Introduction:
Solid organ transplantation is a complex phenomenon made possible by our better understanding of the immune system and the technological advances of modern medicine. Transplantation carries an intrinsic risk of graft-rejection that must be controlled. For this reason, immunosuppressive therapy is always initiated in these patients1. Among the immunosuppressive drugs used in solid organ transplantation, calcineurin inhibitors (CNIs), primarily Tacrolimus, have proven an effective and relatively safe option for these patients, with low rates of graft-rejection 1.
However, patients taking Tacrolimus are not exempt from adverse effects, some of which can be potentially life threatening, if they’re not identified early. Some of the most important side effects described in medical literature include nephrotoxicity, high blood pressure, post-transplant diabetes mellitus (PTMD), new-onset diabetes after transplantation (NODAT), dyslipidemia, and modification of cardiovascular-risk profile 2. Also, multiple electrolyte disorders as hyperkalemia, hypomagnesemia, hypercalciuria and metabolic acidosis have been described 3. Cardiovascular side effects as NODAT, dyslipidemia and hypertension with clinically significant increase and consequently an increment in the risk of stroke, myocardial infarction and heart failure have been described 4.
Tacrolimus - induced cardiomyopathy is an uncommon but important cardiovascular side effect of this drug, which has been described predominantly in pediatric transplant receptors 5. However, it has been also reported in adults receptors of renal, hepatic, cardiac and small bowel transplantation 6-9. Hypertrophic cardiomyopathy due to Tacrolimus has been cataloged as non familial acquired cardiomyopathy by the European Society of Cardiology (ESC) 10, while the American Heart Association (AHA) classifies it as a secondary cardiomyopathy 11.