Introduction: Trimethylamine-N-oxide (TMAO) is a metabolite produced by intestinal microbiota. It is well recognized as an independent risk marker for cardiovascular and renal diseases and mortality. Aim: The aim of the present study was to investigate the effect of Lactobacillus plantarum GLP3 supplementation on TMAO levels in 30 patients with a history of atherosclerotic cardiovascular disease after 12 weeks of treatment. Materials and methods: Thirty consecutive male patients with a history of clinical atherosclerotic cardiovascular disease were randomized in the study. TMAO levels were evaluated in human plasma samples using high-performance liquid chromatography with triple quadrupole tandem mass spectrometry and results were presented as the median (interquartile range). Microbiome sequencing analysis, focusing on bacteria from the genus Lactobacillus, was performed in 21 patients. Results: Patients receiving probiotic treatment showed a significant decrease in the TMAO levels [from 284 (139) µg/L to 202.5 (96.7) µg/L; p=0.044], with no significant change apparent in the placebo group after the treatment [from 176 (120) µg/L to 178 (150) µg/L; p=0.258]. Lactobacillus spp. % in the probiotic group was significantly increased after the interventional procedures [0.6 (0.14) before and 0.79 (0.6) after the treatment; p=0.041]. Conclusion: Probiotic supplementation with Lactobacillus plantarum GLP3 reduced the TMAO levels in very high-risk patients for cardiovascular diseases.

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.

Background: Acute decompensated heart failure (ADHF) is often associated with central sleep apnea (CSA), which exacerbates cardiovascular strain and impacts quality of life. In ADHF patients, CSA contributes to recurrent nocturnal oxygen desaturation, elevated apnea-hypopnea index (AHI), and frequent Cheyne-Stokes respiration episodes, increasing health risks. Echocardiographic monitoring is essential in these patients, providing reliable assessment of heart function over time. Sodium-glucose cotransporter-2 inhibitors (SGLT2i), initially developed for diabetes management, have shown benefi ts for renal function, sleep apnea symptoms, and heart failure outcomes, suggesting potential for multifaceted treatment. Purpose: To evaluate the effects of SGLT2i therapy on echocardiographic parameters and sleep apnea severity in patients with CSA and ADHF with reduced systolic function (HFrEF). Material and methods: We conducted a prospective cohort study with 162 patients, including those with an ejection fraction < 40%, NT-proBNP > 900 pg/ml, and AHIcentral > 5. Exclusions were patients with end-stage renal disease, NYHA class IV heart failure, COPD, or severe respiratory failure. ApneaLink™ and echocardiograms were used for assessments, and patients were followed for three months post-initiation of SGLT2i. Results: Among the 52 eligible patients, 48 completed the study. Echocardiographic improvements were signifi cant, particularly in diastolic function with a reduction in the E/e’ ratio (from 14.74 ± 2.57 to 13.64 ± 2.18, p = 0.002) and right heart function, as shown by decreases in RVOT (from 39.25 ± 4.01 to 38.32 ± 3.59, p = 0.004) and s-PAP (from 41.26 ± 5.74 to 40.07 ± 5.20, p = 0.001). TAPSE also improved (from 18.37 ± 2.17 mm to 18.87 ± 1.96 mm, p < 0.001), and the s-PAP/TAPSE ratio refl ected better right heart effi ciency (from 0.46 ± 0.11 to 0.48 ± 0.10, p < 0.001). Sleep apnea metrics also showed improvement, with reductions in AHI (from 21.35 ± 4.91 to 18.33 ± 4.75, p = 0.015), central AHI (from 13.16 ± 3.70 to 10.04 ± 3.57, p < 0.001), and Cheyne-Stokes respiration episodes (from 33.70 ± 11.20 to 26.58 ± 9.95, p < 0.001). Oxygen desaturation index (ODI) decreased (from 24.29 ± 7.01 to 17.91 ± 5.90, p < 0.001), and NT-proBNP levels, indicating heart failure severity, were reduced (from 1574.89 ± 652.80 pg/ml to 1250.35 ± 484.26 pg/ml, p < 0.001). Conclusion: SGLT2i therapy led to substantial improvements in echocardiographic measures of diastolic and right heart function, along with signifi cant reductions in CSA severity and oxygen desaturation in ADHF patients. These fi ndings support the potential of SGLT2i as an effective treatment option, meriting further study for long-term benefi ts on cardiac and respiratory health.

Introduction: Patients with diverse demographic and clinical characteristics and comorbidities are included in the category of atrial cardiomyopathy (ACM). Aim: Our study aims to evaluate the demographic, clinical, laboratory, and echocardiographic parameters of patients with ACM and to assess their impact on prognosis. Materials and methods: Only 200 of the 724 consecutively evaluated patients with dilated left atrium who met the criteria for advanced ACM were included in the analysis. Forty age- and sex-matched controls with normal left atrial volume were also included. On enrollment, all patients received a detailed echocardiography with volumetric and speckle tracking analysis, and they were followed for 36 months for cardiovascular outcomes, including mortality. Results: The mean age of the ACM population was 73.91±9.74 years, with 58% being women. Hypertension was found in 93% of them, 79% had atrial fibrillation, 60% had heart failure, 37% were obese, and 26% had diabetes. Over a median follow-up of 20.6 months, 35 deaths were registered in the ACM group compared to 1 death in the control group (17.5% vs. 2%, p=0.011). The presence of heart failure (HR 5.2, p=0.004), cancer (HR 3.7, p=0.007), severe tricuspid regurgitation (TR) (HR 5.4, p<0.001), high NT-proBNP (HR 1.4, p−17 %.

Systemic lupus erythematosus is a chronic autoimmune disorder affecting predominantly young women. Cardiac involvement in systemic lupus erythematosus is common and the typical manifestations are pericarditis, myocarditis, valvular disease, coronary artery disease, cardiac arrhythmias, and congestive heart failure. Clinical lupus myocarditis typically occurs early during lupus, in the context of high disease activity. It may present as an acute illness or have a chronic course with the development of cardiomyopathy. We present a clinical case of young patient who developed a severe dilated cardiomyopathy as a fi rst manifestation of systemic lupus erythematosus.