Why the study?
Is wall shear stress associated with carotid atherosclerosis indicators in untreated hypertensive patients?
Is wall shear stress associated with carotid atherosclerosis indicators in untreated hypertensive patients?
Low wall shear stress in the common carotid artery is independently associated with higher resistive and pulsatility indices in untreated hypertensive patients, suggesting a hemodynamic mechanism for atherosclerosis progression.
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May link hypertension to carotid flow changes; hypothesis-generating and requires prospective confirmation before clinical consideration.
BACKGROUND: Wall shear stress (WSS) has been shown to be a critical determinant of vessel diameter implicated in vascular remodeling and atherogenesis. Carotid intima-media thickness (IMT), resistive index (RI), and pulsatility index (PI) have been used as relevant indictors for carotid atherosclerosis. The study aimed to investigate the relationship between hemodynamic parameters in the common carotid artery (CCA) and the severity of carotid atherosclerosis in untreated hypertensive patients. METHODS: Duplex ultrasound was performed in 64 untreated hypertensive patients and 16 age-matched normotensive control subjects. Morphologic and hemodynamic parameters of CCA, including peak and mean WSS, RI, PI, and IMT were calculated after measuring internal diameter (ID) and flow velocity of CCA. RESULTS: Subjects with hypertension had lower peak and mean WSS than did normotensive control subjects (P < 0.05). Both carotid RI and PI were found to correlate inversely with mean WSS in hypertensive subjects. There was no correlation between carotid IMT and WSS. Stepwise multiple regression analysis for carotid RI and PI after adjustment for age, carotid IMT, and high sensitivity C-reactive protein (hsCRP) showed that mean WSS was an independent determinant of RI and PI. CONCLUSIONS: High carotid atherosclerotic indexes as expressed by both RI and PI are associated with low WSS in CCA. These findings indicate that local shear stress is associated with altered vascular pulsatility and resistance. Consequent alteration in local vascular dynamics could be an underlying mechanism for the progression of atherosclerosis.
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Lee et al. (2009) studied this question.
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