Arterial remodeling in [corrected] subclinical carotid artery disease.
OBJECTIVE
We sought to identify clinical and/or plaque characteristics that affect atherosclerotic disease progression and arterial remodeling in the carotid artery with subclinical stenosis.


BACKGROUND
Increasing severity of stenosis has been associated with a higher risk of stroke. Factors that drive subclinical lesions to become stenotic plaques remain ambiguous. Carotid magnetic resonance imaging (MRI) has been validated with histology to accurately quantify in vivo arterial morphology and plaque composition.


METHODS
A total of 67 asymptomatic participants with 16% to 49% carotid stenosis as demonstrated by duplex ultrasonography were imaged at 1.5-T with a carotid MRI protocol at baseline and at 18-month follow-up. Clinical and/or intra-arterial metrics with a significant association with change in plaque burden during multivariate analysis were evaluated for effects on lumen, wall, and total vessel volume.


RESULTS
From multiple regression analysis, intraplaque hemorrhage (IPH) (p < 0.001) and statin therapy (p = 0.015) were identified as key determinants of change in plaque burden. The group with IPH compared with the group without IPH demonstrated luminal narrowing, with a mean +/- SD decrease in lumen volume (-24.9 +/- 21.1 mm(3)/year vs. -0.5 +/- 26.9 mm(3)/year; p = 0.005), a larger increase in wall volume (44.1 +/- 36.1 mm(3)/year vs. 0.8 +/- 34.5 mm(3)/year; p < 0.001), and no difference in total vessel volume (19.3 +/- 27.4 mm(3)/year vs. 0.4 +/- 42.4 mm(3)/year; p = 0.15). The nonstatin group compared with the statin group demonstrated outward remodeling, with an increase in wall volume (22.4 +/- 35.6 mm(3)/year(3)/year vs. 0.9 +/- 38.0 mm(3)/year; p = 0.026) and total vessel volume (19.2 +/- 36.9 mm(3)/year vs. -4.9 +/- 40.4 mm(3)/year; p = 0.019) and no difference in lumen volume (-5.8 +/- 26.6 mm(3)/year vs. -3.2 +/- 29.5 mm(3)/year; p = 0.72).


CONCLUSIONS
IPH may represent an indication of accelerated plaque growth and impending luminal compromise in the subclinical carotid artery. Statin therapy may stabilize lesions by slowing or halting lesion progression. This phase of plaque stenosis (16% to 49%) may be a critical stage for intrinsic and extrinsic factors to affect the atherosclerotic disease process.
Underhill
Hunter R
HR
Yuan
Chun
C
Yarnykh
Vasily L
VL
Chu
Baocheng
B
Oikawa
Minako
M
Polissar
Nayak L
NL
Schwartz
Stephen M
SM
Jarvik
Gail P
GP
Hatsukami
Thomas S
TS
D000368:Aged; D000369:Aged, 80 and over; D001794:Blood Pressure; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000473:pathology*; D016893:Carotid Stenosis / Q000150:complications / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology; D018450:Disease Progression; D005260:Female; D006470:Hemorrhage / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D018810:Magnetic Resonance Angiography; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D011446:Prospective Studies; D012307:Risk Factors; D012720:Severity of Illness Index; D013997:Time Factors; D018616:Ultrasonography, Doppler, Duplex
D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors