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.