Our study aims to evaluate the acute remodeling of the tricuspid valve annulus immediately after the T-TEER by using intraprocedural transesophageal three-dimensional (3D) echocardiography. We prospectively enrolled 62 consecutive symptomatic patients with at least severe TR, who underwent T-TEER with the TriClip System between March 2021 and June 2024. The following parameters were assessed using a multiplanar reconstruction analysis performed off-line using a 3D dataset: septal-lateral (SL) and antero-posterior (AP) annulus diameters; annulus area; annulus perimeter and eccentricity index. The acute procedural success was achieved in 85,5%. We observed an acute reduction in SL (from a median of 43 to 38 mm, p<0,0001), AP (from a median of 46 to 45 mm, p<0,0001), area (from a median of 17,9 to 15,95 cm², p<0,0001), perimeter (from a median of 145,5 to 137 mm, p<0,0001) and eccentricity index (from 0,92 to 0,87, p<0,0001). The TV annulus was progressively larger in patients with higher residual TR. Analysis of the subgroups according to procedural success showed an acute inverse remodeling of the TV annulus independent of the acute procedural success. The TV geometry necessitates the use of 3D echocardiography for accurate assessment of annular remodeling post T-TEER. The reduction in TR grade and TV annulus dimensions begins immediately after TriClip implantation. Concurrently, the baseline TV geometry influences the procedural results.

Background: The Ejection Fraction (EF) represents a fundamental pillar for the phenotypic classification and clinical management of cardiovascular diseases. Although trans-thoracic echocardiography (TTE) acts as the first-line examination and cardiac magnetic resonance (CMR) is the reference gold standard, cardiac computed tomography (CCT) has undergone a technological evolution. The advent of wide-detector scanners and artificial intelligence (AI) models has enabled CCT to transition from a purely morphological tool to a modality capable of comprehensive, three-dimensional morpho-functional assessments. Methods: This narrative review evaluates the literature across Scopus, MEDLINE, and Web of Science regarding the calculation of biventricular function and EF using CCT. It provides an updated summary of current clinical applications, technological advancements, and comparative diagnostic reliability against TTE and CMR. Results: The CCT “one-stop-shop” concept allows for the simultaneous acquisition of anatomical data and systolic function metrics (EDV, ESV, SV, EF), optimizing clinical workflows at no additional cost. Being intrinsically three-dimensional, CCT bypasses the geometric assumptions and apical foreshortening artifacts typical of 2D-TTE, demonstrating high volumetric concordance with CMR. Nevertheless, structural limitations persist, primarily regarding ionizing radiation exposure, contrast media toxicity, dependence on heart rhythm stability, and lower temporal resolution compared to CMR. Conclusions: EF determination via CCT has achieved technical maturity and clinical validation. While it does not intend to replace TTE or CMR, it offers synergistic data when integrated with primary anatomical indications. Furthermore, AI integration has been shown to potentially automate this workflow, transforming CCT into an opportunistic screening tool for subclinical cardiac dysfunction.

Background: Right heart failure (HF) and tricuspid regurgitation (TR) are closely interrelated conditions, linked by a bidirectional and self-perpetuating pathophysiological relationship. Alterations in right-ventricular (RV) loading conditions, pulmonary vascular impedance, and ventriculo-arterial (VA) coupling play a central role in the development and progression of TR, which in turn exacerbates RV volume overload and end-organ dysfunction. Methods: This review provides a comprehensive overview of the pathophysiology of right HF and TR, focusing on the mechanisms underlying RV dysfunction, pressure–volume (PV) relationships, and pulmonary vascular load. We further examine the clinical implications of this interaction and summarize current strategies for risk stratification, with particular emphasis on disease-specific risk models. Results: TR emerges both as a consequence and a driver of RHF. Conditions such as pulmonary hypertension (PH) and left-sided heart disease promote annular dilation and leaflet tethering, leading to functional TR. Conversely, TR increases RV volume overload, worsening chamber dilation, reducing effective forward stroke volume (SV), and accelerating disease progression. This vicious cycle results in progressive RV impairment, impaired left-ventricular filling through ventricular interdependence, and systemic venous congestion affecting renal and hepatic function. Traditional risk scores fail to capture this complex pathophysiology. In this context, TRISCORE integrates clinical, biological, and echocardiographic (TTE) parameters reflecting RV dysfunction and systemic involvement, providing a more comprehensive assessment of disease severity and prognosis. Conclusions: TR should be considered not only a marker but also a key determinant of right HF progression. A multiparametric approach integrating pathophysiology and disease-specific risk stratification is essential to identifying the optimal therapeutic window and guiding clinical decision making.

Mitral valve prolapse (MVP) is generally associated with excellent long-term outcomes when MR is absent or mild. Nonetheless, a small proportion of patients exhibit a distinct arrhythmogenic susceptibility, characterized by complex ventricular ectopy, sustained ventricular arrhythmias (VAs), and in rare instances, sudden cardiac death (SCD). This subgroup—collectively referred to as arrhythmic MVP (AMVP)—has prompted renewed attention in identifying individuals at elevated risk. Among the structural alterations associated with MVP, mitral annular disjunction (MAD) has gained recognition as a major contributor to arrhythmic vulnerability, arising from the pathological separation of the posterior annulus from the adjacent ventricular muscle. Advances in multimodality imaging, including trans-thoracic echocardiography (TTE), cardiac magnetic resonance (CMR), and cardiac computed tomography (cCT), have significantly improved delineation of MAD and clarified its relationship to the broader MVP spectrum. Current evidence suggests that MVP, MAD, and AMVP should not be regarded as isolated conditions but as intersecting phenotypes within a shared pathological framework. In certain patients, especially those without established myocardial fibrosis, abnormal annular dynamics appear to constitute the primary arrhythmogenic driver and may diminish after surgical intervention. In others, persistent arrhythmias despite optimal repair reflect a fibrosis-based substrate. This review synthesizes contemporary insights into the anatomical, biomechanical, and electrophysiological interplay linking MVP, MAD, and ventricular arrhythmogenesis, emphasizing implications for imaging-based risk assessment and individualized surgical management strategies.

While traditionally focused on coronary anatomy, cardiac computed tomography now enables non-invasive myocardial tissue characterization. By evaluating late iodine enhancement (LIE) and extracellular volume (ECV), single-energy CT (SECT) provides a valuable alternative to cardiac magnetic resonance for assessing ischemic and non-ischemic pathologies. However, clinical implementation of SECT faces technical challenges, primarily the low contrast-to-noise ratio (CNR) of iodine and the reliance on image subtraction for ECV quantification, both of which increase radiation exposure and susceptibility to spatial misregistration. To address these issues, protocol optimization is essential. Evidence-based recommendations include using low tube voltages to shift the X-ray spectrum closer to the iodine K-edge, paired with high reference tube currents. Additionally, delayed acquisition timing should be tailored to specific pathological targets to account for differences in contrast kinetics, and advanced iterative or deep learning image reconstructions should be implemented to mitigate noise. Optimized SECT demonstrates diagnostic and prognostic utility in conditions like acute myocardial infarction, hypertrophic cardiomyopathy, cardiac amyloidosis, and left ventricular thrombus detection. While spectral imaging represents the future, optimizing SECT through technical adjustments and standardized training is crucial for integrating myocardial characterization into routine workflows.

Growing evidence indicates that myocardial infarction (MI) is the clinical manifestation of heterogeneous plaque substrates with distinct molecular, cellular, and biomechanical mechanisms. Acute coronary thrombosis (ACT) most commonly arises from plaque rupture (PR), plaque erosion (PE), and calcified nodules (CNs), each associated with different inflammatory profiles, thrombus composition, clinical presentation, and prognosis. This comprehensive review provides a clinician-oriented synthesis of the pathophysiological mechanisms underlying these three principal plaque phenotypes and discusses their implications for the contemporary management of acute coronary syndromes (ACS). We examine the molecular and cellular determinants of plaque instability and highlight how systemic factors such as plaque burden, impaired healing responses, and myocardial jeopardy modulate clinical risk. The role of intracoronary and non-invasive imaging is discussed primarily as a tool to elucidate plaque biology with direct clinical relevance rather than merely as a procedural guide. Building on these insights, we propose a conceptual framework for integrating plaque biology into clinical decision-making across the acute phase, secondary prevention, and long-term follow-up. In particular, recognizing the biological heterogeneity of plaque substrates may support more personalized therapeutic strategies, enabling clinicians to tailor pharmacological and interventional approaches according to the underlying plaque phenotype and patient-specific risk profile. Finally, we briefly address emerging perspectives, including the potential role of artificial intelligence (AI) in refining plaque characterization, risk stratification, and precision cardiovascular prevention. Overall, recognition of PR, PE, and CNs as biologically distinct entities supports a shift toward mechanism-informed and personalized management of MI, aligning advances in plaque biology with the principles of precision cardiovascular medicine.