Jose Fernando Rodriguez Palomares

Tricuspid regurgitation (TR) is associated with adverse clinical outcomes, highlighting the need for echocardiographic assessment beyond conventional severity grading. This narrative review examines the prognostic value and clinical applicability of established and emerging echocardiographic parameters. TR phenotype influences prognosis and response to transcatheter intervention, with more favourable outcomes in atrial than ventricular functional TR. The five-grade TR classification improves risk stratification, with massive or torrential TR associated with worse outcomes despite comparable procedural success. Right ventricular–pulmonary arterial coupling provides valuable prognostic information and may help identify an optimal therapeutic window for transcatheter intervention, particularly in patients with intermediate coupling values. The GLIDE score helps predict anatomical suitability and procedural success for transcatheter edge-to-edge repair, whereas high TRI-SCORE values (≥6) identify patients in whom a significant survival benefit from repair has not been demonstrated. Treatment decisions should therefore integrate symptoms, overall clinical status, procedural feasibility, and expected benefit through individualized Heart Team assessment. Following intervention, the severity of residual TR, ideally mild or less, remains a key determinant of procedural success.

Thoracic and abdominal aortic aneurysms (TAA and AAA) progress silently, and no drug has been shown to slow their growth. Circulating lipids, statins, and metformin are candidate disease modifiers, but the evidence is heterogeneous and largely observational. We searched MEDLINE, Embase, and the Cochrane Library from inception to 24 March 2025, with an update of MEDLINE to 3 October 2026, for randomized and cohort studies of adults with established AAA or TAA. Aneurysm growth was standardized to mm/year and pooled with random-effects models when at least three comparable studies were available. Risk of bias and certainty of evidence were assessed with ROBINS-I and GRADE. Thirty-three studies were included, 32 observational and one randomized; fewer than 20% of participants were women. Circulating lipid fractions showed no consistent association with aneurysm growth. Statin use was associated with slower growth (mean difference −0.78 mm/year; 95% CI −1.13 to −0.43; I² = 92.4%; 95% prediction interval −2.02 to 0.46 mm/year), lower all-cause mortality, and fewer aortic complications. In AAA, metformin use was associated with slower growth in observational studies (−0.34 mm/year; 95% CI −0.48 to −0.20; I² = 46.3%), while the single randomized trial found no difference. Certainty of evidence was low to very low. In these largely observational data, aneurysm progression was more closely related to statin and metformin use than to circulating lipid levels, a pattern that is hypothesis-generating and from which causality cannot be inferred.

As abdominal aortic aneurysms (AAA) rupture results in a high mortality rate, early detection and risk stratification are critical for timely elective intervention. Although the maximum diameter is the sole imaging metric used to assess risk, other factors may provide complementary information. This study investigated the role of inflammation and hemodynamics in AAA progression. Methods: Patients with AAA underwent hybrid 18F-fluorodeoxyglucose ([18F]FDG) PET/CMR imaging, including a four-dimensional flow sequence and contrast-enhanced magnetic resonance angiography, and were followed to assess AAA diameter growth rate. Abdominal aorta hemodynamics and [18F]FDG PET target-to-background (TBR) were quantified at 28 standardized regions. Correlations between AAA diameter, hemodynamics, PET and growth rate were assessed. Results: Thirty-two AAA patients (84.4% men) with a median age of 73 and an interquartile range of [68; 77] years were prospectively recruited. The AAA maximum diameter was 48.1 [44.8; 55.0] mm, and the growth rate was 2.7 [1.3; 4.0] mm/year during a follow-up of 2 [1.1; 3.5] years. The AAA maximum diameter (R = 0.443, p = 0.011) and flow vorticity (R = 0.453, p = 0.009) showed significant bivariate correlation with the growth rate. When correcting for the aneurysm diameter, the helicity density was significantly correlated with the growth rate (p = 0.045), while the AAA thrombus volume was inversely associated with it (p = 0.042). Aneurysms with negative helicity density (counterclockwise rotation) grew significantly faster (p = 0.042) than those with positive helicity. In multivariable analysis, beyond the AAA diameter, the thrombus volume, helicity density and TBR were inversely related to the growth rate. Conclusions: Integrating flow, inflammatory and thrombus information may improve AAA growth rate prediction beyond the maximum aneurysm diameter.

Hypertrophic cardiomyopathy (HCM) is a common inherited myocardial disorder and a leading cause of sudden cardiac death (SCD) across all age groups. Accurate risk stratification remains a clinical challenge, as conventional algorithms fail to fully capture the heterogeneous arrhythmic substrate of the disease. In recent years, cardiac imaging has emerged as a pivotal tool for refining SCD prediction by providing detailed structural, functional, and tissue-characterisation data. This review offers a comprehensive synthesis of imaging-derived predictors of SCD in HCM. We examine established echocardiographic markers, including maximal left ventricular wall thickness, left ventricular ejection fraction and left ventricular outflow tract obstruction, together with advanced cardiovascular magnetic resonance parameters such as late gadolinium enhancement and apical aneurysm detection. In addition, we discuss the emerging role of extracellular volume expansion, quantitative mapping techniques, and strain abnormalities within the framework of contemporary risk stratification models. By bridging imaging biomarkers with underlying pathophysiological mechanisms, this review highlights current evidence, limitations, and future directions to improve precision in SCD risk assessment in HCM.

Background: Cardiac amyloidosis (CA) is frequently diagnosed in clinically stable patients, yet the risk of subsequent heart failure (HF) hospitalization remains difficult to predict using readily available tools. Early identification of high-risk outpatients is crucial to optimize follow-up and therapeutic strategies. Purpose: To develop a simple, non-invasive risk score to predict HF hospitalization in stable patients with cardiac amyloidosis using standard electrocardiographic and echocardiographic parameters. Methods: We prospectively enrolled 100 consecutive patients with confirmed cardiac amyloidosis from three tertiary centers. Baseline evaluation included clinical assessment, electrocardiography, and transthoracic echocardiography. The primary endpoint was HF hospitalization during follow-up; secondary endpoints were HF-related and all-cause mortality. Cox regression analysis was used to identify independent predictors of HF hospitalization and to derive a point-based risk (CAMY-HF) score. Results: During a median follow-up of 36 months, 55% of patients required HF hospitalization and 47% died. Low QRS voltage, interventricular septal thickness ≥14 mm, and left ventricular ejection fraction ≤40% independently predicted HF hospitalization and were incorporated into the CAMY-HF score (range, 0–4). HF hospitalization occurred in 0% of low-risk, 47.9% of intermediate-risk, and 80.6% of high-risk patients at 3 years. Higher CAMY-HF scores were also associated with increased HF-related and all-cause mortality. Conclusions: The CAMY-HF score is a simple, widely applicable tool for early risk stratification in clinically stable patients with cardiac amyloidosis. By relying on routine ECG and echocardiographic parameters, it may help identify outpatients at high risk of HF hospitalization and guide follow-up intensity and management strategies.

Heritable thoracic disease (HTAD) represents a heterogeneous group of genetic conditions predisposing to thoracic aortic aneurysm and dissection, with important implications for patients and families. Accurate diagnosis requires integration of clinical assessment—including subtle syndromic features—and molecular genetic testing, supported by family screening. While aortic root pathology is a hallmark, extra-aortic manifestations such as myocardial dysfunction, arrhythmias, premature atherosclerosis and aneurysms in distal or branch vessels are increasingly recognised, with gene-specific associations informing risk stratification. Imaging plays a central role in diagnosis and longitudinal monitoring. Transthoracic echocardiography remains the first-line tool, but cross-sectional imaging (cardiovascular magnetic resonance or cardiovascular CT) is essential for complete aortic assessment and detection of extra-aortic involvement. Surveillance intervals and imaging techniques must be standardised and tailored to genotype and clinical features. Medical therapy aims to control blood pressure and reduce aortic growth. Beta-blockers and angiotensin receptor blockers are first-line in Marfan syndrome; evidence for other HTAD subtypes is emerging. Surgical thresholds differ by genotype, emphasising the importance of personalised care. Paediatric management follows similar principles but requires adapted imaging techniques, growth-adjusted interpretation and careful timing of intervention. Pregnancy in women with HTAD demands multidisciplinary planning, individualised risk assessment and close follow-up to minimise maternal and fetal complications. Finally, recent data support moderate aerobic activity while avoiding isometric and contact sports; exercise prescriptions should be individualised. Overall, HTAD care requires lifelong, multidisciplinary, gene-informed management, integrating imaging, genetics and lifestyle considerations to optimise outcomes across the lifespan.