title: Statin cardiomyopathy? A potential role for Co-Enzyme Q10 therapy for statin-induced changes in diastolic LV performance: description of a clinical protocol.
abstract: Lipid-lowering statins are thought to have a favorable safety profile. Statins inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting step of mevalonate synthesis. Mevalonate is the substrate for further synthesis of cholesterol and Co Enzyme Q10 (CoQ10). CoQ10 plays an important role during oxidative phosphorylation in the myocardial cell. Since myocardial diastolic function is a highly ATP dependent, we reasoned that early changes of diastolic function may be an early marker of ventricular dysfunction.
  
  
  METHODS
  Patients who are to commence on statin therapy will be enrolled in the trial. Baseline measurements of plasma CoQ10, total cholesterol, LDL, HDL, CoQ10/LDL ratio, peak E, peak A velocities, E/A ratio, deceleration time, isovolumetric relaxation time, color M-mode propagation velocity will be performed and patients will then begin to take Oral atorvastatin (Lipitor, Parke-Davis) 20 mg daily for three to six months. All baseline measurement will be repeated after 3 to 6 months of statin therapy. Those patients demonstrating > 1 measurement of diastolic LV function that worsened during the 3 to 6 months of statin therapy will be supplemented with CoQ10 300 mg. daily for 3 months. A followup echocardiogram and blood CoQ10 level will be measured in patients who received CoQ10 supplementation.
  
  
  RESULTS
  Statistical analysis will be performed using the paired t test to compare coenzyme levels and echocardiographic indices at baseline and after treatment and after supplementation.
authors.affiliation: Heart Failure Institute, Division of Cardiology, Department of Medicine, Advocate Christ Medical Center and the University of Illinois/Christ Cardiovascular Disease Fellowship Program, Oak Lawn, IL 60453, USA. Marc.Silver@Advocatehealth.com
authors.forename: Marc A
authors.initials: MA
authors.lastname: Silver
authors.forename: Peter H
authors.initials: PH
authors.lastname: Langsjoen
authors.forename: Szabolcs
authors.initials: S
authors.lastname: Szabo
authors.forename: Harish
authors.initials: H
authors.lastname: Patil
authors.forename: Allan
authors.initials: A
authors.lastname: Zelinger
mesh_terms: D000069059:Atorvastatin; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D002985:Clinical Protocols; D002986:Clinical Trials as Topic; D003067:Coenzymes; D003971:Diastole; D006538:Heptanoic Acids / Q000008:administration & dosage / Q000009:adverse effects; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000009:adverse effects* / Q000627:therapeutic use; D011758:Pyrroles / Q000008:administration & dosage / Q000009:adverse effects; D014451:Ubiquinone / Q000031:analogs & derivatives* / Q000097:blood / Q000627:therapeutic use*; D018487:Ventricular Dysfunction, Left / Q000139:chemically induced* / Q000188:drug therapy
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D003067:Coenzymes; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D014451:Ubiquinone; D002784:Cholesterol; D000069059:Atorvastatin; C024989:coenzyme Q10