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Homeostatic effects of carotid stenosis
  1. S M OPPENHEIMER
  1. Dr S M Oppenheimer, Cerebrovascular Program, Department of Neurology, Meyer 5–185, Johns Hopkins Hospital, 600 North Wolfe Street, Baltimore, MD 21205, USA. Telephone 00 1 410 502 5356; fax 00 1 410 614 9807.

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Signalling of blood pressure changes is partly the result of carotid sinus function and activity within the afferent glossopharyngeal and vagus nerves. Carotid stenosis is common and often affects the carotid bulb where the arterial baroreceptors are situated. However, little attention has been paid to the homeostatic effects of stenosis at this point. Akinola et al in this issue (pp428–32)1 compare autonomic reflexes in a group of hypertensive patients with transient ischaemic attacks (TIAs) and unilateral or bilateral carotid stenosis to matched groups of hypertensive and normotensive controls. Their findings indicate that baroreflex sensitivity is blunted, the effects being equal in patients with either unilateral or bilateral carotid stenosis compared with both control groups. In other respects, autonomic reflexes are blunted to the same extent as seen in hypertensive controls, indicating no specific involvement of cardiovascular efferents in the stenosis group. There are two main caveats. The first concerns the use of antihypertensive medication. Such treatment, especially with angiotensin converting enzyme activators (which may act on AT receptors in the area postrema) or β-blockers can affect baroreflex sensitivity. Although these medications were stopped within 1 day of the study, their central effects may be longer lasting. Secondly, other mechanoreceptors in the left ventricle and aortic arch may be intact in these patients. However, the shrewd use of a hypertensive control group on similar medication to some extent allays some of the interpretative complications. Why the effects are similar in patients with severe unilateral and bilateral carotid stenosis is a matter of conjecture. This could indicate a complex non-linear compensatory effect within the brain, using baroreceptor input from the aortic arch and other regions. The importance of this study is threefold: firstly, such patients may be at risk of presyncopal symptoms which may be erroneously diagnosed as focal brainstem transient ischaemic attacks; secondly, impaired peripheral blood pressure regulation could affect cerebral blood flow in the post-stroke state as such patients lose cerebral autoregulation. The effects could also be accentuated in patients with tandem intracranial stenosis. Finally, it should not be forgotten that control of blood pressure may be impaired after carotid endarterectomy and the effects of antihypertensive medication in these patients should be monitored most carefully.

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