Date of this Version
J Vasc Surg. 2011 Oct;54(4):1011-20. doi: 10.1016/j.jvs.2011.03.254. Epub 2011 May 28.
Objective: True understanding of carotid bifurcation pathophysiology requires a detailed knowledge of the hemodynamic conditions within the arteries. Data on carotid artery hemodynamics are usually based on simplified, computer-based, or in vitro experimental models, most of which assume that the velocity profiles are axially symmetric away from the carotid bulb. Modeling accuracy and, more importantly, our understanding of the pathophysiology of carotid bifurcation disease could be considerably improved by more precise knowledge of the in vivo flow properties within the human carotid artery. The purpose of this work was to determine the three-dimensional pulsatile velocity profiles of human carotid arteries.
Methods: Flow velocities were measured over the cardiac cycle using duplex ultrasonography, before and after endarterectomy, in the surgically exposed common (CCA), internal (ICA), and external (ECA) carotid arteries (n = 16) proximal and distal to the stenosis/endarterectomy zone. These measurements were linked to a standardized grid across the flow lumina of the CCA, ICA, and ECA. The individual velocities were then used to build mean three-dimensional pulsatile velocity profiles for each of the carotid artery branches.
Results: Pulsatile velocity profiles in all arteries were asymmetric about the arterial centerline. Posterior velocities were higher than anterior velocities in all arteries. In the CCA and ECA, velocities were higher laterally, while in the ICA, velocities were higher medially. Pre- and postendarterectomy velocity profiles were significantly different. After endarterectomy, velocity values increased in the common and internal and decreased in the external carotid artery.
Conclusions: The in vivo hemodynamics of the human carotid artery are different from those used in most current computer-based and in vitro models. The new information on three-dimensional blood velocity profiles can be used to design models that more closely replicate the actual hemodynamic conditions within the carotid bifurcation. Such models can be used to further improve our understanding of the pathophysiologic processes leading to stroke and for the rational design of medical and interventional therapies.