title: Rosuvastatin slows the development of diastolic dysfunction in calcific aortic stenosis.
abstract: OBJECTIVE
  The study aims were to test the effect of rosuvastatin on the progression of left ventricular (LV) diastolic function in patients with aortic stenosis (AS), and to evaluate the use of beta-natriuretic-peptide (BNP) as a marker of diastolic dysfunction in this condition.
  
  
  METHODS
  Sixty-one hypercholesterolemic, consecutive new referrals with moderate AS were administered rosuvastatin (Crestor) 20 mg/day for 18 months, while a further 60 subjects with normal cholesterol levels remained untreated. The LV diastolic function was determined using conventional Doppler echocardiography, tissue Doppler imaging (TDI); BNP plasma levels were monitored when subjects entered the study and then assessed prospectively at six-month intervals until the study end.
  
  
  RESULTS
  After an 18-month (mean 73 +/- 24 weeks) period of treatment with rosuvastatin (Tx group), patients showed a significantly better diastolic function than untreated subjects (uTx group), as indicated by an isovolumic relaxation time (IVRT) (Tx 102.0 +/- 42.8 versus 97.2 +/- 19.1; p < 0.001; uTx 99.7 +/- 21.7 versus 95.2 +/- 21.8 ms; p = 0.032), E/A ratio (Tx 1.0 +/- 0.6 versus 0.9 +/- 0.3, p = 0.52; uTx 1.2 +/- 0.40 versus 0.9 +/- 0.30 versus, p = 0.006), and E/E' ratio (Tx 11.4 +/- 1.5 versus 11.4 +/- 1.8, p = 0.19; uTx 15.4 +/- 1.2 versus 12.3 +/- 1.5, p < 0.001). Similarly, at study end, plasma levels of BNP were significantly lower in the Tx group than in the uTx group [median (1st-3rd quartiles): 37.0 pg/ml (20.1-65.2 pg/ml) versus 57.1 pg/ml (46.9-98.2 pg/ml); p = 0.017].
  
  
  CONCLUSIONS
  The results of this prospective follow up study of asymptomatic patients showed that rosuvastatin treatment delays the progression of diastolic dysfunction in moderate AS when assessed using hemodynamic echocardiographic parameters or by the release of plasma physiological markers. Hence, the benefits of statin treatment in AS, which are known to affect the valve endothelium, also extend to changes affecting myocardial function itself.
authors.affiliation: Department of Medicine, Oporto School of Medicine, University of Oporto, Portugal. luismoura@med.up.pt
authors.forename: Luis M
authors.initials: LM
authors.lastname: Moura
authors.forename: Sandra F
authors.initials: SF
authors.lastname: Ramos
authors.forename: Steen D
authors.initials: SD
authors.lastname: Kristensen
authors.forename: Fausto J
authors.initials: FJ
authors.lastname: Pinto
authors.forename: Isabel M
authors.initials: IM
authors.lastname: Barros
authors.forename: Francisco
authors.initials: F
authors.lastname: Rocha-Gonçalves
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001024:Aortic Valve Stenosis / Q000150:complications* / Q000000981:diagnostic imaging / Q000188:drug therapy*; D002114:Calcinosis / Q000150:complications / Q000000981:diagnostic imaging; D003971:Diastole / Q000187:drug effects; D018450:Disease Progression; D004452:Echocardiography; D005260:Female; D005464:Fluorobenzenes / Q000008:administration & dosage*; D005500:Follow-Up Studies; D054144:Heart Failure, Diastolic / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000209:etiology*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D011446:Prospective Studies; D011743:Pyrimidines / Q000008:administration & dosage*; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000008:administration & dosage*; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000209:etiology
chemical_list: D005464:Fluorobenzenes; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011743:Pyrimidines; D013449:Sulfonamides; D020097:Natriuretic Peptide, Brain; D000068718:Rosuvastatin Calcium