Effect of Rosuvastatin on Left Ventricular Remodeling
|Study Design:||Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Double Blind (Subject, Investigator)
Primary Purpose: Treatment
|Official Title:||A Phase III Study of the Effect of Rosuvastatin on Left Ventricular Remodeling and Inflammatory Markers in Heart Failure|
- End points will be LV end systolic and diastolic volume (LVESV, LVEDV), and LV-ejection fraction (LV-EF). [ Time Frame: 2009 ] [ Designated as safety issue: Yes ]
- the B-type natriuretic peptide (BNP), Effect on immunological variables [ Time Frame: 2009 ] [ Designated as safety issue: Yes ]
|Study Start Date:||July 2007|
|Study Completion Date:||July 2013|
|Primary Completion Date:||July 2013 (Final data collection date for primary outcome measure)|
Placebo Comparator: 2
Active Comparator: 1
Rosuvastatin 10 mg tablets od for 6 months
- Chronic heart failure (HF) is one of the most important public health problems in cardiovascular medicine.
- Idioatic dilated cardiomyopathy (CMP) represents the final common expression of primary myocardial damage produced by a variety of as yet undefined myocardial insults, producing areas of interstitial and perivascular fibrosis, particularly of the left ventricle. Chronic HF, including CMP, is a progressive disease with high morbidity and mortality, suggesting that important pathogenic mechanisms remain active and unmodified by the present treatment modalities. The presence of chronic inflammation in patients with chronic heart failure has been widely recognized and coupled with persistent immune activation may represent such unmodified mechanisms.
The effect of statin therapy on lipids are well known, but recent studies suggest that the beneficial effects of statins also may be related to their anti-inflammatory properties.
To further elucidate this issue we want to study the potent new statin Rosuvastatin on myocardial function and remodeling and their relation to inflammatory markers in patients with IDCM. As hyperlipidemia is not involved in the pathogenesis of IDCM, as opposed to HF secondary to CAD, such studies will also be an interesting approach in separating the lipid lowering from other effects of these medications in HF.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00505154
|Oslo University Hospital|
|Study Director:||Geir Gokstad||Rikshospitalet, Oslo, Norway|