A haemodynamic analysis of intracranial arteriovenous malformations.
Abnormal haemodynamics of intracranial arteriovenous malformations (AVMs) may account for a large spectrum of pathophysiology, including vascular steal, haemorrhage, chronic hypoperfusion, and low-grade ischaemia in adjacent brain tissue. The high blood flow rates present in AVMs may also influence treatment complications including, 'perfusion pressure breakthrough' phenomena. In this paper, a biomathematical analysis of haemodynamic alterations in intracranial arteriovenous malformations is presented, based on fluid dynamic formulations of flow rates, cerebral perfusion pressure, intra-AVM pressure gradients, and haemodynamic resistances. The model demonstrates that (1) vascular steal is inversely proportional to the haemodynamic resistance of the AVM, (2) haemorrhage probability is related to the distribution of cerebral perfusion pressure across large thin-walled shunts, (3) normal reperfusion pressure after AVM obliteration is dependent on the ratio of resistance of surrounding vasculature versus any residual AVM, and (4) hyperemic complications post-treatment are likely to occur in high-flow AVMs that demonstrate steal. These results, in general, agree with current clinical impressions. Although the difficulty of obtaining accurate clinical measurements of some of these model parameters precludes a complete empirical testing of the model, the biomathematical analysis should provide a useful theoretical framework for understanding the complex haemodynamic perturbations that may influence the pathophysiology and treatment approach for intracranial AVMs.
Lo
E H
EH
Center for Imaging and Pharmaceutical Research, Massachusetts General Hospital, Harvard Medical School, Boston 02129.
D002543:Cerebral Hemorrhage / Q000209:etiology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D006940:Hyperemia / Q000209:etiology; D002538:Intracranial Arteriovenous Malformations / Q000150:complications / Q000503:physiopathology*; D008433:Mathematics; D008955:Models, Cardiovascular