Version June 2024
| Disease | EMB processing/staining | Possible findings |
| Myocarditis, DCM | Histopathology Haematoxylin and eosin, Mason or Mallory trichrome, Elastic van Gieson, PAS, Heidenhein's AZAN, and Methylene blue stain (Trypanosoma cruzii) | Dallas criteria for myocarditis: Inflammatory infiltrates associated with myocyte degeneration and necrosis of non-ischaemic origin (active or borderline). Lymphocytic myocarditis: Patchy or diffuse inflammatory infiltrate mostly of lymphocytes and macrophages (viral infections, immune-mediated myocarditis [systemic lupus erythematosus, polymyositis/dermatomyositis, rheumatoid arthritis, organ-specific autoimmune disorders, etc]). Giant cell myocarditis: Myocyte necrosis and diffuse or multifocal inflammatory infiltrates, with T lymphocytes, macrophage-derived multinucleated giant cells and eosinophilic granulocytes. Granulomatous myocarditis: Non-necrotizing granulomas with macrophages and multinucleated giant cells, surrounded by fibrosis and a lymphocytic infiltrate (sarcoidosis). Eosinophilic myocarditis: Interstitial inflammatory infiltrate dominated by eosinophils, often without myocyte damage, frequently accompanied by peripheral eosinophilia (hypersensitivity, parasitic infection, Churg-Strauss syndrome, endomyocardial fibrosis). |
| Quantitative real-time PCR for enteroviruses, adenoviruses, herpesviruses (cytomegalovirus, herpes simplex, Epstein-Barr, human herpesvirus 6), parvovirus B19, influenza A and B, and SARS-CoV-2 virus + Borrelia | Infection confirmed or not by (RT–) PCR | |
| Immunohistochemistry CD3 (T cells), CD68 (macrophages), MHC II, alpha SM-myofibroblasts | Myocarditis confirmed by immunohistochemistry: ≥14 leucocytes/mm2 including up to 4 monocytes/mm2 with the presence of CD3+ T-lymphocytes ≥7 cells/mm2 | |
| DCM, ARVC | Histology and PCR as above, additional immunohistochemical stains for lamin A/C, dystrophin, and plakoglobin (ARVC) | DCM: Non-specific histopathology including hypertrophy and vacuolar changes of myocytes, interstitial fibrosis, foci of micro-scarring. ARVC: Progressive myocyte atrophy/loss with fibrous or fibro-fatty myocardial replacement. |
| Storage diseases | PAS, Congo Red, sulfate alcian blue, or S/T thioflavin, Sudan black or Oil Red O (lipid deposits), Prussian Blue (iron), TEM (Anderson-Fabry, Danon) | PAS+ sarcoplasmic vacuoles and lysosomal glycogen accumulation (Pompe disease); PAS+ and LAMP2 absence, autophagic granules in TEM (Danon disease), PAS+ and lamellar bodies (Anderson-Fabry), Congo Red+ and interstitial deposits (amyloidosis); brownish perinuclear granules in myocytes highlighted in blue by Prussian Blue stain (iron storage disease). |
| Tumours | Standard histopathology + immunohistochemistry for specific tumours | Differential diagnosis between benign and malignant tumours, and in malignant tumour subtyping. |
| Heart transplantation | Haematoxylin and eosin, Giemsa, Movat, Masson trichrome, Weigert-Van Gieson, Ziehl Nielsen, PAS, Gram, Gomori, CD31, CD34, CD45, CD68, C4d | Cellular rejection: Grade 0R (no rejection); Grade 1R (mild) interstitial and/or perivascular infiltrate with up to 1 focus of myocyte damage; Grade 2R (moderate), ≥2 foci of infiltrate with associated myocyte damage; Grade 3R (severe) diffuse infiltrate with multifocal myocyte damage, oedema, haemorrhage, or vasculitis. Humoral rejection: Capillary injury, endothelial cell swelling and aggregation of intravascular macrophages (positive staining for C4d or C3d fragments of complement by endothelial cells). |
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