Differential associations of statin and fibrate treatment with carotid arterial remodeling.
BACKGROUND
The effects of statins on intima-media thickness (IMT) are well documented, whereas those of fibrates are unknown. Therefore we compared IMT under treatment with each class of drugs.


METHODS
We studied a cohort of consecutive dyslipidemic subjects treated with statin (n = 291) or fibrate (n = 82) drugs. Fibrate-treated subjects were matched with the same number of statin-treated subjects to obtain two subgroups of similar demographic and risk factors including LDL cholesterol. Common carotid far wall IMT and lumen diameter were measured by ultrasonography.


RESULTS
In the entire study population, IMT was greater in the fibrate group than in the statin group (P < .001), even after adjustment for LDL cholesterol and other covariates (P < .05). In the matched groups, IMT was greater in fibrate group than in the statin group (P < .01), even after adjustment for LDL cholesterol and other covariates including treatment duration (P < .01). The IMT correlated positively with treatment duration in the fibrate group (P < 0.05) but not in the statin group. In addition, IMT correlated positively with carotid lumen diameter in both the fibrate and statin groups (P < .05, P < .01) but with a lower slope in the former (P < .05).


CONCLUSIONS
In this study fibrate treatment was associated with greater IMT, steeper IMT-time relationship, and lower compensatory carotid enlargement than was statin treatment. These differences were not explained by differences in LDL cholesterol.
Chironi
Gilles
G
Centre de Médecine Préventive Cardiovasculaire, Hôpital Broussais-Assistance Publique-Hôpitaux de Paris and Faculté de Médecine Paris 5, Paris, France.
Simon
Alain
A
Gariepy
Jérome
J
Balice
Maria
M
Del-Pino
Muriel
M
Levenson
Jaime
J
D000328:Adult; D000069059:Atorvastatin; D001629:Bezafibrate / Q000627:therapeutic use; D015992:Body Mass Index; D002339:Carotid Arteries / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D008076:Cholesterol, HDL / Q000097:blood; D002995:Clofibric Acid / Q000031:analogs & derivatives / Q000627:therapeutic use*; D015331:Cohort Studies; D050171:Dyslipidemias / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D005229:Fatty Acids, Monounsaturated / Q000627:therapeutic use; D005260:Female; D011345:Fenofibrate / Q000627:therapeutic use; D058607:Fibric Acids; D000077340:Fluvastatin; D015248:Gemfibrozil / Q000627:therapeutic use; D006538:Heptanoic Acids / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D007211:Indoles / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D017035:Pravastatin / Q000627:therapeutic use; D011725:Pyridines / Q000627:therapeutic use; D011758:Pyrroles / Q000627:therapeutic use; D012307:Risk Factors; D019821:Simvastatin / Q000627:therapeutic use; D016896:Treatment Outcome; D017539:Tunica Intima / Q000000981:diagnostic imaging; D017540:Tunica Media / Q000000981:diagnostic imaging; D014463:Ultrasonography
D008076:Cholesterol, HDL; D005229:Fatty Acids, Monounsaturated; D058607:Fibric Acids; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents; D007211:Indoles; D011725:Pyridines; D011758:Pyrroles; D000077340:Fluvastatin; D002995:Clofibric Acid; D000069059:Atorvastatin; D019821:Simvastatin; C086276:cerivastatin; C019304:ciprofibrate; D017035:Pravastatin; D015248:Gemfibrozil; D011345:Fenofibrate; D001629:Bezafibrate