Histopathological insights into a swinging cardiac calcified amorphous tumor associated with mitral annular calcification: A case report
- 1Department of Cardiovascular Surgery, Kyorin University, Tokyo, Japan
Abstract
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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BibTeX
@article{tsuchiya2026histopathological,
title = {{Histopathological insights into a swinging cardiac calcified amorphous tumor associated with mitral annular calcification: A case report}},
author = {Hiroshi Tsuchiya and Hidehito Endo and Sachito Minegishi and Yu Takahashi and Yusuke Inaba and Hiroshi Kubota},
journal = {Journal of Cardiology Cases},
year = {2026},
month = aug,
doi = {10.1016/j.jccase.2026.07.011},
url = {https://doi.org/10.1016/j.jccase.2026.07.011},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Histopathological insights into a swinging cardiac calcified amorphous tumor associated with mitral annular calcification: A case report
AU - Hiroshi Tsuchiya
AU - Hidehito Endo
AU - Sachito Minegishi
AU - Yu Takahashi
AU - Yusuke Inaba
AU - Hiroshi Kubota
PY - 2026
DA - 2026/08/08
JO - Journal of Cardiology Cases
DO - 10.1016/j.jccase.2026.07.011
UR - https://doi.org/10.1016/j.jccase.2026.07.011
AB - 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.
SN - 1878-5409
ER -