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: 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: 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: Congenital absence of pericardium is a rare cardiac disorder with a reported incidence of less than 1 in 10,000. Although most of the cases are of little clinical significance, some of them are associated with serious complications, including risk of herniation and strangulation or coronary artery compression. Detailed Case Description: We report a case of a 36-year-old male referred for routine cardiovascular examination. He had a medical history of a heart murmur since childhood. Electrocardiogram (ECG) revealed sinus rhythm, normal axis, poor R-wave progression in the precordial leads and repolarization abnormalities with negative T waves in leads V1–V4. On 2D transthoracic echocardiography (TTE), an unusual heart position was noted with poor image quality from the standard acoustic windows. The parasternal long axis view gave the impression of right ventricular dilatation. The findings raised the suspicion of left to right shunt and possible atrial septal defect. For further evaluation, the patient was referred for cardiac magnetic resonance which demonstrated complete left-sided absence of the pericardium. Discussion: Due to indistinct and atypical symptoms and lack of clinical awareness, pericardial congenital absence is frequently misdiagnosed. Patients may complain of atypical chest pain. Patient’s history and physical examination are often nonspecific. In cases with complete pericardial absence, ECG findings may include right axis deviation, right bundle block and sinus bradycardia. Echocardiography findings are also not characteristic, but some may raise the clinical suspicion of this diagnosis. The imaging modalities of choice are computed tomography and cardiac magnetic resonance. Treatment depends on the type of defect and clinical symptoms.

Transthyretin cardiac amyloidosis is a restrictive cardiomyopathy ((ATTR-CM), caused by an extracellular deposition of insoluble amyloid fibrils in the myocardium. It is a life threatening disease with life expectancy of 2 to 6 years after diagnosis. There are two types – hereditary and wild type. Recent data reveal that the wild type ATTR-CM is a common cause of heart failure with preserved ejection fraction, especially in elderly men. Hereditary ATTR amyloidosis is not so rare in Bulgaria. Five different mutations have been diagnosed, the most common being p.Glu89Gln, identified in 62 unrelated families with 117 patients and 72 mutation carriers. ATTR-CM diagnosis is often delayed or even missed, however its early recognition has become very important as a new drug, which is a transthyretin stabilizer is now available and other drugs are under development. Updated knowledge about the clinical presentation, diagnostic algorithm, available and future therapeutic options for ATTR-CM are a prerequisite for an early identification, timely treatment and better prognosis of the affected patients. The diagnosis requires a multidisciplinary approach with the participation of experienced specialists, multimodality imaging, well equipped histopathological and genetic laboratories. Establishing centres of expertise could improve the management of the patients with ATTR-CM.