Coronary atherosclerosis is increasingly recognized as an immuno-inflammatory disease as well as a lipid-driven condition. Despite major advances in lipid lowering, antithrombotic therapy, and contemporary secondary prevention, a substantial proportion of patients continue to experience recurrent coronary events. This persistent vulnerability, residual inflammatory risk, reflects ongoing inflammatory activity within the vascular wall and plaque microenvironment that is not fully captured by traditional risk factors. Rapid progress in vascular biology, circulating biomarkers, multi-omics, computational analytics, and cardiovascular and molecular imaging is expanding our ability to quantify inflammatory burden, define mechanistic endotypes, monitor disease activity, and assess treatment response.
This Research Topic aims to advance the field by integrating (i) mechanistic insights into inflammation-driven coronary atherosclerosis, (ii) biomarker- and imaging-enabled risk stratification, and (iii) precision therapeutic strategies targeting inflammatory and immune pathways. We seek contributions spanning basic, translational, and clinical research that clarify why inflammatory risk persists, how it can be measured and used for patient selection, and how targeted interventions can be implemented to meaningfully reduce coronary events across stable coronary disease and acute coronary syndromes.
Topics of interest include, but are not limited to: • Cellular and molecular mechanisms of vascular inflammation in coronary atherosclerosis; • Plaque biology, microenvironmental drivers of vulnerability, and determinants of plaque destabilization; • Circulating biomarkers and inflammatory signatures for diagnosis, risk stratification, and treatment monitoring; • Genetics and multi-omics (genomics, transcriptomics, proteomics, metabolomics, microbiome) and integrative frameworks to define inflammatory endotypes; • Cardiovascular and molecular imaging of vascular inflammation and plaque phenotype, including quantitative methods and longitudinal assessment; • Artificial intelligence and data-driven phenotyping, prediction, and decision support for inflammation-guided management; • Links between coronary atherosclerosis and comorbid inflammatory conditions (cardiometabolic disease, chronic kidney disease, autoimmune/systemic inflammatory disorders) and their therapeutic implications; • Precision and targeted therapies addressing residual inflammatory risk, including patient selection strategies, monitoring, safety, and clinical outcomes; trial design and implementation considerations.
We welcome original research, methodological and technical advances, and evidence syntheses (systematic reviews and meta-analyses). Submissions that connect mechanistic findings to clinically actionable stratification and/or therapeutic response, and that incorporate robust study design and transparent analytics, are particularly encouraged.
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Article types
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