Hemodynamic significance of internal carotid artery disease

Abstract

— Neurologic symptoms in the region of an internal carotid artery stenosis are considered to be embolic in most instances. Only in a subgroup has carotid occlusive disease with impairment of the collateral supply, caused a state of hemodynamic failure with marked reduction of perfusion pressure. Though unproven, it is reasonable to assume that without surgical intervention, the risk is higher than average for patients with hemodynamic failure. Equally, should there be any postoperative improvement of cerebral blood flow or neurologic deficits, it should be looked for in this group. Thus, it is necessary to distinguish those with low perfusion pressure from the population of patients with carotid artery disease. Preoperative clinical evaluation and direct visualization of the carotid bifurcation should be supplemented by indirect physiological tests which allow assessment of collateral perfusion. Examination of periorbital flow direction or oculoplethysmography could be used as a screening procedure. Negative tests most certainly rule out any severe pressure gradient across the stenosis, irrespective of the luminal reduction. A positive result, on the other hand, should be further quantified since most indirect tests become positive at relatively small pressure gradients. Studies of cerebral blood flow at rest and during cerebral vasodilation makes it possible to identify patients with severe reduction of cerebral perfusion pressure. Such hemodynamic failure of one hemisphere may be identified in most cases by a conventional non-invasive xenon-133 technique and stationary detectors. Smaller focal regions of hypoperfusion may be identified by computer emission tomography, either by the detection of single-photon emission or by paired detection of annihilation photons. Endarterectomy does improve cerebral hemodynamics in terms of increased flow through the reconstructed vessel and elimination of pressure gradients. The cerebral blood flow, though remains unchanged in the majority of patients, at least when measured at baseline. Only in those patients with a reduction in perfusion pressure can a significant improvement in baseline flow occur. Flow reserve determined by cerebral vasodilation, however, will improve in most patients with hemodynamic failure. In addition, some patients in the low-pressure group develop marked, but temporary, hyperperfusion after reconstruction of very high grade carotid stenosis. This is considered a result of chronic low perfusion pressure with subsequent loss of autoregulation, and autoregulatory control is first regained after some days. Hyperperfusion, however, has been associated with increased risk of postoperative neurologic complications as cerebral hemorrhage, seizures and severe headache. Thus, those patients who seem to benefit most from surgery run the highest risk of complications. Future studies of both carotid artery surgery and extracranial-intracranial bypass surgery should include physiologic entry criteria as an adjunct to traditional preoperative assessment. Thus, the underlying hemodynamic state may be evaluated helping to identify patients who may or may not benefit from cerebrovascular reconstructive surgery.