title: Fluvastatin as co-medication in heart transplant recipients with elevated creatine-kinase.
abstract: BACKGROUND
  Statins reduce the risk for transplant vasculopathy and mortality among heart transplant recipients. Interactions between commonly used statins (ie, simvastatin, atorvastatin) and immunosuppressant drugs lead to side effects or withdrawal of statin therapy. Fluvastatin shows fewer interactions with the immunosuppressant agents because it is not metabolized via the cytochrome P-450 3A4 pathway like most immunosuppressants, steroids, or other statins. This study investigated the impact of a switch from other statins to fluvastatin in heart transplant recipients who revealed elevated creatine-kinase levels.
  
  
  METHODS
  A total of 23 heart transplant patients with elevated creatine-kinase levels were included in this study. Statins were replaced with an equal dosage of fluvastatin. We measured on the day of replacement as well as there after at 3, 6, 9, and 12 months creatine-kinase, lipid status, ALT, AST, and creatinine levels.
  
  
  RESULTS
  After 6 months creatine-kinase showed a significant reduction of 25% (P < .05) and after 9 months of 38% (P < .05). The HDL-cholesterol levels were significantly reduced at 6 months (8%; P < .05) and 9 months (23%; P < .05). At 3 months, triglyceride levels were significantly elevated (18%; P < .05). No differences were observed in ALT, AST, creatinine, total, and LDL-cholesterol at any time.
  
  
  CONCLUSIONS
  A conversion from commonly used statins to fluvastatin in heart transplant patients with elevated creatine-kinase was safe, leading to a significant reduction in creatine-kinase levels. Except for an initial raise in triglycerides and a lowering of HDL-cholesterol, no changes in lipid status were seen. This conversion might help to maintain lipid-lowering therapy in transplant recipients who show side effects using conventional statins.
authors.affiliation: Department of Cardiac Surgery, Grosshadern University Hospital, Ludwig-Maximilians-University, Munich, Germany. Sebastian.Sadoni@med.uni-muenchen.de
authors.forename: S
authors.initials: S
authors.lastname: Sadoni
authors.forename: I
authors.initials: I
authors.lastname: Kaczmarek
authors.forename: O
authors.initials: O
authors.lastname: Delgado
authors.forename: M
authors.initials: M
authors.lastname: Schmöckel
authors.forename: B
authors.initials: B
authors.lastname: Reichart
authors.forename: B
authors.initials: B
authors.lastname: Meiser
mesh_terms: D000328:Adult; D000069059:Atorvastatin; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003402:Creatine Kinase / Q000097:blood*; D004359:Drug Therapy, Combination; D005229:Fatty Acids, Monounsaturated / Q000627:therapeutic use*; D005260:Female; D000077340:Fluvastatin; D016027:Heart Transplantation / Q000502:physiology*; D006538:Heptanoic Acids / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D007211:Indoles / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000627:therapeutic use; D019821:Simvastatin / Q000627:therapeutic use; D014280:Triglycerides / Q000097:blood
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005229:Fatty Acids, Monounsaturated; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D011758:Pyrroles; D014280:Triglycerides; D000077340:Fluvastatin; D000069059:Atorvastatin; D019821:Simvastatin; D003402:Creatine Kinase