Clinicopathological features of immune checkpoint inhibitor induced myocarditis
10.3760/cma.j.cn112151-20220704-00576
- VernacularTitle:免疫治疗相关心肌炎临床及病理特征观察
- Author:
Yan XIONG
1
;
Dong LI
;
Jiting DI
;
Cuiyan GUO
;
Pengkang HE
;
Kai ZHAO
Author Information
1. 北京大学第一医院病理科，北京 100034
- Keywords:
Myocarditis;
Adverse drug reaction reporting systems;
Antineoplastic protocols;
Immune checkpoint inhibitor
- From:
Chinese Journal of Pathology
2023;52(3):268-273
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the clinicopathological characteristics and possible pathogenesis of immune checkpoint inhibitor (ICI) induced myocarditis, and to improve understanding of this new type of myocarditis.Methods:Two cases of ICI induced myocarditis with endomyocardial biopsy available for review were selected from the cases with immune-related adverse events treated by ICI in Peking University First Hospital, Beijing, China from 2020 to 2022. The clinical data, histomorphological characteristics, PD-L1 expression of cardiomyocytes, and classification of inflammatory cells in two cases of ICI-induced myocarditis were analyzed. Relevant literature was reviewed.Results:Case 1 was a 64-year-old male diagnosed with gastric signet ring cell carcinoma. Case 2 was a 56-year-old male ad diagnosed with lung squamous cell carcinoma. Both patients developed acute myocarditis during PD-1 inhibitor treatment, and the disease progressed rapidly. Case 2 was more serious than case 1. Endomyocardial biopsy showed definite cardiomyocytic injury and prominent inflammatory infiltration in both cases, which met the full Dallas criteria for myocarditis. The degenerated and necrotic cardiomyocytes accounted for about 10% of the tissues in case 1 and 30% in case 2, respectively. In case 1, the inflammatory cells counted in the densest area were about 150/HPF, comprised of CD20 + cells (about 5/HPF), CD3 + cells (about 60/HPF), CD8 + cells (about 50/HPF) and CD68 + cells (about 70/HPF). In case 2, the inflammatory cells counted in the densest area were about 350/HPF, comprised of CD20 + cells (0/HPF), CD3 + cells (about 100/HPF), CD8 + cells (about 90/HPF) and CD68 + cells (about 200/HPF). In both cases, PD-L1 + cardiomyocytes aggregated in the inflammatory lesions, and the percentage was about 8% and 30% in case 1 and case 2, respectively. Conclusions:ICI-induced myocarditis is frequently acute onset, severe symptoms, and rapid progression. The histological morphology meets the full Dallas criteria for myocarditis. Expression of PD-L1 in cardiomyocytes can be detected in the inflammatory lesions. The inflammatory cells are comprised of CD8 + T lymphocytes and macrophages and the number of macrophages significantly exceeds that of lymphocytes. Combined with the pathological characteristics and the history of ICI treatment, the diagnosis of ICI-induced myocarditis can be made.
