Background: Diabetic cardiomyopathy is a major contributor to cardiovascular morbidity, often progressing silently before overt heart failure. Left atrial (LA) strain, assessed via speckle-tracking echocardiography, could serve as an early indicator of subclinical myocardial dysfunction in patients with type 2 diabetes mellitus (T2DM). Objectives: The objectives of this study were to evaluate LA strain parameters in patients with T2DM versus non-diabetic controls and investigate their association with glycemic control and diabetes duration. Methods: This cross-sectional study, designed according to STROBE reporting guidelines, included 47 participants (25 with T2DM and 22 controls) undergoing comprehensive echocardiographic and biochemical evaluation. LA reservoir (LASr), conduit (LAScd), and booster-pump (LASbp) strain values were measured. Associations with glycosylated hemoglobin (HbA1c) and diabetes duration were assessed via multivariate analysis. ROC curves were used to evaluate predictive performance. Results: Diabetic patients had significantly lower LASr (20.4 ± 7.25% vs. 26.7 ± 8.0%, p = 0.007), LAScd (−10.9 ± 5.4% vs. −15.6 ± 6.5%, p = 0.010), and LASbp (−9.9 ± 4.2% vs. −12.9 ± 5.0%, p = 0.034). LASr and LAScd remained independent predictors in multivariate models. ROC analysis showed good discrimination (AUC: LAScd = 0.78; LASr = 0.73). Conclusions: This study demonstrates that LASr and LAScd are independently associated with type 2 diabetes mellitus and can reliably identify subclinical atrial dysfunction before the onset of structural or symptomatic heart disease.

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.

Background and Objectives: Type 2 diabetes (T2DM) substantially increases cardiovascular risk; beyond the well-recognized left-ventricular involvement in diabetic cardiomyopathy, emerging data indicate subclinical right-ventricular (RV) dysfunction may also be present. This study aimed to evaluate whether speckle-tracking echocardiography identifies subclinical right-ventricular systolic dysfunction in type 2 diabetes, despite normal conventional indices and preserved global systolic function. Materials and Methods: We conducted a cross-sectional, single-center study in accordance with STROBE recommendations, enrolling 77 participants, 36 adults with T2DM, and 41 non-diabetic controls, between December 2024 and July 2025. All participants underwent comprehensive transthoracic echocardiography, including conventional parameters (tricuspid annular plane systolic excursion (TAPSE), tricuspid annular systolic velocity (TV S’), right ventricular fractional area change (RVFAC)) and deformation imaging (right ventricular global longitudinal strain (RV GLS), right ventricular free wall longitudinal strain (RVFWS)) using speckle-tracking echocardiography. Biochemical and clinical data, including glycosylated hemoglobin (HbA1c), were recorded. Correlation and ROC curve analyses were performed to explore associations and predictive value. Results: The mean age was comparable between the two groups (62.08 ± 9.54 years vs. 60.22 ± 13.39 years; p = 0.480). While conventional RV parameters did not differ significantly between groups, diabetic patients had significantly lower RV GLS (−13.86 ± 6.07% vs. −18.59 ± 2.27%, p < 0.001) and RVFWS (−15.64 ± 4.30% vs. −19.03 ± 3.53%, p < 0.001). HbA1c levels correlated positively with RV strain impairment (RVFWS r = 0.41, p < 0.001). Both RV GLS and RVFWS were independent predictors of RV dysfunction in logistic regression analysis. ROC analysis showed good diagnostic performance for RV GLS, AUC = 0.84 with an optimal cut-off −17.2% (sensitivity 86.1% and specificity 80.5%) and RVFWS, AUC = 0.76 with cut-off −17.6% (sensitivity 77.8; specificity 80.5%) in identifying early myocardial involvement. Conclusions: RV systolic dysfunction may occur early in T2DM, even when traditional echocardiographic indices remain within normal limits. Speckle-tracking echocardiography, particularly RV GLS and RVFWS, offers sensitive detection of subclinical myocardial impairment, reinforcing its value in early cardiovascular risk stratification among diabetic patients.

Background/Objectives: To determine whether left atrial (LA) strain by speckle-tracking echocardiography can identify supraventricular arrhythmia risk in patients with type 2 diabetes mellitus (T2DM) without overt structural heart disease. Methods: Prospective, single-center observational cohort study including 107 adults: 57 with T2DM and 50 age-matched controls. Participants underwent clinical assessment and echocardiography at baseline and 12 months. LA reservoir, conduit, and contractile strain (LASr, LAScd, LASct) were measured; left atrial volume indexed (LAVI) and LA stiffness index (LASI) were calculated. The primary endpoint was clinically significant supraventricular arrhythmia at 12 months on 24 h Holter (atrial fibrillation (AF)/atrial flutter (AFL) ≥ 30 s and/or excessive supraventricular ectopy). Predictors were assessed using penalized logistic regression and discrimination by ROC analysis. Results: At baseline and 12 months, T2DM showed impaired LA mechanics versus controls (baseline: LASr 20.1 ± 5.7 vs. 25.8 ± 6.3%, LAScd −11.6 ± 4.2 vs. −15.6 ± 4.9%, LASct −9.9 ± 3.2 vs. −13.1 ± 3.7%; all p < 0.001) and higher LASI (0.4 ± 0.2 vs. 0.3 ± 0.1, p < 0.001). LAVI was higher in T2DM at 12 months (34.0 ± 7.0 vs. 29.9 ± 6.5 mL/m², p = 0.003). Supraventricular arrhythmias occurred in 20/57 patients (35.1%) of the T2DM vs. 1/50 patients (2.0%) of the control group (p < 0.001). Arrhythmias were assessed by 24 h Holter monitoring at the 12-month follow-up. In T2DM, LAScd provided the best single-parameter discrimination (AUC 0.692), with an optimal cut-off around −8% (sensitivity 55.6%, specificity 81.8%); a LAScd+left ventricular ejection fraction (LVEF) model improved AUC to 0.772. Conclusions: In this prospective observational cohort, T2DM was associated with subclinical LA dysfunction and a higher burden of supraventricular arrhythmias. LAScd emerged as the most clinically informative LA deformation marker for arrhythmic risk stratification and may support targeted rhythm surveillance in diabetic patients. These findings require external validation in larger, independent multicenter cohorts.

Background: Acute myocardial infarction (AMI) in younger adults represents a distinct clinical entity with biological features that may differ from those observed in later-onset disease. We aimed to characterize age-dependent clinical, inflammatory, lipid, and echocardiographic phenotypes and to explore their association with in-hospital adverse clinical events. Methods: In this prospective, single-center, age-stratified observational study conducted between 20 January 2024 and 20 January 2025, 90 patients with AMI undergoing successful percutaneous coronary intervention (PCI) were selected from 1051 AMI admissions: 30 aged 25–44 years and 60 aged ≥45 years. Admission biomarkers (including C-reactive protein, leukocyte-derived indices, and lipid parameters) and echocardiographic variables (left ventricular ejection fraction and global longitudinal strain) were assessed, and exploratory receiver operating characteristic analyses were performed for in-hospital adverse clinical events. Results: Younger patients demonstrated a predominantly atherogenic profile, with higher smoking prevalence (63.3% vs. 13.3%; p < 0.001) and markedly higher lipoprotein(a) concentrations (76.18 ± 10.10 vs. 17.61 ± 11.42 mg/dL; p < 0.001). Older patients exhibited higher inflammatory indices (NLR and SII), higher hs-cTnI and NT-proBNP concentrations, and worse ventricular function. STEMI predominated in both age groups (83.3% in each), and infarct localization did not differ significantly between younger and older patients. The rate of in-hospital adverse clinical events was numerically higher in older patients (18.3% vs. 10.0%), but this difference was not statistically significant. In exploratory ROC analyses, CRP (AUC = 0.874) and LVEF (AUC = 0.868) showed the highest discriminatory performance. Conclusions: AMI appears to manifest through age-related baseline phenotypes: a more atherogenic/thrombotic profile in younger patients and a more inflammatory/ventricular dysfunction profile in older patients. CRP and LVEF emerged as the strongest exploratory discriminators of in-hospital adverse clinical events, but these findings require validation in larger cohorts.