Statin cardiomyopathy? A potential role for Co‐Enzyme Q 10 therapy for statin‐induced changes in diastolic LV performance: Description of a clinical protocol

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 Q 10 (CoQ 10 ). CoQ 10 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 CoQ 10 , total cholesterol, LDL, HDL, CoQ 10 /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 CoQ 10 300 mg. daily for 3 months. A followup echocardiogram and blood CoQ 10 level will be measured in patients who received CoQ 10 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.