Elevated lipoprotein(a) (Lp[a]) is a prevalent, lifelong, and genetically determined causal cardiovascular risk factor, associated with a wide spectrum of cardiovascular disease, including atherosclerotic coronary artery disease, aortic stenosis, ischemic stroke, and peripheral vascular disease. This review aims to: examine the evolving therapeutic landscape for Lp(a), concisely summarize results from preclinical work and ongoing clinical trials of novel pharmacologic and gene-based therapies, and contextualize their potential role in cardiovascular disease prevention.

The Konect Resilia valved conduit (Edwards Lifesciences) was designed for aortic valve and root replacement. This article aims to describe its use in the pulmonary position (off-label). This graft is particularly convenient when the pulmonary bifurcation needs to be reconstructed. In the described case, prosthetic replacement and reimplantation of the pulmonary artery branches were necessary. Of note, in patients with previous Lecompte maneuver, bifurcated Dacron conduits should not be used to replace pulmonary artery branches given the risk of severe stenosis in the short term.

Calcific aortic valve disease is common in older adults and a major cause of aortic stenosis. Despite its clinical impact, there are still no effective drugs that slow disease progression, and treatment largely relies on surgical or transcatheter valve replacement once stenosis becomes severe and symptomatic. Beyond established roles for inflammation and tissue remodeling, recent evidence suggests that chemical modifications of RNA may influence how valve cells shift toward fibro-calcific states. In this study, we compared human valvular interstitial cells isolated from non-calcified valves and from fibro-calcific stenotic valves, profiling RNA modifications using direct RNA sequencing. The resulting epitranscriptomic patterns clearly separated control from diseased cells and revealed an overall increase in detected modification sites in disease, alongside site-specific gains and losses across selected transcripts. Network-based prioritization highlighted genes linked to extracellular matrix remodeling and inflammatory signaling, pointing to stress-responsive regulators as notable candidates. Overall, these findings support the idea that disease-associated RNA modification remodeling accompanies, and may help shape, key cellular programs in calcific valve disease, providing a focused set of targets for future functional validation and potential non-surgical therapeutic exploration.

Congenital Heart Disease (CHD) encompasses a range of structural abnormalities of the heart and great vessels present at birth and is associated with significant lifelong morbidity, including heart failure and arrhythmias. Early diagnosis is critical for optimizing perinatal management and improving outcomes. This review focuses on early fetal echocardiography, a specialized ultrasound technique that enables detection of cardiac abnormalities in utero, as early as 11-14 weeks of gestation, compared to traditional imaging performed at approximately 20 weeks. Advancements in early imaging have improved the identification of high-risk fetuses, particularly those with genetic predispositions or family history of CHD, allowing for earlier clinical decision-making and intervention planning. In select cases, prenatal detection facilitates in utero management of conditions such as aortic stenosis and hypoplastic left heart syndrome. Additionally, emerging applications of artificial intelligence (AI) have enhanced image analysis and diagnostic accuracy, supporting clinicians in the early recognition of CHD. Despite these advances, challenges remain, including variability in diagnostic accuracy in early gestation, risk of false positives, and limited access to specialized imaging technologies. Continued integration of AI-driven tools and the development of standardized screening protocols hold promise for improving diagnostic consistency and long-term outcomes in patients with CHD.

Cardiac Damage Staging (CDS) is associated with prognosis and may evolve after transcatheter aortic valve replacement (TAVR). However, the prognostic value of CDS at 1-year and the trajectory of CDS, and its underlying factors, remains unclear. From a single-center registry, patients who underwent TAVR between 2016 and 2023 and had echocardiographic assessment at baseline, immediately post-TAVR, and 1-year, were included. We evaluated (1) temporal changes in CDS, (2) factors associated with CDS evolution, and (3) the association between 1-year CDS and long-term survival. CDS was assessed using the original schema and dichotomized as early stage (stage 0-2) versus advanced stage (stage 3-4). Among 762 patients, 676 were classified as early stage and 86 as advanced stage at baseline. In the baseline early stage group, 25 (3.7%) worsened to advanced stage immediately post-TAVR, and 48 (7.1%) had worsened by 1-year. Among baseline advanced stage group, 39 (45.3%) improved to early stage immediately post-TAVR, increasing to 50 (58.1%) at 1-year. Absence of baseline atrial fibrillation (AF) was associated with CDS improvement, whereas baseline AF and mild tricuspid regurgitation (TR) were associated with CDS worsening. Advanced stage CDS at 1-year was associated with higher all-cause mortality (adjusted HR 1.90; 95% CI 1.10-3.29; p = 0.02). Among the baseline early stage group, worsening to advanced stage was associated with a two-fold higher mortality risk. CDS evolves during the first year post-TAVR and is influenced by AF and TR. CDS at 1-year after TAVR was associated with long-term survival.