TY - JOUR
T1 - 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)
AU - Nicholls, Stephen J.
AU - Tuzcu, E. Murat
AU - Sipahi, Ilke
AU - Schoenhagen, Paul
AU - Hazen, Stanley L.
AU - Ntanios, Fady
AU - Wun, Chuan Chuan
AU - Nissen, Steven E.
N1 - Funding Information:
This study was supported by Pfizer, Inc., New York, New York.
PY - 2006/6/1
Y1 - 2006/6/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=33646686191&partnerID=8YFLogxK
U2 - 10.1016/j.amjcard.2005.12.042
DO - 10.1016/j.amjcard.2005.12.042
M3 - Article
C2 - 16728212
AN - SCOPUS:33646686191
SN - 0002-9149
VL - 97
SP - 1553
EP - 1557
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 11
ER -