Effects of low and high doses of atorvastatin on arterial compliance.
At the beginning of atherosclerosis before evidence of morphological lesions or plaques, vascular distensibility or arterial compliance decreased gradually. This endothelial dysfunction is regarded as an early feature of atherosclerosis. In a randomized, double-blind study design, group 1 (12 patients; 7 males, 5 females) with serum LDL-C levels higher than 170 mg/dL and without any other risk factor for atherosclerosis received three months of 20 mg/day atorvastatin treatment while group 11 (8 males, 4 females) with the same characteristics received 80 mg/day. Baseline and posttreatment serum lipid fractions and arterial compliance were measured. Arterial compliance was measured noninvasively in the left common carotid artery with color Doppler ultrasound. Atorvastatin reduced total cholesterol (TC), LDL-C, and triglyceride levels by 32% (P < 0.001), 40.8% (P < 0.001), and 19% (P < 0.001), respectively, and increased HDL-C by 6.9%, (P = 0.002) in the first group. In the second group these reductions were 38.5% (P < 0.001), 46.2% (P < 0.001), and 26.78% (P < 0.001), respectively, and the increase in HDL was 7.8% (P = 0.03). It was observed that the decrease in serum TC, LDL-C and triglyceride levels were significantly higher in the second group than the first group. With atorvastatin, the distensibility coefficient (DC) and compliance coefficient (CC) increased from 18.7 +/- 3.4 to 21.3 +/- 2.9 10(-3) x kPa(-1) (P < 0.001) and from 0.69 +/- 0.05 to 0.77 +/- 0.03 mm2 x kPa(-1) (P < 0.001) in the first group while they changed from 18.3 +/- 3.6 to 21.9 +/- 3.0 10(-3) x kPa(-1) (P < 0.001) and from 0.70 +/- 0.04 to 0.81 +/- 0.01 mm2 x kPa(-1) (P < 0.001) respectively, in the second group. DC and CC increased in both groups, but the differences between the groups were not significant. High doses of atorvastatin reduce blood lipid levels more than conventional doses, however, the change in compliance is not dose-dependent. As endothelial dysfunction is regarded as an early feature of atherosclerosis, there would be no need to administer aggressive doses in a patient without any risk factors other than hyperlipidemia.
Karter
Yesari
Y
Department of Internal Medicine, Cerrahpasa Medical Faculty, Istanbul University, Turkey.
Curgunlu
Asli
A
Ertürk
Nurver
N
Vehid
Suphi
S
Mihmanli
Ismail
I
Ayan
Faruk
F
D000924:Anticholesteremic Agents / Q000008:administration & dosage* / Q000494:pharmacology; D001161:Arteriosclerosis / Q000209:etiology; D000069059:Atorvastatin; D017536:Carotid Artery, Common / Q000000981:diagnostic imaging* / Q000503:physiopathology; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003187:Compliance / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004311:Double-Blind Method; D004334:Drug Administration Schedule; D005260:Female; D006538:Heptanoic Acids / Q000008:administration & dosage* / Q000494:pharmacology; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000008:administration & dosage* / Q000494:pharmacology; D014280:Triglycerides / Q000097:blood; D018615:Ultrasonography, Doppler, Color; D018084:Ultrasonography, Interventional
D000924:Anticholesteremic Agents; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D011758:Pyrroles; D014280:Triglycerides; D002784:Cholesterol; D000069059:Atorvastatin