Hemodynamics and oxygen extraction in chronic large artery steno-occlusive disease: Clinical applications for predicting stroke risk

J Cereb Blood Flow Metab. 2018 Sep;38(9):1584-1597. doi: 10.1177/0271678X17732884. Epub 2017 Sep 19.

Abstract

Depending on the adequacy of collateral sources of blood flow, arterial stenosis or occlusion may lead to reduced perfusion pressure and ultimately reduced blood flow in the distal territory supplied by that vessel. There are two well-defined compensatory mechanisms to reduced pressure or flow - autoregulatory vasodilation and increased oxygen extraction fraction. Other changes, such as metabolic downregulation, are likely. The positive identification of autoregulatory vasodilation and increased oxygen extraction fraction in humans is an established risk factor for future ischemic stroke in some disease states such as atherosclerotic carotid stenosis and occlusion. The mechanisms by which ischemic stroke may occur are not clear, and may include an increased vulnerability to embolic events. The use of hemodynamic assessment to identify patients with occlusive vasculopathy at an increased risk for stroke is very appealing for several different patient populations, such as those with symptomatic intracranial atherosclerotic disease, moyamoya phenomenon, complete internal carotid artery occlusion, and asymptomatic cervical carotid artery stenosis. While there is very good data for stroke risk prediction in some of these groups, no intervention based on these tools has been proven effective yet. In this manuscript, we will review these topics above and identify areas for future research.

Keywords: Arterial stenosis; cerebrovascular disease; occlusion; oxygen extraction; stroke.

Publication types

  • Review

MeSH terms

  • Arterial Occlusive Diseases / metabolism
  • Arterial Occlusive Diseases / physiopathology*
  • Cerebrovascular Circulation / physiology*
  • Hemodynamics / physiology*
  • Humans
  • Oxygen / metabolism*
  • Stroke / etiology
  • Stroke / metabolism
  • Stroke / physiopathology*

Substances

  • Oxygen