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Evaluating the effectiveness of rosuvastatin in preventing the progression of diastolic dysfunction in aortic stenosis: A substudy of the aortic stenosis progression observation measuring effects of rosuvastatin (ASTRONOMER) study

Davinder S Jassal123*, Kapil M Bhagirath1, Erin Karlstedt1, Matthew Zeglinski2, Jean G Dumesnil4, Koon K Teo5, James W Tam1 and Kwan L Chan6

Author Affiliations

1 Cardiology Division, Department of Internal Medicine, St. Boniface General Hospital, Winnipeg, Manitoba, Canada

2 Institute of Cardiovascular Sciences, Cardiology Division, Department of Cardiac Sciences, St. Boniface General Hospital, Winnipeg, Manitoba, Canada

3 Department of Radiology, St. Boniface General Hospital, Winnipeg, Manitoba, Canada

4 Hopital Laval, Sainte-Foy, Quebec, Canada

5 McMaster University, Hamilton, Ontario, Canada

6 University of Ottawa Heart Institute, Ontario, Canada

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Cardiovascular Ultrasound 2011, 9:5  doi:10.1186/1476-7120-9-5

Published: 7 February 2011



Tissue Doppler imaging (TDI) is a noninvasive echocardiographic method for the diagnosis of diastolic dysfunction in patients with varying degrees of aortic stenosis (AS). Little is known however, on the utility of TDI in the serial assessment of diastolic abnormalities in AS.


The aim of the current proposal was to examine whether treatment with rosuvastatin was successful in improving diastolic abnormalities in patients enrolled in the Aortic Stenosis Progression Observation Measuring Effects of Rosuvastatin (ASTRONOMER) study.


Conventional Doppler indices including peak early (E) and late (A) transmitral velocities, and E/A ratio were measured from spectral Doppler. Tissue Doppler measurements including early (E') and late (A') velocities of the lateral annulus were determined, and E/E' was calculated.


The study population included 168 patients (56 ± 13 years), whose AS severity was categorized based on peak velocity at baseline (Group I: 2.5-3.0 m/s; Group II: 3.1-3.5 m/s; Group III: 3.6-4.0 m/s). Baseline and follow-up hemodynamics, LV dimensions and diastolic functional parameters were evaluated in all three groups. There was increased diastolic dysfunction from baseline to follow-up in each of the placebo and rosuvastatin groups. In patients with increasing severity of AS in Groups I and II, the lateral E' was lower and the E/E' (as an estimate of increased left ventricular end-diastolic pressure) was higher at baseline (p < 0.05). However, treatment with rosuvastatin did not affect the progression of diastolic dysfunction from baseline to 3.5 year follow-up between patients in any of the three predefined groups.


In patients with mild to moderate asymptomatic AS, rosuvastatin did not attenuate the progression of diastolic dysfunction.