title: Effects of obesity on lipid-lowering, anti-inflammatory, and antiatherosclerotic benefits of atorvastatin or pravastatin in patients with coronary artery disease (from the REVERSAL Study).
abstract: The effect of obesity on atherosclerotic burden and its modulation by lipid-lowering therapy is unknown. The Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) study was analyzed to determine the influence of increasing body mass index (BMI) on plasma lipids, C-reactive protein, plaque burden as determined by intravascular ultrasound, and the serial change in these parameters with a moderate or intensive lipid-lowering strategy. Patients with a higher BMI were younger, more likely to be women, and had a greater prevalence of hypertension, diabetes, and the metabolic syndrome. Although a higher BMI was associated with a lower high-density lipoprotein level and higher triglyceride and C-reactive protein levels, there was no apparent influence of BMI on plaque burden. However, with the intensive lipid-lowering strategy, a greater BMI was associated with a lower proportionate decrease in low-density lipoprotein (49.1 +/- 21.4% vs 43.0 +/- 22.4%, p = 0.008) and a greater proportionate decrease in C-reactive protein (39.7% vs 33.3%, p <0.04). Further, although moderate and intensive lipid-lowering strategies halted plaque progression in subjects with a lower BMI (median progression rates +1.5% and +1.2%, respectively), a significant effect on plaque progression rates was seen only with adoption of an intensive lipid-lowering strategy in the most obese subjects (median progression rate -1.88% vs +6.5% with the moderate lipid-lowering strategy, p = 0.01). In conclusion, plaque progression in obese patients is attenuated using an intensive, but not moderate, lipid-lowering strategy. These results highlight the need for aggressive risk factor modification and a decrease in vascular inflammation in obese patients.
authors.affiliation: Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Cleveland, Ohio, USA.
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Nicholls
authors.forename: E Murat
authors.initials: EM
authors.lastname: Tuzcu
authors.forename: Ilke
authors.initials: I
authors.lastname: Sipahi
authors.forename: Paul
authors.initials: P
authors.lastname: Schoenhagen
authors.forename: Stanley L
authors.initials: SL
authors.lastname: Hazen
authors.forename: Fady
authors.initials: F
authors.lastname: Ntanios
authors.forename: Chuan-Chuan
authors.initials: CC
authors.lastname: Wun
authors.forename: Steven E
authors.initials: SE
authors.lastname: Nissen
mesh_terms: D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism*; D003327:Coronary Disease / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D003331:Coronary Vessels / Q000000981:diagnostic imaging; D018450:Disease Progression; D019160:Endosonography; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D007249:Inflammation / Q000097:blood; D008055:Lipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000150:complications*; D017035:Pravastatin / Q000627:therapeutic use*; D011758:Pyrroles / Q000627:therapeutic use*; D012307:Risk Factors
chemical_list: D000924:Anticholesteremic Agents; D015415:Biomarkers; D006538:Heptanoic Acids; D008055:Lipids; D011758:Pyrroles; D002097:C-Reactive Protein; D000069059:Atorvastatin; D017035:Pravastatin