title: Effect of statin treatment on aortic valve and coronary artery calcification.
abstract: OBJECTIVE
  Conflicting data exist regarding statins and the progression of aortic valve disease. Hence, further information is required to determine if statin treatment has a beneficial effect on aortic valve calcification, and whether the inflammatory status of the patient affects aortic valve disease progression. The study aim was to evaluate the concomitant effect of statin treatment on aortic valve and coronary artery calcification and to compare results with the inflammatory status of the patient.
  
  
  METHODS
  Sixty-one patients with moderate to severe aortic stenosis (AS) were enrolled in this single-center, prospective observational study evaluating progression of aortic valve calcification. Patients underwent baseline and one-year echocardiography and electron-beam computed tomography. Blood samples were withdrawn at baseline and at one year for measurement of inflammatory biomarkers.
  
  
  RESULTS
  There was no significant reduction in calcium accumulation in the aortic valve of the statin group compared to the non-statin group, but there was trend towards less progression of calcification for the statin group. A significant inhibition of the coronary artery calcification volume score was observed for the statin group compared to the non-statin group. On echocardiography, statin treatment had no significant impact on aortic valve stenosis. Patients with serum LDL level >130 mg/dl showed less progression of coronary artery calcification when treated with statin drugs. The level of high-sensitivity C-reactive protein (hsCRP) significantly correlated with the progression of calcification for both the aortic valve and coronary arteries.
  
  
  CONCLUSIONS
  Whilst there was no significant benefit of statin treatment on aortic valve calcification over one year, there was a decreased progression of coronary artery calcification. The baseline level of hsCRP was predictive of progression of both aortic valve and coronary artery calcification, and may identify a high-risk population requiring aggressive control, either with statins or emerging drugs targeted at the inflammatory process of atherosclerosis.
authors: Department of Medicine, Cardiovascular Division, University of Pennsylvania School of Medicine, University Hospital, Philadelphia 19104, USA. mohlere@uphs.upenn.edu
authors: Emile R
authors: ER
authors: Mohler
authors: Hao
authors: H
authors: Wang
authors: Elizabeth
authors: E
authors: Medenilla
authors: Craig
authors: C
authors: Scott
mesh_terms: D000328:Adult; D000368:Aged; D001024:Aortic Valve Stenosis / Q000097:blood / Q000175:diagnosis* / Q000517:prevention & control; D002097:C-Reactive Protein / Q000378:metabolism; D002114:Calcinosis / Q000097:blood / Q000175:diagnosis* / Q000517:prevention & control; D023921:Coronary Stenosis / Q000097:blood / Q000175:diagnosis* / Q000517:prevention & control; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D015850:Interleukin-6; D002097:C-Reactive Protein