Does shear stress modulate both plaque progression and regression in the thoracic aorta? Human study using serial magnetic resonance imaging.
OBJECTIVE
The purpose of this study was to investigate the role of shear stress (SS) in plaque regression.


BACKGROUND
A condition favorable to the development of atherosclerotic lesions is low oscillating SS. In the descending thoracic aorta, the relationship between plaque distribution and SS has never been characterized. The regression of plaque as the result of lipid-lowering therapy is associated with reverse atherogenic mechanisms. Therefore, we investigated the role of SS in plaque regression. Magnetic resonance imaging (MRI) provides a unique opportunity to noninvasively study morphology and hemodynamics.


METHODS
Cross-sectional images of atherosclerotic plaques in the descending thoracic aorta of 10 asymptomatic, hypercholesteremic patients were acquired at baseline and 24 months after starting lipid-lowering therapy by using a black-blood sequence on a 1.5-T clinical MRI system (5 mm x 780 microm x 780 microm). Average wall thickness (WT) was derived per quadrant. The aorta was subdivided in segments 2 cm in length starting 1 cm from the aortic arch.


RESULTS
Average WT decreased with increasing distance from the arch (3.0 +/- 0.7 mm vs. 2.5 +/- 0.3 mm; p < 0.05) and showed a helical pattern from the proximal to distal segments. Phase-contrast MRI was performed in the thoracic aorta of eight healthy volunteers to derive typical average SS distribution. Shear stress predicted the location of WT (r(2) = 0.29, p < 0.05) but did not predict plaque regression. The best predictor of plaque regression was baseline WT.


CONCLUSIONS
Our data showing an association between WT and average low SS locations support the role of local hemodynamics in the development of atherosclerotic lesions in descending thoracic aorta. Furthermore, SS does not seem to be the major predictor for plaque regression by lipid-lowering interventions. Therefore, our data suggest that other mechanisms are involved in the lipid-reversal mechanism.
Wentzel
Jolanda J
JJ
Cardiovascular Institute, Mount Sinai School of Medicine, New York, New York, USA.
Corti
Roberto
R
Fayad
Zahi A
ZA
Wisdom
Paul
P
Macaluso
Frank
F
Winkelman
Mark O
MO
Fuster
Valentin
V
Badimon
Juan J
JJ
D000328:Adult; D000368:Aged; D001013:Aorta, Thoracic / Q000000981:diagnostic imaging / Q000473:pathology*; D001018:Aortic Diseases / Q000175:diagnosis* / Q000188:drug therapy / Q000503:physiopathology; D001783:Blood Flow Velocity / Q000187:drug effects; D018450:Disease Progression; D017548:Echocardiography, Transesophageal; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D006937:Hypercholesterolemia / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D007091:Image Processing, Computer-Assisted; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011237:Predictive Value of Tests; D011859:Radiography; D013223:Statistics as Topic; D013314:Stress, Mechanical; D016896:Treatment Outcome
D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents