Effects of atorvastatin versus other statins on fasting and postprandial C-reactive protein and lipoprotein-associated phospholipase A2 in patients with coronary heart disease versus control subjects.
The effects of atorvastatin (40 mg/day) versus placebo on fasting and postprandial plasma levels of high-sensitivity C-reactive protein (hs-CRP) and lipoprotein-associated phospholipase A2 (Lp-PLA2) were examined over 36 weeks in 84 patients who had coronary heart disease and low-density lipoprotein cholesterol levels >130 mg/dl and compared directly with the effects of fluvastatin, lovastatin, pravastatin, and simvastatin. Results were also compared with those obtained in age- and gender-matched control subjects (n = 84). Feeding increased median hs-CRP levels by 2% in patients (p = NS) and 22% in controls (p <0.01) and increased mean Lp-PLA2 values by 9% in patients (p = NS) but decreased values by 21% in controls (p <0.0001). Patients had 51% higher median hs-CRP values and 29% higher mean Lp-PLA2 values than did controls (p <0.05 for hs-CRP and Lp-PLA2) in the fasting state; however, Lp-PLA2 values were 62% higher (p <0.0001) in the fed state in patients compared with controls. Atorvastatin decreased median hs-CRP levels by 32% (p <0.01) and mean Lp-PLA2 values by 26% in patients (p <0.0001), with similar decreases in the fed state, and none of the other statins had any significant effect on these parameters. Change in Lp-PLA2 was significantly related to change in low-density lipoprotein cholesterol (p <0.01), with no significant relations with change in hs-CRP. Our data indicate greater differences in patients with coronary heart disease compared with controls in Lp-PLA2 in the fed state than in the fasting state and that atorvastatin is more effective than fluvastatin, lovastatin, pravastatin, or simvastatin for decreasing not only low-density lipoprotein cholesterol but also hs-CRP and Lp-PLA2.
Schaefer
Ernst J
EJ
Cardiovascular Research and Lipid Metabolism Laboratories, Tufts University School of Medicine, Friedman School of Nutrition Science and Policy at Tufts University, Boston, Massachusetts 02111, USA. ernst.schaefer@tufts.edu
McNamara
Judith R
JR
Asztalos
Bela F
BF
Tayler
Timothy
T
Daly
Jennifer A
JA
Gleason
Joi L
JL
Seman
Leo J
LJ
Ferrari
Andrea
A
Rubenstein
Joel J
JJ
D000924:Anticholesteremic Agents / Q000145:classification / Q000378:metabolism / Q000627:therapeutic use*; D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000187:drug effects*; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000188:drug therapy*; D005215:Fasting; D005260:Female; D006538:Heptanoic Acids / Q000378:metabolism / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000145:classification / Q000378:metabolism / Q000627:therapeutic use*; D008074:Lipoproteins / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D010741:Phospholipases A / Q000187:drug effects*; D054467:Phospholipases A2; D010919:Placebos; D019518:Postprandial Period; D011758:Pyrroles / Q000378:metabolism / Q000627:therapeutic use*
D000924:Anticholesteremic Agents; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008074:Lipoproteins; D010919:Placebos; D011758:Pyrroles; D002097:C-Reactive Protein; D000069059:Atorvastatin; D010741:Phospholipases A; D054467:Phospholipases A2