Lack of tacrolimus-induced cardiomyopathy

Citation
Kc. Coley et al., Lack of tacrolimus-induced cardiomyopathy, ANN PHARMAC, 35(9), 2001, pp. 985-989
Citations number
9
Categorie Soggetti
Pharmacology
Journal title
ANNALS OF PHARMACOTHERAPY
ISSN journal
10600280 → ACNP
Volume
35
Issue
9
Year of publication
2001
Pages
985 - 989
Database
ISI
SICI code
1060-0280(200109)35:9<985:LOTC>2.0.ZU;2-3
Abstract
BACKGROUND: Hypertrophic cardiomyopathy (HCM) has been reported in pediatri c transplant patients receiving tacrolimus. It is unclear whether tacrolimu s is associated with HCM in adult transplant recipients. OBJECTIVE: To determine the prevalence of HCM in noncardiac adult transplan t patients receiving tacrolimus. METHODS: A retrospective analysis of nonheart transplant recipients who rec eived tacrolimus at our institution from January 1982 to April 1996 was con ducted. Patients with left-ventricular hypertrophy (LVH) defined as a poste rior or septal wall thickness greater than or equal to1.3 cm by echocardiog raphy (ECHO) were independently evaluated. RESULTS: There were 3609 patients who met entry criteria including 2257 liv er, 1333 kidney, and 19 other organ transplants. Of the 502 patients who ha d undergone ECHOs after transplantation, 171 had LVH. The etiology of LVH w as categorized as valvular disease (36%), hypertensive disease (29%), ische mic heart disease (17%), or multifactorial (15%). There were six patients i n whom, after detailed chart review, no underlying cause of LVH was evident . Five of these patients had HCM, representing an overall prevalence of 0.1 % in the entire group of tacrolimus-treated patients, and 1% in patients re ferred for ECHO. CONCLUSIONS: The prevalence of HCM in our tacrolimus-treated adult transpla nt population is similar to that reported in general population studies. Th ese data suggest that tacrolimus is not a risk factor for HCM in adult tran splant recipients.