Despite all the important advances in its diagnosis and treatment, acute myocardial infarction (AMI) is still one of the most prominent causes of morbidity and mortality worldwide. Early identification of patients at high risk of poor outcomes through the measurement of various biomarker concentrations might contribute to more accurate risk stratification and help to guide more individualized therapeutic strategies, thus improving prognoses. The aim of this article is to provide an overview of the role and applications of cardiac biomarkers in risk stratification and prognostic assessment for patients with myocardial infarction. Although there is no ideal biomarker that can provide prognostic information for risk assessment in patients with AMI, the results obtained in recent years are promising. Several novel biomarkers related to the pathophysiological processes found in patients with myocardial infarction, such as inflammation, neurohormonal activation, myocardial stress, myocardial necrosis, cardiac remodeling and vasoactive processes, have been identified; they may bring additional value for AMI prognosis when included in multi-biomarker strategies. Furthermore, the use of artificial intelligence algorithms for risk stratification and prognostic assessment in these patients may have an extremely important role in improving outcomes.

Cardiovascular disease (CVD) and chronic kidney disease (CKD) often coexist and have a major impact on patient prognosis. Organ fibrosis plays a significant role in the pathogenesis of cardio-renal syndrome (CRS), explaining the high incidence of heart failure and sudden cardiac death in these patients. Various mediators and mechanisms have been proposed as contributors to the alteration of fibroblasts and collagen turnover, varying from hemodynamic changes to the activation of the renin–angiotensin system, involvement of FGF 23, and Klotho protein or collagen deposition. A better understanding of all the mechanisms involved has prompted the search for alternative therapeutic targets, such as novel inhibitors of the renin–angiotensin–aldosterone system (RAAS), serelaxin, and neutralizing interleukin-11 (IL-11) antibodies. This review focuses on the molecular mechanisms of cardiac and renal fibrosis in the CKD and heart failure (HF) population and highlights the therapeutic alternatives designed to target the responsible pathways.

Speckle tracking echocardiography is an innovative imaging technique that evaluates myocardial motion, including the function of the left atrium (LA). The assessment of the left atrium’s function across its dimensions can have diagnostic and prognostic roles in various cardiovascular conditions. Left atrial strain has been recognized as a valuable predictor of mortality and cardiovascular incidents in the general population across various conditions. For individuals with type 2 diabetes mellitus (T2DM), left atrial dysfunction, as gauged by speckle tracking echocardiography, appears particularly prognostic. Parameters such as peak atrial longitudinal strain (PALS) and left atrial stiffness have been linked with heightened risks of severe cardiovascular events, including atrial fibrillation (AF), heart failure (HF) hospitalizations, or mortality. Consequently, recognizing left atrial dysfunction early is crucial for accurate diagnosis, guiding treatment choices, comprehensive patient management, and prognosis evaluation. Using two-dimensional (2D) speckle tracking echocardiography, results from recent studies report that treatment with empagliflozin significantly enhanced LA function in patients with type 2 diabetes mellitus, improving left atrial strain (LAS) contraction and reservoir values. Furthermore, treatments with glucagon-like peptide-1 (GLP)-1 receptor agonists and sodium–glucose cotransporter-2 (SGLT-2) inhibitors were shown to improve LA reservoir strain more effectively than insulin alone, suggesting their potential in reducing cardiovascular complications in T2DM patients. This narrative review further addresses ongoing challenges and potential enhancements needed to boost the clinical value of left atrium strain, emphasizing its significance in managing and improving outcomes for diabetic patients.

Coronary artery disease is the leading cause of death worldwide, and its main pathological substrate is represented by atherosclerosis. Inflammation is a major promoter of the atherosclerotic process and is involved in both the initiation and progression of atherosclerosis, as well as in the occurrence of fatal complications. Until the present moment, Colchicine Cardiovascular Outcomes Trial is the largest trial to demonstrate a major benefit of low-dose colchicine on major adverse cardiac events in patients with recent myocardial infarction (MI), but the mechanisms behind this relation are not completely known. The purpose of this review is to emphasize the possible pathways through which colchicine improves the clinical outcomes in the acute setting of acute coronary syndromes by referring to the results of the studies published in the past 5 years. Aside from its stated systemic anti-inflammatory effect, colchicine could be a valuable addition to the therapeutic approach of acute MI by reducing the infarct size, stabilizing the coronary plaque, as well as reducing platelet aggregation. Moreover, colchicine may improve endothelial function, reduce the transcoronary release of cytokines, and prevent a rise in inflammatory markers after percutaneous coronary intervention, thus diminishing the residual inflammatory risk.

Background/Objectives: As population aging increases the prevalence of atrial fibrillation (AF), the use of direct oral anticoagulants (DOACs) has expanded for thromboembolism prevention. Although DOACs offer advantages over vitamin K antagonists (VKAs), gastrointestinal bleeding (GIB) remains the most common extracranial adverse event. Current guidelines address global bleeding risk but provide limited guidance on site-specific gastrointestinal risk assessment and prevention. This narrative review aims to summarize current evidence on the mechanisms, etiologies, and risk factors for DOAC-associated gastrointestinal bleeding and to propose a pragmatic, risk-based framework to support clinicians in individualized bleeding prevention. Methods: A narrative review of studies published between 2004 and 2025 was conducted, including randomized clinical trials, real-world evidence, meta-analyses, and major society guidelines. Evidence addressing DOAC safety profiles, gastrointestinal bleeding etiologies, patient-level risk factors, medication interactions, and preventive strategies was analyzed. Results: Gastrointestinal bleeding in patients treated with DOAC is strongly influenced by underlying gastrointestinal pathology, comorbid conditions, and concomitant medications. Established risk factors include prior gastrointestinal hemorrhage, Helicobacter pylori infection, gastrointestinal malignancy, diverticulosis, and angiodysplasia, as well as the use of nonsteroidal anti-inflammatory drugs (NSAIDs), antiplatelet therapy, or selective serotonin reuptake inhibitors (SSRIs). DOACs differ in gastrointestinal safety: apixaban consistently demonstrates the most favorable profile, whereas rivaroxaban and high-dose dabigatran show higher GIB rates. Preventive strategies such as H. pylori testing and eradication, proton pump inhibitor use in high-risk individuals, avoidance of NSAIDs and unnecessary antiplatelet therapy, and individualized DOAC selection may help reduce bleeding risk. Conclusions: Gastrointestinal bleeding risk in patients receiving DOAC therapy should be assessed using a site-specific and dynamic approach. A structured strategy integrating baseline risk evaluation, correction of modifiable factors, tailored anticoagulant selection, and risk-adapted follow-up may improve the safety of anticoagulation. The proposed framework may provide a pragmatic approach to individualized bleeding risk mitigation while preserving the benefits of DOAC therapy; however, prospective validation is required before its routine implementation can be recommended.