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.