Key result
Wall shear stress (WSS) was inversely related to carotid plaque thickness (R=-0.28 and -0.37, p<0.01), while oscillatory shear index (OSI) was directly related (R=0.22 and 0.52, p<0.05).
Why the study?
Do baseline wall shear stress and oscillatory shear index correlate with carotid plaque thickness, composition, and regression after 6 months of statin treatment?
Observational (n=8)
Do baseline wall shear stress and oscillatory shear index correlate with carotid plaque thickness, composition, and regression after 6 months of statin treatment?
p-value: p=<0.01
Patient-specific CFD enables efficient WSS/OSI mapping in carotid plaques; leaves open their link to statin-related thickness changes.
PURPOSE: Low wall shear stress (WSS) and high oscillatory shear index (OSI) influence plaque formation, yet little is known about their role in progression/regression of established plaques because of lack of practical means to calculate them in individual patients. Our aim was to use computational fluid dynamics (CFD) models of patients with carotid plaque undergoing statin treatment to calculate WSS and OSI in a time-efficient manner, and determine their relationship to plaque thickness (PT), plaque composition (PC), and regression. METHODS: Eight patients (68 +/- 9 yr, one female) underwent multicontrast 3 T MRI at baseline and six-month post statin treatment. PT and PC were measured in carotid segments (common-CC, bifurcation-B, internal-IC) and circumferentially in nonoverlapping 600 angles and correlated with CFD models created from MRI, ultrasound, and blood pressure. RESULTS: PT was highest in B (2.42 +/- 0.98 versus CC: 1.60 +/- 0.47, IC: 1.62 +/- 0.52 mm, p < 0.01). Circumferentially, plaque was greatest opposite the flow divider (p < 0.01), where the lowest WSS and highest OSI were observed. In B and IC, PT was inversely related to WSS (R = -0.28 and -0.37, p < 0.01) and directly related to OSI (R = 0.22 and 0.52, p < 0.05). The total plaque volume changed from 1140 +/- 437 to 974 +/- 587 mm3 at six months (p = 0.1). Baseline WSS, but not OSI, correlated with changes in PT, necrotic tissue, and hemorrhage in B and IC, but not CC. CFD modeling took 49 +/- 18 h per patient. CONCLUSIONS: PT and PC correspond to adverse WSS and OSI in B and IC, and WSS is modestly but significantly related to changes in PT after short-term statin treatment. Regional hemodynamics from CFD can feasibly augment routine clinical imaging for comprehensive plaque evaluation.
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LaDisa et al. (2010) conducted an observational in Carotid plaque (n=8). Wall shear stress (WSS) and oscillatory shear index (OSI) was evaluated on Relationship of wall shear stress (WSS) and oscillatory shear index (OSI) to plaque thickness (PT) (p=<0.01). Wall shear stress (WSS) was inversely related to carotid plaque thickness (R=-0.28 and -0.37, p<0.01), while oscillatory shear index (OSI) was directly related (R=0.22 and 0.52, p<0.05).
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