Background: Acute decompensated heart failure (ADHF) is a condition with a high frequency of hospitalizations and mortality, and obstructive sleep apnea (OSA) is a common comorbidity. Continuous positive airway pressure (CPAP) therapy at home can be a good adjunctive non-drug therapy for these patients. Methods: We conducted a single-center, prospective cohort study from 150 consecutive patients hospitalized for heart failure exacerbation in the cardiology department. Of these, 57 patients had obstructive sleep apnea. After discharge, CPAP therapy at home was offered. We divided them into two groups and followed them for 1 year. All patients received optimal medical treatment. At the end of the period, patients underwent a follow-up physical examination, a follow-up echocardiography, and a follow-up evaluation of the Epworth Sleepiness Scale (ESS). Results: From 81 patients with sleep apnea, 72.8% (n = 59) had obstructive sleep apnea (OSA) and 27.2% (n = 22) had central sleep apnea (CSA). There was a statistically significant difference in body mass index (BMI), ESS, systolic blood pressure (SBP), diastolic blood pressure (DBP), and left ventricular ejection fraction (LVEF%) in the group with CPAP therapy compared to the no-CPAP group. The CPAP group had a median survival of 11.7 months vs. 10.1 months in the no-CPAP group (log-rank (Mantel–Cox) p = 0.044). Conclusions: This study suggests that obstructive sleep apnea is a common comorbidity in patients with acute decompensated heart failure. The addition of CPAP therapy in these patients improves the symptoms and the prognosis.

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: 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/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.

Serum uric acid (UA) is a routinely measured laboratory parameter, and elevated levels have been associated with adverse cardiovascular outcomes. However,