Journal of Pathology and Translational Medicine

Original Article

Indirect pathological indicators for cardiac sarcoidosis on endomyocardial biopsy: Myung-Jin Cha, Jeong-Wook Seo, Seil Oh, Eun-Ah Park, Sang-Han Lee, Moon Young Kim, Jae-Young Park; J Pathol Transl Med. 2020;54(5):396-410. Published online July 29, 2020; DOI: https://doi.org/10.4132/jptm.2020.06.10

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Background
The definitive pathologic diagnosis of cardiac sarcoidosis requires observation of a granuloma in the myocardial tissue. It is common, however, to receive a “negative” report for a clinically probable case. We would like to advise pathologists and clinicians on how to interpret “negative” biopsies.
Methods
Our study samples were 27 endomyocardial biopsies from 25 patients, three cardiac transplantation and an autopsied heart with suspected cardiac sarcoidosis. Pathologic, radiologic, and clinical features were compared.
Results
The presence of micro-granulomas or increased histiocytic infiltration was always (6/6 or 100%) associated with fatty infiltration and confluent fibrosis, and they showed radiological features of sarcoidosis. Three of five cases (60%) with fatty change and confluent fibrosis were probable for cardiac sarcoidosis on radiology. When either confluent fibrosis or fatty change was present, one-third (3/9) were radiologically probable for cardiac sarcoidosis. We interpreted cases with micro-granuloma as positive for cardiac sarcoidosis (five of 25, 20%). Cases with both confluent fibrosis and fatty change were interpreted as probable for cardiac sarcoidosis (seven of 25, 28%). Another 13 cases, including eight cases with either confluent fibrosis or fatty change, were interpreted as low probability based on endomyocardial biopsy.
Conclusions
The presence of micro-granuloma could be an evidence for positive diagnosis of cardiac sarcoidosis. Presence of both confluent fibrosis and fatty change is necessary for probable cardiac sarcoidosis in the absence of granuloma. Either of confluent fibrosis or fatty change may be an indirect pathological evidence but they are interpreted as nonspecific findings.

Citations

Citations to this article as recorded by

Advances in cellular and tissue-based imaging techniques for sarcoid granulomas
Junwoo Kim, Girish Dwivedi, Berin A. Boughton, Ankur Sharma, Silvia Lee
American Journal of Physiology-Cell Physiology.2024; 326(1): C10. CrossRef
Cardiac sarcoidosis: phenotypes, diagnosis, treatment, and prognosis
Jukka Lehtonen, Valtteri Uusitalo, Pauli Pöyhönen, Mikko I Mäyränpää, Markku Kupari
European Heart Journal.2023; 44(17): 1495. CrossRef
Cardiac sarcoidosis: a comprehensive review of risk factors, pathogenesis, diagnosis, clinical manifestations, and treatment strategies
Hussain Haider Shah, Syeda Alishah Zehra, Aliza Shahrukh, Radeyah Waseem, Tooba Hussain, Muhammad Sheheryar Hussain, Fareeha Batool, Muhammad Jaffer
Frontiers in Cardiovascular Medicine.2023;[Epub] CrossRef
Histology of Cardiac Sarcoidosis with Novel Considerations Arranged upon a Pathologic Basis
Shu Kato, Yasuhiro Sakai, Asako Okabe, Yoshiaki Kawashima, Kazuhiko Kuwahara, Kazuya Shiogama, Masato Abe, Hiroyasu Ito, Shin’ichiro Morimoto
Journal of Clinical Medicine.2022; 11(1): 251. CrossRef
Cardiac sarcoidosis: A multimodal approach to reach the diagnosis
Nicolas Piriou, Patrick Bruneval
International Journal of Cardiology.2021; 323: 264. CrossRef
Value of 3D mapping‐guided endomyocardial biopsy in cardiac sarcoidosis
Danielle M. Haanschoten, Ahmet Adiyaman, Nils A. ‘t Hart, Piet L. Jager, Arif Elvan
European Journal of Clinical Investigation.2021;[Epub] CrossRef
Cardiac Sarcoidosis: A Clinical Overview
Ana Carolina Alba, Shyla Gupta, Lakshmi Kugathasan, Andrew Ha, Alejandro Ochoa, Meyer Balter, Alvaro Sosa Liprandi, Maria Inés Sosa Liprandi
Current Problems in Cardiology.2021; 46(10): 100936. CrossRef

Case Report

Giant Cell Myocarditis: A case report.: Ho Jung Lee, Jae Gul Chung, In Chul Lee, Myeong Gun Song, Jae Jung Kim, Jong Goo Lee; Korean J Pathol. 1996;30(6):523-527.

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Abstract PDF: Giant cell myocarditis(GCM) is a rare inflammatory heart disease which is characterized by multinucleated giant cells and a granulomatous reaction. It usually progresses rapidly and results in a fatal course. We report a patient with giant cell myocarditis who was treated by cardiac transplantation. A 35-year-old male was admitted with dyspnea which had developed 4 months before. On echocardiography, the right and left ventricles were markedly dilated and severe global hypokinesia was noted. He was diagosed with dilated cardiomyopathy with secondary severe mitral regurgitation. His cardiac function deteriorated progressively. He underwent orthotopic heart transplantation. Grossly the heart was enlarged, weighing 420gm and round with a blunt apex. Both right and left ventricles were markedly dilated. There were numerous white patches, measuring up to 4cm, throughout the epi- and myocardium. Microscopically, extensive fibrosis and multiple exuberant granulomas with numerous scattered multinucleated giant cells were seen. Lymphocytes and eosinophils were also frequent. Coronary arteries were unremarkable. Neither microorganisms nor foreign materials were found. By serial endomyocardial biopsies of the transplanted heart, only mild perivascular lymphocytic infiltration was occasionally observed without any evidence of rejection or recurrence of giant cell myocarditis. The patient's postoperative course has been uneventful so far(postoperative 21 months). The etiology of GCM remains to be clarified, although various factors are suspected. No matter what the cause, our experience suggests that this grave disease might be treated well by heart transplantation.

Original Articles

Altered Expression of Tissue Inhibitor of Matrix Metalloproteinase-2 in Complicated Mice Heart Secondary to Experimentally Induced Viral Myocarditis.: Sung Sook Kim, Dae Woon Eom, Yeong Ju Woo, Jae Hee Suh, Jooryung Huh, Young Me Hong, Inpyo Choi; Korean J Pathol. 2001;35(3):196-200.

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Abstract PDF: BACKGROUND
The pathogenesis of transition from viral myocarditis to dilated cardiomyopathy is elusive, although the incidence of dilated cardiomyopathy in human is increasing.
METHODS
To clarify the role of the tissue inhibitor of matrix metaloproteinase-2 (TIMP-2) in this event, we performed immunohistochemistry, immunoblotting and immunoassay of matrix metalloproteinase-9 (MMP-9) and TIMP-2 in the serum and heart tissue of mice, which were inoculated with 4000 plaque-forming units of coxsackie B virus.
RESULTS
The MMP-9 was expressed in damaged cardiomyocytes, and the TIMP-2 was expressed in mainly interstitial connective tissue between cardiac muscle bundles by immunohistochemistry. The level of serum MMP-9 was higher in the complicated than non-complicated group (p<0.001), but the level of TIMP-2 was much lower in complicated than non-complicated group (p<0.05). These findings were similar to the results of immunohistochemistry and immunoblotting in tissues.
CONCLUSIONS
These results suggest that an imbalance in the level of MMP-9 and its inhibitor might activate cardiac complication in viral myocarditis.

Expression of Interleukin-6 in Induced Viral Myocarditis in Mice.: Soo Yeon Cho, Hye Kyung Jin, Min Sun Cho, Sung Sook Kim, Woon Sup Han, Dong Sun Han, Hak Chung Lee; Korean J Pathol. 1995;29(2):212-220.

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Abstract PDF: Viral myocarditis is considered an important cause of dilated cardiomyopathy. At preseent, two mechanisms are known to be involved in the pathogenesis of viral myocarditis and subse-quent cardiomyopathy: viral direct toxicity and immune mediated toxicity. Some authors have reported that IL-6 influences the immunologic mechanism and the virus-induced tissue damage in myocarditis. We injected encephalomyocarditis(EMC) virus to induce viral myocarditis in ICR mice. In order to study the lymphocyte subset and IL-6 expression to clarify the immune mechanism and to demonstrate the role of IL-6 in viral induced myocardial damage. The following results were obtained: 1) In virus inoculated mice, inflammation was severest at 10 days, and some serious complications developed, indicating a possible transition to dilated cardiomyopathy. 2) On analysis of the lymphocyte subset, CD4 cells were most prevalent at 5 days and CD8 cells were most prevalent at 10 and 20 days. 3) IL-6 was significantly increased and expression of IL-6 was constant, but its intensity was strongest at 5 days. In conclusion, IL-6, produced by inflammatory cells, fibroblasts, and endothelial cells, might play an important role in myocardial damage in experimentally induced EMC viral myocarditis by its direct cytotoxicity or cytokine mediated activation of cytotoxic cells.

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