Mitral annular calcification (MAC) is the most common calcific disorder of the mitral valve; however, other calcified lesions, including cardiac calcified amorphous tumor (CAT) and its highly mobile subtype, swinging CAT (S-CAT), have been reported. These entities differ markedly in their growth patterns and structural characteristics. This study aimed to clarify the mechanism underlying the development of S-CAT arising from MAC by focusing on detailed pathological findings of resected specimens, particularly along the long-axis. Histopathological analysis demonstrated that the lesion could be divided into three distinct zones, each characterized by different morphologies of calcified nodules and varying degrees of inflammatory cell infiltration. In particular, the distribution of macrophages and neutrophils differed among these regions, suggesting heterogeneity in inflammatory exposure over time. These findings indicate that localized and time-dependent inflammatory processes associated with circulating blood components may contribute to the development of S-CAT on the roughened endocardial surface overlying pre-existing MAC. Furthermore, clinical backgrounds frequently included end-stage renal disease, diabetes mellitus, obesity, and hypercholesterolemia, supporting the role of systemic metabolic and inflammatory conditions in this process. Understanding these pathological features may provide insight into the pathogenesis of S-CAT and its clinical behavior. Learning objective Previous pathological reports of swinging cardiac calcified amorphous tumor (S-CAT) have mainly focused on the distal tip of the lesion. By examining longitudinal pathological specimens from root to tip, this case demonstrates distinct regional histological differences and suggests that S-CAT develops through a chronological process involving thrombosis, inflammation, and progressive calcification arising from mitral annular calcification.
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