Severe aortic stenosis represents a significant prognostic burden, particularly in symptomatic patients. The advent of transcatheter aortic valve replacement (TAVR) has revolutionized the treatment of patients previously considered ineligible for surgical aortic valve replacement (SAVR). TAVR provides a relatively safe intervention that leads to improvements in survival, symptoms, and functional status within months of implantation. A major complication following TAVR is the occurrence of paravalvular leaks (PVLs), which have been associated with increased mortality and higher rates of heart failure-related hospitalizations. PVLs refer to abnormal blood flow between the implanted valve and the aortic wall, which can compromise the functionality of the device. Careful pre-procedural planning enables the identification of patients at higher risk for PVL development. Although the incidence of PVLs has decreased with the introduction of newer-generation transcatheter valves, the condition remains clinically relevant. Due to the complex anatomy of the aortic valve apparatus and interference from the prosthetic frame, accurate evaluation of PVLs requires a multimodal diagnostic approach. Current evidence on PVL management is limited. In most cases, a conservative approach is adopted, while interventional strategies (such as pre- and post-dilatation, percutaneous PVL closure, and TAVR-in-TAVR) are reserved for selected patients. We performed a systematic literature review to summarize the incidence, predictors, diagnostic techniques, and management strategies of PVLs following TAVR.

Non-obstructive coronary artery disease (NOCAD) encompasses a heterogeneous group of conditions in which patients present with angina, ischemia or myocardial infarction despite the absence of obstructive epicardial stenoses. This spectrum includes myocardial infarction with non-obstructive coronary arteries (MINOCA) and angina or ischemia with non-obstructive coronary arteries (ANOCA/INOCA), entities increasingly recognized as clinically significant and associated with adverse outcomes. Advances in cardiac computed tomography (CT) have expanded the diagnostic capabilities beyond the exclusion of obstructive coronary artery disease, enabling comprehensive anatomical, functional and tissue-level assessment relevant to NOCAD. CT allows precise identification of non-obstructive atherosclerosis, high-risk plaque features, myocardial bridging and structural vascular remodelling. Quantitative and qualitative characterization of plaque burden correlates with ischemic risk and provides prognostic information that complements traditional stenosis-based evaluation. Emerging CT-derived biomarkers, such as pericoronary fat attenuation index and epicardial adipose tissue metrics, offer insight into vascular inflammation and microvascular dysfunction, key mechanisms in NOCAD. Functional CT techniques, such as CT-derived fractional flow reserve and CT perfusion imaging, enable non-invasive assessment of hemodynamic significance and microvascular impairment, although their routine use is limited by methodological variability and evolving clinical evidence. Beyond coronary evaluation, CT also provides myocardial tissue characterization, detects extracardiac causes of symptoms and contributes to comprehensive differential diagnosis. Despite its strengths, cardiac CT remains limited by spatial resolution, radiation exposure and its inability to directly visualize the microcirculation. Nevertheless, ongoing technological refinement and integration of computational modelling are likely to enhance its diagnostic and prognostic role.

Despite major advances in reperfusion strategies and guideline-directed medical therapy, patients surviving myocardial infarction (MI) remain at substantial risk of recurrent cardiovascular events. Among the multiple determinants of post-MI cardiovascular risk, persistent atherothrombotic vulnerability remains a major therapeutic challenge despite guideline-directed secondary prevention. This review provides an integrated overview of residual atherothrombotic risk after MI, focusing on the complementary roles of lipid, inflammatory, and thrombotic pathways. Current evidence supports the use of biomarkers such as apolipoprotein B, lipoprotein(a), remnant cholesterol, triglyceride-rich lipoproteins, and high-sensitivity C-reactive protein to improve risk stratification beyond LDL-C. Landmark clinical trials have demonstrated that intensive lipid-lowering therapy, selected anti-inflammatory agents, and individualized antithrombotic strategies can further reduce recurrent cardiovascular events in appropriately selected patients. However, these pathogenic pathways rarely occur in isolation and frequently overlap, generating heterogeneous residual risk phenotypes. We propose a pragmatic multi-layered model in which lipid, inflammatory, and thrombotic mechanisms are viewed as interconnected biological processes rather than independent entities. This framework supports a personalized approach to secondary prevention based on comprehensive risk assessment, targeted therapeutic intensification, and longitudinal reassessment. Integrating these complementary domains may provide a framework for more individualized secondary prevention after MI, although its clinical utility requires prospective validation.

Left atrial appendage closure has emerged as an established nonpharmacological strategy for stroke prevention in selected patients with atrial fibrillation, particularly those in whom long-term oral anticoagulation is problematic. Its contemporary role, however, is defined by a central tension between procedural precision and clinical uncertainty. Advances in multimodality imaging, including transesophageal echocardiography, cardiac computed tomography, three-dimensional echocardiography, fusion imaging, and emerging computational tools, now allow highly accurate assessment of left atrial appendage anatomy, device sizing, intraprocedural guidance, and postprocedural surveillance. These techniques are essential to minimize peri-device leak, device-related thrombus, and other procedure-related complications in a structure characterized by marked interindividual variability. At the same time, the randomized evidence base remains nuanced. Early warfarin-era trials established the feasibility of LAAC, whereas contemporary comparisons with direct oral anticoagulants and best available medical therapy have yielded more heterogeneous results, reflecting differences in patient selection, comparator regimens, and endpoint design. Taken together, the available data support LAAC as a reasonable option in carefully selected patients at elevated bleeding risk or with limited tolerance for chronic anticoagulation, but not as a universal substitute for oral anticoagulant therapy. Future progress will depend on more refined phenotyping, standardized imaging pathways, and longer-term comparative data to better define which patients derive the greatest net clinical benefit from LAAC.

Background: Myocardial infarction (MI) remains a leading cause of morbidity and mortality despite major advances in reperfusion and secondary prevention. Inflammation contributes throughout the MI continuum, from atherosclerotic plaque development and destabilization to myocardial injury, adverse ventricular remodeling, and recurrent cardiovascular events. Objective: This narrative review summarizes current evidence on inflammation across the MI continuum, focusing on inflammatory biomarkers, cardiovascular imaging, residual inflammatory risk, and emerging anti-inflammatory therapies. Methods: We reviewed current evidence on the pathophysiological and clinical relevance of inflammation in MI, with particular emphasis on circulating biomarkers, multimodality imaging, and inflammation-targeted therapeutic strategies. Results: High-sensitivity C-reactive protein remains the best-established biomarker of residual inflammatory risk, while interleukin-6, myeloperoxidase, suPAR, and GlycA provide complementary information. Advanced imaging, including coronary computed tomography-derived perivascular fat attenuation index, cardiac magnetic resonance, and positron emission tomography, may further characterize vascular and myocardial inflammation. Clinical trials support inflammation as a potentially modifiable component of cardiovascular risk; however, therapeutic benefit has been inconsistent across inflammatory targets, agents, and clinical settings. Canakinumab and low-dose colchicine have demonstrated cardiovascular benefit in selected secondary-prevention populations, although recent neutral trials highlight heterogeneity across clinical settings. Similarly, IL-6-targeted strategies have yielded mixed results, with the neutral ZEUS trial underscoring that biomarker reduction does not necessarily translate into cardiovascular benefit, while NLRP3-targeted approaches remain investigational. Conclusions: Integrating inflammatory biomarkers, multimodality imaging, and targeted therapies may improve risk stratification and support personalized secondary prevention. Further evidence is needed to define optimal patient selection and determine whether biomarker- or imaging-guided anti-inflammatory strategies improve clinical outcomes.