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Lack of objective improvement in ventricular systolic function in patients with myocarditis treated with azathioprine
Insights
Azathioprine and prednisone treatment for myocarditis did not demonstrate clear benefits. Decreased heart rate and pulmonary wedge pressure may be due to increased heart failure medications, not the immunosuppressants, which had significant side effects.
Area of Science:
- Cardiology
- Immunology
Background:
- Myocarditis is an inflammatory condition of the heart muscle.
- Immunosuppressive therapy is sometimes considered for myocarditis, but its efficacy is debated.
Purpose of the Study:
- To evaluate the efficacy and safety of azathioprine and prednisone in patients with biopsy-proven myocarditis.
Main Methods:
- Six patients with myocarditis underwent baseline right heart catheterization and echocardiogram.
- Treatment with azathioprine and prednisone was administered for 3 months.
- Repeat assessments included biopsy, right heart catheterization, and echocardiogram.
Main Results:
- Mean heart rate and pulmonary wedge pressure decreased significantly after treatment.
- No significant changes were observed in cardiac index, end-diastolic dimension, or fractional shortening.
- One patient each experienced severe soft tissue infection, acute psychosis, and adrenal insufficiency.
Conclusions:
- Azathioprine and prednisone did not show clear benefits for myocarditis in this small group.
- Observed hemodynamic improvements may be attributed to increased conventional heart failure therapy.
- High incidence of severe side effects suggests limiting this therapy to experimental settings.
Abstract:
Six patients with myocarditis documented by biopsy, after a baseline right heart catheterization and echocardiogram, underwent treatment with azathioprine and prednisone. After 3 months of treatment, biopsy, right heart catheterization and echocardiogram were repeated. In addition to the immunosuppressive therapy, most patients received additional conventional medications for heart failure between evaluation periods (mean number of cardiac drugs increased from 1.7 +/- 1.0 to 2.7 +/- 0.05, p = 0.041). Mean heart rate decreased (105 +/- 14 to 84 +/- 13 beats/min, p = 0.016), as did pulmonary wedge pressure (23 +/- 8 to 12 +/- 4 mm Hg, p = 0.012). There were no significant changes in cardiac index (3.1 +/- 0.8 to 2.9 +/- 1.0 liters/min), end-diastolic dimension (62 +/- 13 to 62 +/- 12 mm) or fractional shortening (11 +/- 6 to 12 +/- 3%) with treatment. Complications from immunosuppressive therapy included severe soft tissue infection, acute psychosis and adrenal insufficiency in one patient each. The benefits from prednisone and azathioprine in this group of patients have not been demonstrated. Although heart rate and pulmonary wedge pressure decreased, these changes could be ascribed to increases in the conventional therapy for heart failure. Finally, there is a high incidence of side effects from prednisone and azathioprine therapy. These findings suggest that this unproven therapy for myocarditis should be limited to experimental protocols.