Natalia Spasova

Background: Serum albumin reflects nutritional status, inflammation, congestion, and organ dysfunction in heart failure (HF). We examined its association with recorded all-cause mortality and compared it with the prognostic nutritional index (PNI) and hemoglobin–albumin–lymphocyte–platelet (HALP) index. Methods: This retrospective single-center study included 492 patients hospitalized with decompensated HF with available serum albumin, left ventricular ejection fraction (LVEF), and N-terminal pro-B-type natriuretic peptide (NT-proBNP), classified as heart failure with reduced ejection fraction (HFrEF; LVEF < 50%) or heart failure with preserved ejection fraction (HFpEF; LVEF ≥ 50%) using the 2026 European Society of Cardiology (ESC) framework. Exact death dates were unavailable, and potential observation time varied between patients. Logistic regression evaluated each marker separately after adjustment for clinical characteristics, NT-proBNP, and renal function. Results: There were 177 recorded deaths. Lower albumin (odds ratio [OR] 1.60 per 5 g/L decrease, 95% confidence interval [CI] 1.30–1.96), PNI (OR 1.43 per 5-unit decrease, 95% CI 1.21–1.67), and HALP (OR 1.15 per 10-unit decrease, 95% CI 1.04–1.27) were associated with mortality. Adding albumin to the clinical + NT-proBNP model improved model fit (likelihood-ratio p < 0.001) and increased apparent area under the receiver operating characteristic curve (AUC) from 0.689 to 0.731; PNI and HALP yielded AUCs of 0.730 and 0.710. For the primary albumin model, bootstrap optimism correction reduced the AUC from 0.735 to 0.702, with a corrected calibration slope of 0.822. Associations were similar in the sensitivity analysis restricted to at least 12 months of potential observation. Interaction tests provided no evidence that the associations differed by HF phenotype, but did not establish equivalence. Conclusions: Lower serum albumin was associated with recorded mortality and added information beyond clinical variables and NT-proBNP. Comparisons with PNI and HALP remain exploratory. Clinical use requires external validation and follow-up with known event dates.

Background: Inflammation is increasingly recognized as an important contributor to the progression of heart failure and may partly explain differences in prognosis beyond conventional clinical characteristics. Simple laboratory-based inflammatory indices may offer additional prognostic information, but their value across different heart failure phenotypes remains uncertain. Objectives: To investigate the association between the systemic immune-inflammation index and recorded all-cause mortality across the spectrum of heart failure and to evaluate its incremental prognostic value beyond conventional clinical and laboratory variables. Patients and Methods: We evaluated the association between the systemic immune-inflammation index (SII) and recorded all-cause mortality in patients with heart failure. Multivariable logistic regression models included age, sex, heart failure phenotype, cardiovascular comorbidities, NT-proBNP, renal function, and hemoglobin. Model discrimination and calibration were assessed, and additional analyses evaluated multicollinearity, interaction with heart failure phenotype, and the functional form of the association. Results: Among 637 patients, mortality status was available for 634, of whom 165 died (26.0%). After multivariable adjustment, each doubling of SII was associated with higher odds of recorded all-cause mortality (OR 1.42, 95% CI 1.19–1.70; p < 0.001). Previous myocardial infarction, atrial fibrillation, and NT-proBNP also remained independently associated with mortality, whereas LVEF phenotype was not. No significant interaction was observed between SII and heart failure phenotype. Adding SII improved overall model fit (likelihood-ratio χ² = 16.17; p < 0.001) and increased the AUC from 0.710 to 0.732, although the difference in discrimination was not statistically significant (DeLong p = 0.076). There was no convincing evidence of marked non-linearity. Conclusions: A higher systemic inflammatory burden was independently associated with recorded all-cause mortality across the heart failure spectrum. This readily available marker may provide complementary prognostic information, but its incremental value appears modest. External validation is needed before it can be considered for routine risk assessment.

Background: Cancer-associated thrombosis is a clinically important complication of malignancy. The systemic immune–inflammation index (SII), calculated from platelet, neutrophil, and lymphocyte counts, may reflect the inflammatory background of cancer, but its value in matched heterogeneous cancer cohorts remains unclear. Objective: To evaluate whether SII is associated with thrombotic status and recorded all-cause mortality in patients with solid cancers. Methods: This retrospective matched cohort study was derived from 2020 consecutive adult patients hospitalized with solid malignancies between September 2023 and December 2025 at the Oncology Clinic of University Hospital “Tsaritsa Yoanna—ISUL”, Sofia, Bulgaria. Patients with documented thrombosis were matched 1:2 to non-thrombotic controls using a nearest propensity-score approach, with preference for exact matching on sex and cancer type. The final cohort included 110 thrombotic patients and 220 matched controls. SII was analyzed in relation to thrombotic status and recorded all-cause mortality using logistic regression. Results: Thrombotic patients and controls were well balanced for matching variables. Mortality was similar between groups: 29.1% versus 28.2%. SII did not differ significantly between thrombotic patients and controls: 772 (516–1471) versus 783 (501–1292), p = 0.655, and showed poor discrimination for thrombotic status, with an AUC of 0.515. In the overall matched cohort, higher SII was associated with recorded all-cause mortality after adjustment for thrombotic status, age, sex, cancer type, stage, and metastatic disease: OR 1.31 per 1000-unit increase, 95% CI 1.05–1.64, p = 0.016. The association was numerically stronger among thrombotic patients, but interaction testing was not statistically significant. Conclusions: SII was not associated with thrombotic status in this matched cancer cohort. Higher SII was associated with recorded all-cause mortality, suggesting that SII may better reflect systemic inflammatory burden than cancer-associated thrombosis itself.

Background/Objectives: Cardiovascular comorbidities are frequent in patients with solid malignancies, but their distribution across tumor types and their association with recorded all-cause mortality remain insufficiently defined. This study assessed clinically defined cardiovascular phenotypes across major cancer groups and examined their association with recorded all-cause mortality. Methods: We performed a retrospective cohort study of 2020 consecutive adult patients hospitalized with malignancies at University Hospital “Tsaritsa Yoanna—ISUL” between September 2023 and December 2025. Patients were classified as having respiratory, gastrointestinal, genitourinary, breast, or other solid malignancies. Four non-mutually exclusive cardiovascular phenotypes were predefined: atherosclerotic, cardiometabolic, structural heart disease, and thromboembolic. Mortality status was ascertained through the National Health Insurance Fund database and hospital electronic records. As complete time-to-event data were unavailable, mortality was analyzed as a binary outcome using multivariable logistic regression. Results: Recorded all-cause mortality occurred in 471 patients (23.3%) and differed significantly across solid tumor types (p < 0.001). Mortality was highest in respiratory cancers (42.3%), followed by gastrointestinal cancers (30.2%), other malignancies (23.5%), genitourinary cancers (14.9%), and breast cancer (9.1%). Cardiovascular phenotypes also differed across tumor groups. In the fully adjusted model, structural heart disease was associated with recorded all-cause mortality status after multivariable adjustment (OR 1.61, 95% CI 1.16–2.23, p = 0.004). The atherosclerotic phenotype showed a borderline association (OR 1.42, 95% CI 1.00–2.02, p = 0.051), whereas cardiometabolic and thromboembolic phenotypes were not associated with recorded mortality after multivariable adjustment. Model AUC was 0.771. When cardiovascular burden was modeled continuously, each additional cardiovascular factor was associated with higher odds of recorded all-cause mortality status (OR 1.12, 95% CI 1.03–1.21, p = 0.005). Conclusions: Cardiovascular profiles differed across cancer types. Structural heart disease was the most consistent cardiovascular phenotype associated with recorded all-cause mortality, while overall cardiovascular burden provided additional but modest mortality-related information. In our cohort, routinely recorded cardiovascular diagnoses helped characterize mortality-related clinical profiles. However, these findings should be viewed as observational and hypothesis-generating, and further longitudinal studies are needed before any clinical use can be recommended.

Background/Objectives: Systemic inflammation is common in patients with cancer and may reflect tumor activity, disease extent, and the patient’s overall clinical condition. The systemic immune-inflammation index (SII), calculated from neutrophil, platelet, and lymphocyte counts, is a simple marker, but its relationship with tumor type, cardiovascular burden, and mortality is not fully clarified. To compare patients with respiratory system malignancies (RSM) and gastrointestinal tract malignancies (GITM) in terms of cardiovascular comorbidity, inflammatory profile, tumor-related characteristics, and recorded all-cause mortality, and to assess the association between SII and mortality. Methods: We analyzed 879 patients with solid malignancies, including 350 with RSM and 529 with GITM. SII was calculated as platelet count × neutrophil count/lymphocyte count. Cardiometabolic and cardiovascular burden was assessed according to the number of recorded cardiometabolic risk factors and cardiovascular diseases. The main outcome was recorded all-cause mortality. Results: Patients with RSM were younger and more often male, and more frequently had stage IV disease, whereas patients with GITM had a more pronounced cardiometabolic risk profile. Mortality was higher in RSM than in GITM (42.3% vs. 29.9%), and SII was also higher in RSM (median 1117.8 vs. 716.8). In the overall cohort, higher SII was associated with mortality after adjustment for age, sex, cancer type, stage, and metastatic disease (OR 1.11 per 1000-unit increase, 95% CI 1.02–1.21; p = 0.013). Mortality increased across SII tertiles from 22.5% to 34.5% and 47.4%. Adding SII to the clinical model led to only a small increase in AUC, from 0.719 to 0.729. Conclusions: SII was higher in patients with RSM and was associated with recorded all-cause mortality. However, its added prognostic value was modest. SII should therefore be interpreted as a supportive inflammatory marker, together with tumor stage, metastatic disease, and the broader clinical condition of the patient.

Background: Obstructive sleep apnea (OSA) is a major modifiable risk factor for atrial fibrillation (AF), promoting arrhythmogenesis through intermittent hypoxia, autonomic activation, and atrial remodeling. Although continuous positive airway pressure (CPAP) effectively treats OSA, real-world evidence linking objectively measured CPAP exposure to clinically relevant AF recurrence remains limited. Aims: We aimed to evaluate the association between CPAP adherence and risk of recurrent paroxysmal AF, and to compare time to first recurrence between patients with mean nightly CPAP use ≥4 h/night versus 30 events/h) and documented paroxysmal atrial fibrillation (AF) were enrolled. Persistent and long-standing persistent AF were excluded to ensure a homogeneous population with respect to atrial substrate. OSA was assessed using home sleep apnea testing (ResMed ApneaLink), and all patients initiated continuous positive airway pressure (CPAP) therapy (ResMed AirSense 10). Objective adherence data were obtained via the ResMed AirView telemonitoring platform. Exclusion criteria included permanent AF, prior pulmonary vein isolation, central sleep apnea, left ventricular ejection fraction < 50%, end-stage chronic kidney disease (eGFR < 15 mL/min/1.73 m² or dialysis), or inability to initiate or maintain CPAP therapy. Patients were followed for 12 months. The primary endpoint was time to first documented recurrence of paroxysmal AF (≥30 s on 12-lead electrocardiography or 24-h Holter monitoring). Progression to permanent AF, defined after unsuccessful rhythm control attempts and subsequent transition to a rate control strategy, was assessed as a secondary endpoint. Time-to-event analyses used Kaplan–Meier estimates with log-rank testing, and Cox proportional hazards regression adjusted for age, body mass index, apnea–hypopnea index, heart failure, left atrial volume index, and antiarrhythmic drug therapy. Results: The final analysis included 91 patients (mean age 62.15 ± 8.29 years; 68.13% men). Mean nightly CPAP use was ≥4 h/night in 49 patients and p = 0.11). In multivariable Cox regression, binary adherence (≥4 h/night) was not independently associated with recurrence (HR 0.52, p = 0.13), whereas mean nightly CPAP use analyzed as a continuous variable remained independently associated with delayed recurrence (per 1-h increase: HR 0.66, 95% CI 0.48–0.91, p = 0.01). Progression to permanent AF occurred in 4/49 (10.0%) versus 9/42 (17.6%) patients, respectively (p = 0.29). Conclusions: In this real-world cohort of patients with severe OSA and paroxysmal AF, higher objectively measured CPAP exposure was independently associated with delayed AF recurrence when analyzed as a continuous variable, suggesting a graded association between objectively measured CPAP exposure and AF recurrence. Larger studies with extended follow-up and continuous rhythm monitoring are warranted to confirm long-term rhythm benefits and effects on AF progression.

This prospective cohort study explored the cardiometabolic, sleep-related, and biomarker effects of glucagon-like peptide-1 receptor agonists (GLP-1RA), sodium–glucose cotransporter-2 inhibitors (SGLT2i), and their combination in patients with heart failure with preserved ejection fraction (HFpEF), type 2 diabetes mellitus (T2DM), obesity, and obstructive sleep apnea (OSA). The findings revealed that therapies including GLP-1RA – either alone or in combination – consistently improved sleep apnea severity, inflammatory and glycemic biomarkers, and right ventricular–pulmonary arterial coupling. In contrast, SGLT2i monotherapy had modest effects in these domains. Notably, the addition of SGLT2i to GLP-1RA did not yield substantial additive benefits regarding sleep-related or inflammatory parameters, suggesting a dominant role of GLP-1RA. These results underscore the clinical relevance of GLP-1RA-based therapies in patients with multimorbid cardiometabolic conditions, particularly in targeting systemic inflammation and obstructive sleep apnea, both of which are critical yet often overlooked contributors to adverse outcomes in HFpEF.

Background: Sleep-disordered breathing (SDB), particularly Cheyne–Stokes respiration (CSR), is highly prevalent among patients hospitalized with acute decompensated heart failure (ADHF) and is associated with worse clinical outcomes. Sodium-glucose cotransporter-2 inhibitors (SGLT2i) have demonstrated cardiorenal benefits in heart failure, but their effects on nocturnal respiratory parameters remain underexplored. Objectives: This study aims to evaluate the impact of SGLT2i therapy on key respiratory and cardiac indices including CSR burden, oxygenation, and right heart function in patients with ADHF and reduced left ventricular ejection fraction. Methods: In this single-center prospective cohort study, 60 patients with ADHF, LVEF < 40%, and a baseline apnea–hypopnea index (AHI) > 5 were assessed before and three months after the initiation of SGLT2i therapy. Sleep respiratory parameters were measured using home polygraphy (ApneaLink^TM), while cardiac and renal indices were evaluated by echocardiography, NT-proBNP, and the estimated glomerular filtration rate (eGFR). Structural and functional echocardiographic changes were analyzed both at baseline and following the 3-month treatment period. Patient-reported outcomes were assessed using the Epworth Sleepiness Scale (ESS) and Kansas City Cardiomyopathy Questionnaire (KCCQ). Results: After 3 months of SGLT2i therapy, significant improvements were observed in daytime sleepiness (ESS: −2.68 points; p < 0.001), CSR index (−5.63 events/h; p < 0.001), AHI (−3.07 events/h; p < 0.001), ODI (−6.11 events/h; p < 0.001), and mean nocturnal SpO₂ (+1.95%; p < 0.001). KCCQ scores increased by 9.16 points (p < 0.001), indicating improved quality of life. Cardiac assessments revealed reductions in NT-proBNP (−329.6 pg/mL; p < 0.001) and E/e′ ratio (−1.08; p < 0.001), with no significant change in LVEF or chamber dimensions. Right ventricular function improved, as evidenced by the increased TAPSE/sPAP ratio (+0.018; p < 0.001). Renal function remained stable, with a non-significant upward trend in eGFR. Conclusions: This exploratory study suggests that SGLT2 inhibitors may be associated with the attenuation of Cheyne–Stokes respiration and an improvement in right heart function in patients with ADHF, warranting further investigation in controlled trials. These findings highlight the potential of SGLT2is to address overlapping cardio-respiratory dysfunction in this high-risk population.

Background: Managing acute decompensated heart failure (ADHF) is complex, particularly when combined with comorbidities like sleep apnea. Effective treatment requires personalized approaches, focusing on quality of life (QoL) and mental health outcomes. Purpose: This study explored the prevalence and characteristics of sleep apnea in patients with obesity and AHF exacerbations. It assessed how different sleep apnea phenotypes impact QoL and mental health, applying personalized medicine strategies. Methods: A prospective cohort study was conducted on 150 patients admitted for AHF exacerbation. Inclusion criteria included an Apnea–Hypopnea Index (AHI) > 5, an Epworth Sleepiness Scale (ESS) > 8, NT-proBNP > 900 pg/mL and informed consent obtained prior to participation. Optimized medical treatment was provided. QoL and mental health were evaluated using the Kansas City Cardiomyopathy Questionnaire (KCCQ) and the Beck Depression Inventory (BDI). Results: Among 81 patients with sleep apnea, 73% (n = 59) had obstructive sleep apnea (OSA) and 27% (n = 19) had central sleep apnea (CSA). OSA patients reported a higher QoL (61.12 ± 17.88) compared to CSA patients (37.18 ± 19.98, p < 0.001). CSA patients exhibited more severe depression (BDI: 26.18 ± 5.5 vs. 16.64 ± 4.1, p < 0.001). Significant correlations were noted between KCCQ and BDI scores (r = −0.849, p < 0.001) and central apnea events (r = −0.485, p < 0.001). Conclusions: Sleep apnea is common in ADHF patients, with CSA being linked to poorer QoL and greater depression. Personalized medicine offers promising strategies to enhance care and outcomes.

Transthyretin amyloidosis (ATTR) is a systemic disease characterized by the deposition of amyloid fi brils in various tissues, leading to progressive neurological manifestations and the development of cardiomyopathy, necessitating timely diagnosis and treatment. This article presents a clinical case of a 74-year-old patient with hereditary transthyretin amyloidosis (ATTRv), diagnosed using non-invasive imaging methods – echocardiography, magnetic resonance imaging, and single-photon emission computed tomography (SPECT-CT) – and confi rmed through molecular genetic analysis revealing a mutation in the TTR gene. The main clinical features of the disease, imaging fi ndings, and therapeutic strategies in the context of the presented case are discussed.