Plaque regression in one artery is not necessarily associated with parallel changes in other vascular beds.
It remains unclear whether atherosclerosis in one vascular bed progresses in parallel with that in other vascular beds. We investigated serial changes in vessel wall areas (VWAs) in various vessels over 2 years of follow-up. Vessel wall areas in the thoracic descending aorta (TDA), common carotid artery (CCA), right (RCA), and left main trunk (LMT) of coronary artery were determined in 52 patients with coronary artery disease (CAD) using 64-slice multidetector computed tomography. Plasma levels of high-sensitivity CRP (hs-CRP) and matrix metalloproteinase (MMP)-9, as well as urinary 8-iso-prostaglandin F2α (PGF2α) were determined at the baseline. After the follow-up period, plaque progression in a specific vessel did not parallel that of other vessels, although changes in TDA-VWAs were weakly correlated with those of LMT-VWAs. Basal levels of hs-CRP, MMP-9, and PGF2α did not predict progression or regression of VWAs in any vessels. Multivariate analyses showed that LDL-cholesterol < 100 mg/dl and use of statin emerged as predictors of regressing VWAs in TDA (p < 0.05 and p < 0.05, respectively) and LMT (p < 0.05 and p = 0.13, respectively). Changes in soft plaques over 2 years paralleled those of VWAs in both coronary arteries. In conclusion, the progression or regression of atherosclerotic plaques is inhomogeneous among the vascular beds of patients with CAD.
Second Department of Internal Medicine, Graduate School of Medicine, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Takayuki
T
Suzuki
Takashi
T
Nozawa
Nozomu
N
Fujii
Mitsuo
M
Sobajima
Takashi
T
Ohori
Takuya
T
Shida
Akira
A
Matsuki
Tomoki
T
Kameyama
Hiroshi
H
Inoue
D000368:Aged; D001013:Aorta, Thoracic / Q000000981:diagnostic imaging / Q000473:pathology*; D001018:Aortic Diseases / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000473:pathology* / Q000652:urine; D001027:Aortography / Q000379:methods; D050197:Atherosclerosis / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000473:pathology* / Q000652:urine; D015415:Biomarkers / Q000097:blood / Q000652:urine; D002097:C-Reactive Protein / Q000032:analysis; D002340:Carotid Artery Diseases / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000473:pathology* / Q000652:urine; D017536:Carotid Artery, Common / Q000000981:diagnostic imaging / Q000473:pathology*; D008078:Cholesterol, LDL / Q000097:blood; D017023:Coronary Angiography / Q000379:methods; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000473:pathology* / Q000652:urine; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007564:Japan; D016015:Logistic Models; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000097:blood; D008875:Middle Aged; D013997:Time Factors; D014057:Tomography, X-Ray Computed
D015415:Biomarkers; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; C075750:8-epi-prostaglandin F2alpha; D002097:C-Reactive Protein; D015237:Dinoprost; D020780:Matrix Metalloproteinase 9