Introduction: The aim of this prospective study was to evaluate the impact of hemodialysis (HD) on myocardial injury, of both right and left ventricle function as well as their association with venous oxygen saturation (ScvO2) alterations.Material and methods: We included in the study stable consecutive patients with end-stage renal disease (ESRD) undergoing regular HD. Right and left ventricular speckle-tracking echocardiographies were performed in all patients. The examination calculates the global systolic longitudinal strain (GLS). Blood samples were obtained from the central vein in order to measure the O2 saturation (ScvO2) levels prior and post HD. High sensitive troponin (HST) was also measured in all patients before and after HD.Results: Thirty seven patients were evaluated. We found that both mean ScvO2 and left ventricle GLS (LV GLS) were deteriorated after the dialysis session: 76.47 ±1.98 to 71.54 ±5.10, p < 0.05 and –17.73 ±3.44 to –14.21 ±3.44%, p < 0.01, respectively. HST levels were increased at the end of hemodialysis, 22.45 ±13.26 to 106.78 ±146.19 pg/ml, p < 0.01. A significant correlation was also found between the decrease of LV GLS with the ScvO2 reduction, p = 0.001, as well as with the increase of the HST levels, p = 0.001.Conclusions: Our data demonstrate that there is a significant worsening of the GLS of the left ventricle at the end of the dialysis, which is strongly associated with the concomitant deterioration of ScvO2. The may be a reliable index of circulatory stress indicating a subclinical myocardial dysfunction during HD.

Coronary artery aneurysm (CAA) and ectasia (CAE) are characterized by an abnormal dilation exceeding 1.5 times the reference diameter of the adjacent normal vessel segment. Usually, these vascular anomalies are detected incidentally during coronary computed tomography angiography or invasive coronary angiography. Their clinical significance has become increasingly recognized over time because they may be associated with myocardial ischemia, thrombosis, distal embolization, acute coronary syndromes, and adverse long-term outcomes. In adults, atherosclerosis remains the most frequent cause, while Kawasaki disease is the leading etiology in children. Many patients remain asymptomatic, and the diagnosis is often incidental. Given their variable natural history and poorly delineated prognostic implications, individualized clinical risk stratification is essential. Coronary angiography remains the gold standard for invasive assessment. Management remains controversial in the absence of randomized controlled trials establishing an optimal therapeutic strategy.

Introduction: The evaluation of myocardial contractility is essential in cardiology practice. The gold standard for this evaluation is the end-systolic elastance, but it the method involved is complex. Echocardiographic measurement of the ejection fraction (EF) is the most commonly used parameter in clinical practice, but it has significant limitations, especially in patients with afterload mismatch. In this study, the area under the curve (AUC) of the isovolumetric contraction was measured to evaluate the myocardial contractility in patients with pulmonary arterial hypertension and severe aortic stenosis. Methods: 110 patients with severe aortic stenosis and pulmonary arterial hypertension were included in this study. The AUC of the isovolumetric contraction was measured using pressure curves of the right ventricle–pulmonary artery and left ventricle–aorta ascendens. This AUC was then correlated with the echocardiographically measured EF, stroke volume (SV), and total ventricular work. Results: The AUC of the isovolumetric contraction showed a statistically significant correlation with the EF of the corresponding ventricle (p < 0.0001). Both the AUC of the isovolumetric contraction and the EF showed a statistically significant correlation with the total work of the ventricle (AUC: R2 0.49, p < 0.001; EF: R2 0.51, p < 0.001). However, the SV only showed a statistically significant correlation with the EF. A statistically significant one-sample t-test could be found for the EF (decreased, p < 0.001) and for the AUC of the isovolumetric contraction (increased, p < 0.001), but not for the total work of the ventricle. Conclusion: The AUC space of the isovolumetric contraction is a useful marker of ventricular performance in patients with afterload mismatch, showing a statistically significant correlation with the EF and the total ventricular work. This method may have potential for use in clinical practice, especially in challenging cardiological cases. However, further studies are needed to evaluate its usefulness in healthy individuals and in other clinical scenarios.

Percutaneous left atrial appendage occlusion (LAAO), patent foramen ovale (PFO) closure, and atrial septal defect (ASD) closure rely on temporary antithrombotic therapy to prevent device-related thrombus during endothelialization, yet optimal regimens remain uncertain and vary widely across clinical practice. This review synthesizes contemporary evidence on postprocedural antithrombotic strategies, comparing efficacy and safety data and identifying key gaps in knowledge. After LAAO, therapeutic approaches range from short-term anticoagulation with vitamin K antagonists or direct oral anticoagulants to dual or single antiplatelet therapy in patients with high bleeding risk; observational data increasingly support DOAC-based regimens, although device-related thrombus remains a significant concern, and follow-up imaging protocols are inconsistent. Following PFO and ASD closure, antiplatelet-only regimens—typically brief dual antiplatelet therapy followed by aspirin—are widely used, with evidence suggesting that simplified or abbreviated strategies may be sufficient in selected patients. Despite extensive clinical experience, high-quality comparative trials are limited, and optimal therapy, duration, and surveillance remain debated. Standardized imaging definitions, randomized studies, and individualized risk-based frameworks are needed to optimize antithrombotic care after atrial structural interventions.

Background: Titin (TTN), a giant structural and signaling protein of striated muscle, participates in intracellular signaling networks and cytoskeletal organization, potentially influencing cell activation, trafficking, and interactions with other tissues, including the heart. Methods: In this pilot study, 29 patients with acute myocarditis and 10 healthy individuals were prospectively enrolled. Peripheral blood was obtained on the first day of hospital admission, total RNA was isolated from peripheral blood mononuclear cells (PBMCs), and TTN mRNA expression was quantified. Results: TTN expression in PBMCs was significantly higher in patients with acute myocarditis compared with healthy controls (p = 0.015), corresponding to a 2.8-fold median increase. Moreover, TTN expression showed a strong positive correlation with global longitudinal strain impairment (Spearman’s r = 0.576, p < 0.001), a moderate positive correlation with peak hs-cTnI levels (r = 0.435, p = 0.021; and a moderate inverse correlation with baseline LVEF (r = −0.421, p = 0.025). Conclusions: These findings support a pathophysiological link between TTN-related pathways in peripheral immune cells and myocardial injury in acute myocarditis and raise the hypothesis that TTN expression in PBMCs may serve as a novel biomarker of disease severity and long-term ventricular remodeling. Further studies in larger cohorts are warranted to validate these results and to elucidate the mechanistic role of titin in immune–cardiac cross-talk.