Shear stress in cerebral arteries supplying arteriovenous malformations

Abstract

Arteries supplying cerebral arteriovenous malformations (AVMs) are known to dilate with time. These changes are reversible, and the feeders have been shown to slowly decrease in calibre after removal of the AMV. There is evidence that arteries alter their internal diameters in response to sustained changes of blood flow so that shear stress is kept constant. This implies that blood flow-induced shear stress might be the driving force for remodelling of the cerebral vascular network in the presence of an AVM, and for reversion of these changes after radical operation. The objective of this study is to examine the hypothesis that the shear stress in cerebral arteries supplying AMVs is of the same magnitude as in arteries supplying normal brain tissue in spite of larger blood flow rate. Fifteen patients with supratentorial cerebral AVMs admitted for endovascular treatment were examined with transcranial Doppler ultrasound in the distal Willisian vessels. Vessel calibres were measured in angiograms with magnification correction. Shear stress was estimated assuming a constant value for blood viscosity. Corresponding arteries in the cerebral hemisphere with AVM and in the contralateral one were compared in pairs. Thirty-four pairs of homonymous arteries were studied. The arteries on the AVM side presented larger calibres, higher axial blood flow velocities, lower pulsatility index and larger blood flow rates than the contralateral side. There was a clear positive correlation between blood flow velocities and vessel calibres. The estimates of shear stress did not differ significantly in corresponding arteries of both hemispheres (p = 0.18). The results indicate a precise adjustment of cerebral arterial calibre and blood flow-induced shear stress that presumably induces the progressive dilation of AVM feeders, and the slow regression of the vessel calibres to average dimensions after removal of the lesion. Each vessel seems to remodel itself in response to long-term changes in blood flow rate so that the vessel calibre is reshaped to maintain a constant level of wall shear stress.

Changes in Wall Shear Stress of Cerebral Arteriovenous Malformation Feeder Arteries After Embolization and Surgery

“…4 The first and only other study to measure WSS in patients with cerebral AVMs was published by Rossitti and Svendsen in 1995. 12 They calculated WSS in a total of 17 feeder arteries in 15 patients (27% with hemorrhagic presentation) by obtaining blood flow velocity within the principal feeder arteries (anterior, middle, and posterior cerebral arteries) and their normal contralateral counterparts (also anterior, middle, and posterior cerebral arteries) using transcranial Doppler ultrasound (TCD) and assessing vessel size from digital subtraction angiography. They found that mean vessel caliber was significantly larger within the AVM feeder arteries compared with the corresponding arteries in the contralateral hemisphere (0.14 cm versus 0.12 cm; P=0.0008).…”

“…This result reveals that cerebral AVMs are a high WSS pathology, which disputes Rossitti and Svendsen's hypothesis that WSS in arteries supplying AVMs is the same as in arteries within normal brain parenchyma. 12 This difference may be attributed to varying methods of blood flow measurement-Rossitti and Svendsen used TCD, whereas we used QMRA. Indeed, TCD is considered to be highly operatordependent and inferior to QMRA that provides better resolution and 3D localization capability.…”

Cooperation of Nature and Physiologically Inspired Mechanisms in Visualisation

“…Specifically, chronic increases in blood flow, and consequently shear stress, lead to the expansion of the luminal radius such that mean shear stress is returned to its baseline level (Kamiya & Togawa, 1980, Girerd et al, 1996. This is clearly demonstrated in the radial artery of dialysis patients proximal to their arteriovenous fistula (Girerd et al, 1996) or in feeder arteries supplying cerebral arteriovenous malformations (Rossitti & Svendsen, 1995), both of which lead to the expansion of the blood vessels calibre as a result of increased shear stress in the vessel lumen. Conversely, decreased shear stress resulting from lower flow or blood viscosity induces a decrease in internal vessel radius (Lowell & O'Donnell, 1986).…”

A DNA Sequence Polymorphism in the Endoglin Gene Is Not Associated with Intracranial Aneurysm or Aneurysmal Subarachnoid Hemorrhage

“…For example, it is well documented that hemodynamic shear stress is a major contributor to IA pathogenesis [14, 15]. Arteriovenous malformations are characteristic of HHT and are thought to be characterized in part by alterations in shear stress [16, 17]. Therefore, one important pathogenic factor that may affect endoglin expression and/or function is hemodynamic stress.…”