Knowledge Structure and Thematic Organization of PFAS-Associated Cardiac Toxicity: A Bibliometric Analysis

Per- and polyfluoroalkyl substances (PFAS) are persistent environmental contaminants increasingly associated with cardiovascular outcomes. While mechanistic studies have reported oxidative stress, developmental toxicity, and gene expression alterations in cardiac models, it remains unclear how these findings integrate with structural cardiomyopathy frameworks. A bibliometric analysis was conducted using 469 publications retrieved from Scopus, PubMed, and Web of Science (1992–2025) using PFAS and cardiac-related search terms. Knowledge structure was evaluated using co-occurrence network analysis (VOSviewer), thematic mapping (Biblioshiny), overlay visualization, and citation timeline analysis (CiteSpace). Keyword co-occurrence analysis identified two dominant thematic domains: (1) mechanistic and developmental cardiotoxicity (e.g., oxidative stress, gene expression, zebrafish), and (2) clinical cerebrovascular outcomes centered on patent foramen ovale and stroke. Thematic mapping positioned PFAS exposure descriptors as central but broadly defined themes, whereas structural cardiomyopathy constructs did not form cohesive or central clusters. Overlay analysis demonstrated temporal expansion toward molecular toxicology after 2018, without parallel growth in myocardial remodeling descriptors. Citation burst analysis revealed stable thematic progression rather than rapid cardiomyopathy-centered acceleration. PFAS-associated cardiac research demonstrates progressive growth but remains structurally segmented. Mechanistic toxicology and clinical cardiovascular outcome studies operate largely in parallel, with limited integration into adult structural cardiomyopathy frameworks. These findings suggest the need for greater incorporation of myocardial phenotyping and remodeling endpoints in PFAS cardiac toxicology research. • PFAS cardiac research shows a dual-domain knowledge structure. • Mechanistic and clinical studies evolve with limited integration. • Structural cardiomyopathy themes are underrepresented. • Recent growth emphasizes molecular, not structural, endpoints. • Fragmentation limits translation to chronic cardiac disease models.