O uso de estatinas em pacientes com distrofia muscular submetidos a transplante cardíaco
USA – as estatinas fazem parte do protocolo de tratamento de pacientes submetidos a transplante cardíaco. Estas drogas podem causar lesão muscular, podendo chegar a rabdomiólise. Nesta pesquisa são relatados poucos casos de pacientes com distrofia muscular submetidos a transplante e tratados com corticóides. O tratamento foi bem tolerado, não havendo alterações musculares graves.
O resumo em inglês pode ser lido abaixo:
Preliminary Observations about Statin Therapy in Heart Transplant Recipients with Muscular Dystrophy
Ekta Singh, Sudhir Kushwaha, Walter K Kremers, and Yogish C Kudva – USA
Background: Statin use is standard practice after heart transplantation (HT) to prevent/delay cardiac allograft vasculopathy. HT recipients with muscular dystrophy (MD) represent a special cohort, since statins are generally avoided in myopathies.Methods: We reviewed the HT database at Mayo Clinic Rochester, MN from January 1996 through December 2011, and studied the medical record for documentation of muscle-related complications from statin use in HT recipients with MD.Results: 4 patients (all males) with MD underwent HT between Jan.1996 and Dec. 2011. Two (50%) patients had Becker’s MD, one had Emery Dreifuss MD, and one had an unclassifiable, poorly defined MD. The median age at the time of HT was 29.5 years (25-36). All patients had minimal myopathic symptoms, and were fully functional prior to HT.All patients received pravastatin post-HT with the dose titrated to achieve an LDL-C goal of 100 mg/dL. The mean dose was 45 mg (20-80). One patient was changed to Simvastatin 40 mg due to suboptimal LDL-C control. The patients tolerated pravastatin well, without any functional impairment for a median duration of 54 months (13-96). The median LDL-C during therapy was 84 mg/dL (70-119).One patient developed progressive weakness 7 years after HT, and 1 year after changing treatment to simvastatin, prompting statin discontinuation, that was followed by mild improvement in symptoms. One patient experienced myalgias 2 years after HT, after pravastatin dose was increased to 40 mg. One patient reported myalgias on pravastatin 40 mg 8 years after HT, prompting its discontinuation that did not result in any symptomatic improvement. One patient reported no adverse events 1 yr after HT, on pravastatin 20 mg. There were no serious adverse effects, including rhabdomyolysis. EMG was not performed on any patient. Creatine kinase levels fluctuated widely, and did not correlate with patients’ muscular symptoms.With the exception of 1 case of mild subclinical hypothyroidism, all patients had normal thyroid function. Three patients were on Sirolimus, and one on Tacrolimus-based immunosuppression. There was no reported use of medications interfering with statin metabolism. Conclusion: Long-term, medium-dose pravastatin therapy is well tolerated by patients with MD undergoing HT. Creatine kinase is not a reliable predictor of adverse muscle-related events. Since these patients are rare, a multi-center effort is required to study them.
