TACROLIMUS-INDUCED ACUTE CARDIOMYOPATHY: A CASE REPORT AND REVIEW OF THE LITERATURE

A Bedi, M Raman, M Alghamdi, V McAlister*, K Peltekian

Atlantic Liver Transplantation Program, Halifax, NS, & *London Health Sciences Centre, London, ON

Tacrolimus (FK506), a calcineurin inhibitor, is commonly used in solid organ transplantation. We present a case of acute cardiomyopathy secondary to FK506 occurring three weeks after FK506 was initiated, and resolving only two weeks after FK506 was discontinued, with a review of the literature regarding the prevalence and mechanism of FK506 induced cardiomyopathy in comparison to cirrhotic cardiomyopathy.
A literature search from 1965 to present using PubMed revealed only two cases of cardiomyopathy. The first case was diagnosed at autopsy, more than three months after FK506 was initiated. The second case occurred five months after FK506 was started, and resolved over a period of three months after discontinuation of FK506.
A fifty-five year old male with decompensated Laennec's cirrhosis received an orthotopic liver transplantation. Post-transplantation, the patient was given FK506 with levels in the range of 6.4 and 18.5. Eleven days post-transplantation, the patient began to experience hypotension and syncope. On the following day, the patient experienced upper extremity tremors and renal insufficiency, all secondary to FK506 toxicity. Echocardiography, three weeks post-transplantation, revealed marked left ventricular hypertrophy with a small cavity and diastolic dysfunction, together with mild to moderate mitral regurgitation. Echocardiography two months prior to transplantation had revealed normal chamber dimensions, and mild concentric left ventricular hypertrophy. Left ventricular wall motion and systolic function were both documented as normal. Repeat echocardiography, two weeks after discontinuation of FK506, was consistent with the pre-transplant echocardiography with normal left ventricular size, left ventricular hypertrophy, mild mitral regurgitation, and no ventricular outflow tract obstruction.
The mechanism of cardiomyopathy secondary to FK506 is not known. It has been postulated that FK506 induced cardiomyopathy may be due to the removal of the FK506 binding protein (FKBP) that regulates calcium influx, and thus growth of the myocardial cell.