Introduction: Patients with bladder cancer have a high risk of venous thrombosis that represents a key challenge for physicians in the decision-making for initiating anticoagulation therapy. Non-muscle-invasive bladder cancer (NMIBC) represents more than 70% of all diagnosed bladder malignancies; therefore, we aimed to evaluate the relationship of the neutrophil to lymphocyte ratio (NLR), lymphocyte to monocyte ratio (LMR), and risk of thrombosis by using the International Medical Prevention Registry on Venous Thromboembolism (IMPROVE) score as well as the risk of bleeding by using the IMPROVE Bleeding Risk Assessment Score in a study cohort. Material and Methods: This was a retrospective observational study involving 130 patients who met the inclusion criteria: age > 18 years, stage pTa-pT1 NMIBC. The exclusion criteria were age < 18 years; stage pT2 or higher; or a presentation of metastasis, inflammatory, liver or autoimmune diseases, or other systemic neoplasms. In order to evaluate the risk of thromboembolic events as well as those of bleeding, the IMPROVE scores were calculated for each patient. Subjects were categorized in a Low IMPROVE group (< 4 points) or a High IMPROVE group. By using uni- and multivariate regression models, we analyzed CBC-derived parameters which could be associated with a higher risk of venous thrombosis in subjects with low or high IMPROVE scores. Results: Patients with IMPROVE score greater than 4 were associated with higher NLR, LMR and lymphocyte values (p < 0.05). In a multivariate regression model, the IMPROVE score was significantly influenced by lymphocyte count (p = 0.007) as well as the NLR value (p < 0.0001). Conclusions: In our study population, subjects with NMIBC with low lymphocytes and NLR > 3 were at a higher risk of developing venous thromboembolic events, reflected by an IMPROVE score of greater than 4. The IMPROVE and IMPROVE Bleeding Risk Assessment Scores are easy to use, and, complemented with the CBC-derived lymphocyte to monocyte ratio as a prothrombotic marker, could aid in the decision of prophylactic anticoagulation therapy during admission.

We discovered a rare pathology described in adulthood, followed by the development of a long asymptomatic evolution, which underlined the importance of multidisciplinary collaboration. We present the case of a 62-year-old female smoker patient, with a known previous medical history of chronic ischemic heart disease, hypertension, chronic obstructive pulmonary disease (COPD), gastric ulcer and gastritis. The patient was rushed to the emergency room (ER) with acute respiratory failure, chest discomfort, ankle and facial edema and a chest X-ray showing a right lower pulmonary lobe consolidation, with an alarming ischemic electrocardiogram (ECG) modification without increasing myocardial cytolysis indicators. This led our medical team to investigate a possible cardiovascular event that might have been in development. After immediate admission, thoracic computer tomography (CT) imaging was carried out, which found a Morgagni diaphragmatic hernia, containing adipose tissue and the hepatic flexure of the colon with approximate dimensions of 50/100 mm. We faced differential diagnostic problems. We knew the subject’s existing cardiac and chronic respiratory tract pathologies from their previous medical history; therefore, multiple investigations and check-ups were carried out. A chest CT and surgery intervention were needed to resolve this case. Subsequently, the acute respiratory failure and alarming ischemic ECG modification disappeared.

The study of the gut microbiome is a relatively new, rapidly growing field of medicine. Alterations in intestinal microbial composition have been implicated in a range of cardiovascular pathologies, primarily atherosclerosis, coronary artery disease, heart failure, and hypertension. Dysbiosis disrupts the balance between commensal and pathogenic bacterial species, impairs gut barrier function, activates pro-inflammatory mechanisms, and modulates the production of microbiome-derived metabolites, such as trimethylamine-N-oxide, short chain fatty-acids, and secondary bile acids. Current data underline a bidirectional relationship between cardiovascular pharmacotherapy and gut barrier dysfunction, as well as changes in gut microbial ecosystem. Commonly used drugs in heart failure management, including statins and angiotensin-converting enzyme inhibitors, may exhibit higher efficacy and better bioavailability in the presence of specific bacterial phyla. Other agents, such as cardiac glycosides, are susceptible to microbial inactivation. Certain microbial taxa can also mitigate drug-induced gut barrier injury and help restore gut homeostasis - for instance, by ameliorating aspirin-related mucosal damage. This review explores the multifaceted relationship between cardiovascular medication and the gut microbiome, synthesizes current evidence, and highlights its potential significance for precision medicine in heart failure management.

Gut microbiome composition influences cardiovascular drug efficacy and safety, yet its integration into heart failure (HF) management remains underexplored. Alterations in intestinal microbial communities have been linked to atherosclerosis, coronary artery disease, heart failure, and hypertension through multiple mechanisms. Dysbiosis disrupts the balance between commensal and pathogenic bacterial species, impairing gut barrier function and activating inflammatory pathways. The altered microbial ecosystem modulates the production of key metabolites—such as trimethylamine-N-oxide (TMAO), short-chain fatty acids (SCFAs), and secondary bile acids (BAs)—that directly impact cardiovascular function. This narrative review synthesizes current evidence on bidirectional interaction between heart failure pharmacotherapy and gut microbiome composition. Commonly used drugs in heart failure management show microbiome-dependent pharmacokinetics. Digoxin undergoes bacterial inactivation by Eggerthella lenta, while angiotensin converting enzyme inhibitors and beta-blockers demonstrate enhanced efficacy with specific Firmicutes populations. Conversely, certain probiotic strains attenuate drug-induced gut barrier injury and restore gut homeostasis. Sodium–glucose cotransporter 2 inhibitors (SGLT2i), mineralocorticoid receptor antagonists, and angiotensin receptor–neprilysin inhibitors exhibit beneficial microbiome-modulating effects beyond their primary cardiovascular actions. These findings underscore the potential for microbiome-informed precision medicine in heart failure. However, significant methodological challenges must be addressed, including lack of standardization in microbiome profiling, small sample sizes, and limited longitudinal data. Future research should focus on identifying specific microbial signatures that predict drug response, developing targeted probiotic interventions, and conducting prospective clinical trials to validate pharmacomicrobiomics approaches in heart failure management.