Arterial destiffening with atorvastatin in overweight and obese middle-aged and older adults.
We hypothesized that atorvastatin (ATOR) treatment would reduce arterial stiffness in overweight and obese middle-aged and older adults. Twenty-six (11 men and 15 women) overweight or obese (body mass index: 31.6+/-0.7 kg/m(2)) middle-aged and older adults (age: 54+/-2 years) were randomly assigned to receive either ATOR (80 mg/d) or placebo for 12 weeks. Arterial stiffness (beta-stiffness and pulse wave velocity) was measured before and after the intervention. At baseline, the ATOR (n=16) and placebo (n=10) groups did not differ with respect to age, body mass index, blood pressure, serum lipid and lipoprotein concentrations, high-sensitivity C-reactive protein, indices of arterial stiffness, or compliance (all P>0.05). After the 12-week treatment period, the ATOR group experienced a 47% reduction in low-density lipoprotein cholesterol (149+/-6 to 80+/-8 mg/dL) and a 42% reduction in high-sensitivity C-reactive protein (3.6+/-0.8 to 2.1+/-0.5 mg/L; both P<0.05). In addition, beta-stiffness (9.4+/-0.6 to 7.6+/-0.5 U) and aortic pulse wave velocity (1096+/-36 to 932+/-32 cm/s), but not brachial pulse wave velocity, decreased (both P<0.05) with ATOR. In contrast, there were no significant changes in beta-stiffness (9.1+/-0.8 to 9.1+/-0.7 U) or aortic pulse wave velocity (1238+/-89 to 1191+/-90 cm/s; both P>0.05) in the placebo group. There were no relations between the reductions in arterial stiffness indices and any of the baseline cardiometabolic risk factors (all P>0.05). However, the reductions in arterial stiffness were correlated with the reduction in low-density lipoprotein cholesterol but not high-sensitivity C-reactive protein or any other cardiometabolic variables (all P<0.05). Taken together, these findings suggest that ATOR reduces arterial stiffness in overweight and obese middle-aged and older adults, and these favorable changes occur irrespective of baseline cardiometabolic risk factors.
Orr
Jeb S
JS
Human Integrative Physiology Laboratory, Department of Human Nutrition, Foods and Exercise, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA.
Dengo
A Laura
AL
Rivero
Jose M
JM
Davy
Kevin P
KP
D000328:Adult; D000368:Aged; D000375:Aging / Q000502:physiology*; D000069059:Atorvastatin; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D002097:C-Reactive Protein / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000503:physiopathology; D002339:Carotid Arteries / Q000187:drug effects / Q000503:physiopathology*; D008078:Cholesterol, LDL / Q000097:blood; D004311:Double-Blind Method; D004548:Elasticity / Q000187:drug effects*; D005260:Female; D005263:Femoral Artery / Q000187:drug effects / Q000503:physiopathology*; D006538:Heptanoic Acids / Q000494:pharmacology*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000503:physiopathology*; D050177:Overweight / Q000503:physiopathology*; D011758:Pyrroles / Q000494:pharmacology*; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D012307:Risk Factors
D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D002097:C-Reactive Protein; D000069059:Atorvastatin