Effect of bezafibrate therapy on atherosclerotic aortic plaques detected by MRI in dyslipidemic patients with hypertriglyceridemia.
Fibrates reduce triglycerides (TG) and increase HDL-cholesterol levels, but there was no report showing plaque regression by fibrates. Using MRI, we investigated the effects of bezafibrate on aortic plaques in 22 dyslipidemic patients. All patients were asked to receive 400mg bezafibrate, but 8 who declined to have bezafibrate became the control group. Changes in vessel wall area (VWA) and lumen area (LA) from baseline to 1-year were evaluated. Bezafibrate reduced TG (-55%) and increased HDL-cholesterol levels (+29%). Bezafibrate reduced HDL size and increased LDL size. In thoracic plaques, bezafibrate reduced VWA (-6%, P<0.001) with no LA change, but VWA slightly progressed without bezafibrate (+5%). In abdominal plaques, bezafibrate reduced VWA (-8%, P<0.001) with LA increase (+3%, P<0.02), but VWA progressed without bezafibrate (+6%). VWA changes in thoracic and abdominal plaques correlated with TG reduction and HDL-cholesterol increase. Notably, VWA change in only abdominal plaques correlated with HDL size reduction and LDL size increase. Thus, bezafibrate induced plaque regression in thoracic and abdominal aortas with marked TG reduction and HDL-cholesterol increase, but the processes of plaque regression and vascular remodeling may differ between thoracic and abdominal aortas. However, because our study was not a controlled, randomized trial, further study is needed.
Ayaori
Makoto
M
First Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
Momiyama
Yukihiko
Y
Division of Cardiology, National Hospital Organization Tokyo Medical Center, Tokyo, Japan. Electronic address: ymomiyamajp@yahoo.co.jp.
Fayad
Zahi A
ZA
Mount Sinai School of Medicine, New York, USA.
Yonemura
Atsushi
A
First Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
Ohmori
Reiko
R
First Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
Kihara
Teruyoshi
T
Iruma Heart Hospital, Saitama, Japan.
Tanaka
Nobukiyo
N
First Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
Nakaya
Kazuhiro
K
First Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
Ogura
Masatsune
M
First Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
Sawada
Shojiro
S
First Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
Taniguchi
Hiroaki
H
First Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
Kusuhara
Masatoshi
M
First Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
Nagata
Masayoshi
M
Iruma Heart Hospital, Saitama, Japan.
Nakamura
Haruo
H
First Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
Ohsuzu
Fumitaka
F
First Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
D000368:Aged; D001011:Aorta / Q000187:drug effects / Q000473:pathology; D050197:Atherosclerosis / Q000188:drug therapy* / Q000473:pathology; D001629:Bezafibrate / Q000494:pharmacology*; D038524:Diffusion Magnetic Resonance Imaging; D005260:Female; D006801:Humans; D015228:Hypertriglyceridemia / Q000188:drug therapy*; D000960:Hypolipidemic Agents / Q000494:pharmacology*; D018810:Magnetic Resonance Angiography; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies
D000960:Hypolipidemic Agents; D001629:Bezafibrate