noninvasive vascular system imaging methods may suggest the need for extending IHD diagnostics even in relatively young patients without clinical symptoms. Full article

The prevalence of diabetes and heart failure rises sharply with age, and their coexistence amplifies cardiovascular and renal risk. Elderly patients display unique clinical and biological profiles characterised by frailty, multimorbidity, and pharmacodynamic variability that challenge conventional treatment strategies. Sodium–glucose co-transporter-2 inhibitors (SGLT2i) have emerged as a cornerstone of cardio–renal–metabolic protection, with the most consistent cardiovascular benefit being the reduction in heart failure hospitalisation, whereas effects on cardiovascular death and major adverse cardiovascular events vary according to baseline cardiovascular risk, heart failure phenotype, diabetic status, and trial design. However, real-world use among the elderly remains limited due to concerns about tolerability, polypharmacy, and cost. This review analyses the pharmacological rationale and evidence base for SGLT2i therapy in older adults, highlighting mechanisms beyond glucose control, quantitative data from pivotal trials, and practical issues for geriatric implementation. Full article

Background/Objectives: Daytime sleepiness in obstructive sleep apnea (OSA) shows substantial variability and is not fully explained by disease severity. This study aimed to evaluate whether a history of cancer is associated with subjective daytime sleepiness independently of respiratory burden. Methods: In this observational cohort study, 402 untreated patients with OSA were included. Cancer history was defined as a documented diagnosis of malignancy prior to baseline polygraphy. Daytime sleepiness was assessed using the Epworth Sleepiness Scale (ESS). Multivariable linear and logistic regression models were used to evaluate the association between cancer history and ESS (continuous and dichotomized as >10), adjusting for age, sex, body mass index, smoking status, chronic obstructive pulmonary disease, and apnea–hypopnea index (AHI). Sensitivity analyses additionally adjusted for heart disease and nocturnal hypoxic burden. Results: Sixty-two patients (15%) had a history of cancer. OSA severity and hypoxemia indices were comparable between groups. In multivariable analysis, cancer history was independently associated with modestly lower ESS scores (B = −1.66, 95% confidence interval [CI] −2.96 to −0.37; p = 0.012) and a reduced likelihood of excessive daytime sleepiness (ESS > 10) (odds ratio [OR] = 0.25, 95% CI 0.07 to 0.85; p = 0.027). Conclusions: In this real-world cohort of untreated patients with OSA, cancer history is associated with modestly lower subjective daytime sleepiness despite comparable disease severity, supporting a potential dissociation between physiological burden and symptom perception. These findings indicate that reliance on subjective sleepiness alone may contribute to under-recognition of clinically relevant OSA in patients with a cancer history. Full article

Background: Advanced chronic kidney disease (CKD) and cardiovascular comorbidities frequently coexist in patients with multiple myeloma and are particularly common among hospitalized patients. However, the relationship between common cardiovascular comorbidities and advanced CKD in routine clinical practice remains incompletely characterized. Methods: We conducted a retrospective single-center cohort study including 137 hospitalized patients diagnosed with multiple myeloma between January 2015 and February 2026. Demographic, clinical, and laboratory data were extracted from electronic medical records. Advanced CKD was defined as eGFR < 30 mL/min/1.73 m², calculated using the CKD-EPI 2021 equation. Patients with isolated acute kidney injury were excluded. Cross-sectional associations between cardiovascular comorbidities and advanced CKD were assessed using logistic regression models. Results: The median age was 69 years (IQR 63–77), and 56.9% of patients were women. Renal impairment was common, with a median creatinine level of 2.82 mg/dL and a median eGFR of 22.4 mL/min/1.73 m². Advanced CKD was identified in 55 of 116 patients (47.4%) with available CKD classification. Cardiovascular comorbidities were common, including hypertension (42/55, 76.4%), diabetes mellitus (18/55, 32.7%), myocardial ischemia (41/55, 74.5%), and heart failure (25/55, 45.5%). In univariate analysis, atrial fibrillation showed a significant cross-sectional association with advanced CKD (OR 4.43, 95% CI 1.30–15.07, p = 0.017), as was myocardial ischemia (OR 2.89, 95% CI 1.07–7.80, p = 0.039). In multivariable analysis, atrial fibrillation demonstrated a trend toward an association with advanced CKD but did not remain statistically significant after adjustment. Conclusions: Advanced CKD and cardiovascular comorbidities frequently coexist in hospitalized patients with multiple myeloma. Atrial fibrillation and myocardial ischemia were associated with advanced CKD in univariate analyses; however, these associations were attenuated after multivariable adjustment. Overall, these findings provide insight into the coexistence of advanced CKD and cardiovascular comorbidities in hospitalized patients with multiple myeloma. Full article

Carbonyl stress, chronic inflammation, and progressive tissue injury accompany type 2 diabetes mellitus (T2DM) and obesity. Yet, the molecular systems that connect these processes with cardiac, vascular and neuronal complications are incompletely defined. This review examines the AGE–RAGE–DIAPH1 axis as a mechanistic link between metabolic dysfunction and diabetic myocardial and neuronal injury, with emphasis on vascular and myocardial remodeling and emerging implications for autonomic neuronal vulnerability. We summarize current evidence on the formation and accumulation of advanced glycation end-products and other RAGE ligands in metabolic disease, DIAPH1’s structural and signaling role as an intracellular effector of RAGE, and the cellular consequences of pathway activation in vascular, neural, and cardiac tissues. Across experimental models, this signaling axis promotes oxidative stress and inflammatory activation, leading to endothelial dysfunction and barrier failure. Subsequent fibrotic remodeling provides a biologically plausible route through which metabolic stress may be translated into persistent organ injury. In the heart, these mechanisms are linked to coronary microvascular dysfunction, altered cardiomyocyte phenotype, calcium handling abnormalities, and myocardial fibrosis. In the autonomic nervous system, limited but emerging data connect RAGE activation to oxidative injury and mitochondrial dysfunction, abnormal neuronal excitability, and structural vulnerability. Direct evidence linking DIAPH1 to autonomic neurons is lacking. We also review biomarker candidates related to this pathway, including circulating AGEs and soluble RAGE isoforms, skin AGE measurements, imaging markers of myocardial remodeling, and autonomic functional measures. Finally, we discuss pharmacological and natural compounds that target AGE formation, ligand accumulation, RAGE signaling, or intracellular protein interactions linked to this axis. Overall, the available evidence supports the AGE–RAGE–DIAPH1 axis as a credible mechanistic concept and a potentially informative translational hypothesis in T2DM. However, the AGE–RAGE component is supported more strongly than DIAPH1-specific involvement in human diabetic myocardial disorder or cardiovascular autonomic neuropathy. The value of DIAPH1 as a biomarker or therapeutic target in these neurocardiac complications remains to be established. Full article

Background/Objectives: Disease count alone does not show which multimorbidity combinations diversify or persist. We examined longitudinal changes in clinically recognisable multimorbidity profiles across three national ageing cohorts. Methods: Harmonised data from the China Health and Retirement Longitudinal Study (CHARLS), the English Longitudinal Study of Ageing (ELSA), and the U.S. Health and Retirement Study (HRS) were analysed. Eight physician-diagnosed chronic conditions were encoded as binary states, and wave-to-wave transitions (four windows in CHARLS and ELSA; five in HRS) were assessed within each cohort. State-level measures characterised accumulation, branching, persistence, and stabilisation sensitivity, supplemented by sensitivity analyses, BranchScore decomposition, prevalence-adjusted enrichment, and a disease-count-preserving permutation null model. Results: The analysis included 17,142 CHARLS, 10,272 ELSA, and 22,034 HRS participants, with baseline multimorbidity of 23.7%, 41.0%, and 58.5%, respectively. Transitions are concentrated around common profiles. One- and two-condition states (hypertension, diabetes, heart disease, chronic lung disease, psychiatric or emotional disorders) showed faster accumulation and greater branching; later persistent states were dominated by cardiometabolic-musculoskeletal combinations, particularly hypertension-heart disease-arthritis and hypertension-diabetes-arthritis. Targeted stabilisation produced modest perturbations exceeding random benchmarks. Count-preserving null models showed that early branching was largely structural, whereas selected lock-in states exceeded null expectations. Conclusions: Across three ageing cohorts, multimorbidity trajectories reflected disease composition as well as count. Because branching was strongly influenced by disease-count geometry, early branching states should be interpreted as structural cohort-level features of the cumulative framework rather than inherently predictive clinical entities. Selected cardiometabolic-musculoskeletal profiles were more persistent and may help frame integrated long-term management; patient-level prediction requires outcome-based studies. Full article

Vericiguat is currently indicated for patients with heart failure with reduced ejection fraction (HFrEF) following recent clinical worsening, based on evidence demonstrating a reduction in cardiovascular death or heart failure hospitalization in a high-risk population. While this positioning is clinically justified, it may underestimate the broader pathophysiological context in which soluble guanylate cyclase (sGC) stimulation may be relevant, particularly in phases of persistent biological activation following apparent clinical stabilization. In routine practice, acute coronary syndromes (ACS), acute heart failure (AHF), and chronic HFrEF are approached as distinct clinical entities. However, these conditions often represent sequential manifestations of a continuous disease trajectory driven by persistent endothelial dysfunction, impaired nitric oxide–sGC–cyclic guanosine monophosphate (NO–sGC–cGMP) signaling, and residual vascular risk. In this perspective, we revisit the mechanistic and clinical rationale for vericiguat and propose a reframing of its therapeutic role. Its greatest utility may lie in patients with recently worsening HFrEF who remain biologically vulnerable after stabilization. Extension of this concept to post-ACS populations remains hypothesis-generating and is not supported by direct clinical evidence. This “post-stabilization vulnerable state” represents a clinically recognizable yet insufficiently targeted phase, characterized by ongoing biological activation despite apparent clinical improvement. Adopting a continuum-based view of cardiovascular disease may improve alignment between pathophysiology and treatment, refine patient selection, and inform future trial design focused on this early post-event window. Importantly, this perspective is hypothesis-generating and reflects an effort to align emerging mechanistic insights with clinical trajectory, rather than to extend current indications beyond the available evidence base. Full article

Background/Objectives: Diuretic resistance is a recognized complication in patients with heart failure (HF) and is associated with worse clinical outcomes; however, information regarding its frequency and associated factors in hospitalized patients in Mexico is limited. This study aimed to describe the frequency of diuretic resistance in patients hospitalized with HF in a hospital unit in western Mexico and to identify factors associated with diuretic resistance. Methods: This retrospective study used data obtained from clinical records. Patients older than 18 years with decompensated HF whose complete clinical records included the variables of interest were included. Patients were classified according to the presence or absence of diuretic resistance. Bivariate and multivariate analyses were performed to evaluate factors associated with diuretic resistance. Results: A total of 76 patients were analyzed, and the frequency of diuretic resistance was 35.5% (n = 27). In bivariate analysis, type 2 diabetes mellitus, chronic kidney disease, elevated creatinine, urea, blood urea nitrogen (BUN), and urine protein levels, decreased glomerular filtration rate (GFR) and serum albumin, and prior treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) and angiotensin-converting enzyme inhibitors/angiotensin II receptor antagonists (ACEI/AARII) were significantly associated with diuretic resistance. In the multivariate logistic regression model, prior ACEI/AARII treatment, history of type 2 diabetes mellitus, BUN levels, and serum albumin levels remained independently associated with diuretic resistance classification. Conclusions: Diuretic resistance was frequent in this cohort of patients hospitalized with decompensated heart failure, and several clinical and biochemical factors were independently associated with its occurrence. These findings may help identify patients at higher risk of diuretic resistance, although they should be confirmed in future prospective studies. Full article

Purpose: To review the long-term cardiovascular risks associated with three common perinatal endocrine disorders—gestational diabetes mellitus (GDM), hypertensive disorders of pregnancy (HDP), and thyroid dysfunction (including postpartum thyroiditis)—and to identify opportunities for early risk stratification and prevention. Materials and Methods: We conducted a structured literature search of PubMed and Web of Science for peer-reviewed articles published between January 2000 and December 2025. Search terms included combinations related to GDM, HDP, thyroid dysfunction, and cardiovascular disease (CVD). We prioritized prospective cohort studies, meta-analyses, systematic reviews, and major clinical guidelines. Key findings were synthesized thematically. Results: GDM is associated with a 1.6- to 2-fold increased risk of future CVD, HDP with a 1.8-fold increase, and subclinical hypothyroidism with a two-fold increase. These risks persist for decades, are independent of traditional risk factors, and are amplified by obesity, recurrence, and social determinants of health. Converging pathophysiological mechanisms include persistent insulin resistance, chronic low-grade inflammation, endothelial dysfunction, autonomic dysregulation, epigenetic modifications, and subclinical myocardial remodeling. The placenta serves as a central endocrine–cardiovascular interface, releasing anti-angiogenic factors, pro-inflammatory cytokines, and exosomal microRNAs. Despite this evidence, postpartum screening uptake remains below 50%, care is fragmented, and pregnancy history is not incorporated into CVD risk calculators. Conclusion: A life-course approach integrating structured postpartum screening (6–12 weeks and annually), lifestyle interventions, targeted pharmacotherapy, and multidisciplinary cardio-obstetrics programs is urgently needed to reduce the global burden of premature heart disease, stroke, and heart failure in women. Full article

Diabetes mellitus is a complex metabolic disorder whose management has moved from glycemic control to the control of risk factors through the use of new antihyperglycemic drugs with pleiotropic effects. Despite the multiple cardio–renal benefits of sodium-glucose co-transporter 2 (SGLT2) inhibitors, their prescription is often avoided due to concerns regarding side effects. This review aims to discuss the multiple benefits of SGLT2 inhibitors in balance with one of the most concerning side effects, the risk of euglycemic diabetic ketoacidosis (EDKA). A literature search was performed to identify and select articles relevant to this topic. We accessed several databases, including PubMed, Web of Science and Scopus, using appropriate keywords. We selected and evaluated randomized controlled trials, retrospective studies, systematic reviews and meta-analysis published between 2014 and 2024 supporting the multifaceted benefits of SGLT2 inhibitors and the limitations of their recommendations and focusing on the risk of EDKA. Initially designed as antidiabetic agents, SGLT2 inhibitors have demonstrated important cardio–renal benefits, these drugs being the first-line medication in patients with established cardiovascular disease, heart failure and chronic kidney disease. SGLT2 inhibitors are associated with some potential side effects, but with contradictory data concerning their prevalence and clinical relevance. From the possible side effects, EDKA is a life-threatening metabolic emergency whose incidence and recognition has increased, in particular with the use of SGLT2 inhibitors. These drugs can cause this disorder through several mechanisms, including reduced insulin secretion and increased glucagon levels, leading to free fatty acid production, which generally occurs in the presence of some risk factors such as reduced dietary carbohydrates, intercurrent illnesses, surgical stress and alcohol consumption. Through awareness of these risk factors as well as of the clinical symptoms, this condition could be promptly avoided or managed and SGLT2 inhibitors could be safely used. Full article

Introduction: Adipose tissue (AT) is increasingly recognized as an active endocrine and immunological organ involved in the pathophysiology of heart failure with preserved ejection fraction (HFpEF). Dysfunctional AT, particularly visceral, promotes chronic low-grade inflammation, endothelial dysfunction, and microvascular damage. At the same time, higher body mass is associated with paradoxically lower natriuretic peptide (NP) levels, which may impact diagnostic accuracy in HFpEF. Methods: This narrative review summarizes the current evidence on the interplay between adipose tissue, NPs, and HFpEF, focusing on pathophysiological mechanisms, AT distribution, and clinical implications. Results: Adipokine-mediated inflammation contributes to the myocardial stiffness, fibrosis, and cardiac remodeling characteristic of HFpEF. Visceral adipose tissue, including epicardial fat, exhibits a more proinflammatory profile than subcutaneous fat. Obesity is associated with decreased NP levels due to increased clearance and decreased production. Consequently, lower NP levels may lead to underdiagnosis or misclassification of HFpEF, particularly in diagnostic algorithms such as HFA-PEFF and H₂FPEF. Patients with low BMI or cachexia exhibit elevated NP levels, reflecting advanced disease and catabolic states. Conclusions: The obesity-natriuretic paradox poses a key diagnostic challenge in HFpEF. Interpretation of natriuretic peptide levels should take body composition into account, and refinement of biomarker cutoff values may improve diagnostic accuracy. Full article