Key result
Switching from cyclosporine to azathioprine and prednisolone normalizes hemodynamics in post-transplant severe heart failure.
Why the study?
Cyclosporine may cause severe diastolic myocardial dysfunction after cardiac transplantation, but its reversibility upon withdrawal is not well documented.
Does cyclosporine withdrawal improve diastolic cardiac dysfunction in a cardiac transplant recipient with unexplained graft failure?
Case Report (n=1)
Does cyclosporine withdrawal improve diastolic cardiac dysfunction in a cardiac transplant recipient with unexplained graft failure?
Cyclosporine may cause reversible severe diastolic heart failure in cardiac transplant recipients, which resolves upon withdrawal and switching to alternative immunosuppression.
Cyclosporine may contribute to late diastolic graft failure after heart transplant; single-case data leaves open need for prospective confirmation.
Severe heart failure developed in a 49-year-old patient 18 months after orthotopic cardiac transplantation. Acute rejection as well as other overt causes of graft failure were excluded. Haemodynamic measurements suggested severe diastolic myocardial dysfunction. Since no other causes of diastolic heart failure were identified, a potential side effect from cyclosporine was considered. Cyclosporine was therefore withdrawn and immunosuppressive treatment was switched to conventional therapy consisting of azathioprine and prednisolone. Withdrawal of cyclosporine was followed by an impressive clinical improvement and by complete haemodynamic normalization. Therefore, in cases of otherwise unexplained graft failure, a potentially reversible side effect from cyclosporine should be taken into consideration.
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Siostrzonek et al. (1993) conducted a case report in Severe heart failure after orthotopic cardiac transplantation (n=1). Cyclosporine withdrawal was evaluated on Clinical improvement and haemodynamic normalization. Withdrawal of cyclosporine and switching to azathioprine and prednisolone led to complete haemodynamic normalization and clinical improvement in a cardiac transplant recipient with severe heart failure.
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