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Three autopsied cases of postmyocarditic cardiomegaly. Comparison with dilated cardiomyopathy
Insights
This study examined three patients with myocarditis who developed dilated cardiomyopathy (DCM)-like features. Postmyocarditic cardiomegaly shares histological similarities with non-fibrosis type DCM.
Area of Science:
- Cardiovascular Pathology
- Infectious Disease Cardiology
Background:
- Myocarditis can lead to dilated cardiomyopathy (DCM).
- Understanding the pathological progression from myocarditis to DCM is crucial for patient outcomes.
Observation:
- Three young patients with clinically proven myocarditis developed DCM-like features after upper respiratory tract infections.
- Histological examination revealed mononuclear cell infiltration, layer-unit depletion, and fibrosis in affected myocardium.
- Elevated Coxsackie B2 virus titers were noted in one patient.
Findings:
- Postmyocarditic cardiomegaly (PMC) showed distinct histological patterns compared to other DCM subtypes.
- Fibrosis and interstitial cellularity in PMC cases were significantly lower than in chronic myocarditis and fibrosis-type DCM.
- PMC most closely resembled the non-fibrosis type of DCM in terms of fibrosis and cellularity.
Implications:
- These findings suggest a specific pathological pathway for myocarditis leading to DCM.
- Distinguishing PMC from other DCM types may inform targeted therapeutic strategies.
- Further research into the viral etiology and long-term sequelae of myocarditis is warranted.
Abstract:
Three patients with clinically proven myocarditis who later developed dilated cardiomyopathy (DCM)-like features were studied pathologically at necropsy and compared with 42 other cases with DCM. The patients were an 18 year old female, a 20 year old male and a 28 year old male. They all had an upper respiratory tract infection as a prodromal symptom and then developed dyspnea on effort, electrocardiographic changes and cardiomegaly. In case 1, the antibody titers for Coxsackie B2 virus were elevated. In cases 1 and 3, myocardial biopsies revealed a mononuclear cell infiltrate. All 3 died of congestive heart failure. Histologically, layer-unit depletion of the myocardium (the myocardial damage and its sequelae (loss or minimal fibrosis) are restricted to certain layers), infiltration of mononuclear cells and moderate fibrosis were noted. In case 3, fibrosis and layer-unit depletion of the myocardium were mild. In our 42 DCM cases, the mean area of fibrosis was 40% in the fibrosis type, 15% in the nonfibrosis type and 30% in chronic myocarditis. In postmyocarditic cardiomegaly (PMC), the areas of fibrosis were 21.6%, 21.7% and 13.1% for the 3 cases. Mean cellularity indexes were 3.9% in PMC, 5.1% in the fibrosis type of DCM, 19.4% in the chronic myocarditis cases and 27% in the nonfibrosis type of DCM. With respect to fibrosis and interstitial cellularity, PMC most resembles the nonfibrosis type of DCM.