Mapping the Inflammation Research Landscape in Myocardial Infarction, 1995-2025: A Bibliometric Analysis of WoSCC and
Yang Liu1, Sicheng Chen2, Ting Li3
1Department of Cardiology, The First Affiliated Hospital of Guangdong Pharmaceutical University, The First Clinical Medical School of Guangdong Pharmaceutical University, Guangzhou, 510080, People's Republic of China.
Purpose:
Inflammation contributes to coronary plaque instability, myocardial injury, tissue repair, ventricular remodeling, recurrent cardiovascular events, and heart failure after myocardial infarction. This study aimed to map the publication patterns, conceptual structure, and thematic evolution of myocardial infarction-related inflammation research from 1995 to 2025.
Methods:
English-language articles and reviews published from 1995 to 2025 were retrieved from the Web of Science Core Collection (WoSCC) and PubMed on July 29, 2026, using database-specific but conceptually harmonized strategies. All retrieved records underwent title and abstract screening against prespecified eligibility criteria, and proposed exclusions were independently verified by two authors. WoSCC was used for the primary bibliometric and science-mapping analyses and PubMed for complementary Medical Subject Headings (MeSH)-based analyses. The datasets were processed separately and were not merged or deduplicated across databases. Bibliometrix, VOSviewer, CiteSpace, and Microsoft Excel were used to examine publication growth, geographic and institutional contributions, collaboration networks, conceptual structure, thematic evolution, citation bursts, and interdisciplinary knowledge flow.
Results:
After screening, 5,446 WoSCC records and 4,494 PubMed records were included. Publication output increased substantially in both databases, although the timing of short-term fluctuations differed. China and the United States were the leading national contributors, while major academic medical centers occupied central positions in collaboration networks. Multiple correspondence analysis of the WoSCC dataset yielded four algorithmic clusters that supported an interpretive framework of three broader domains: clinical inflammatory risk and prognosis, coronary vascular inflammation, and post-infarction inflammatory injury and repair. PubMed MeSH analyses provided complementary clinical and mechanistic patterns. Temporal analyses showed a shift from thrombolysis, conventional inflammatory markers, adhesion molecules, and vascular complications toward ischemia-reperfusion injury, inflammasome signaling, systemic immune-inflammatory indices, immune-cell regulation, biomarkers, and post-infarction remodeling.
Conclusion:
Myocardial infarction-related inflammation research has expanded from conventional biomarker and vascular studies toward a broader literature encompassing coronary inflammation, inflammatory injury and repair, ventricular remodeling, and risk stratification. The separate WoSCC and PubMed analyses provide complementary maps of research prominence and thematic relationships. The proposed domain framework and translational gaps should be interpreted as hypotheses generated from bibliometric patterns rather than evidence of biological causality, clinical validity, or therapeutic efficacy.
