Dynamic cerebral autoregulation and beat to beat blood pressure control are impaired in acute ischaemic stroke. (Paper).

Objectives: Hypertension and chronic cerebrovascular disease are known to alter static cerebral autoregulation (CA) but the effects of acute stroke on dynamic CA (dCA) have not been studied in detail. Those studies to date measuring dCA have used sympathetically induced blood pressure (BP) changes, which may themselves directly affect dCA. This study assessed whether dCA is compromised after acute stroke using spontaneous blood pressure (BP) changes as the stimulus for the dCA response.

Methods: 56 patients with ischaemic stroke (aged 70 (SD 9) years), studied within 72 hours of ictus were compared with 56 age, sex, and BP matched normal controls. Cerebral blood flow velocity was measured using transcranial Doppler ultrasound (TCD) with non-invasive beat to beat arterial BP levels, surface ECG, and transcutaneous [CO.sub.2] levels and a dynamic autoregulatory index (dARI) calculated.

Results: Beat to beat BP, but not pulse interval variability was significantly increased and cardiac baroreceptor sensitivity (BRS) decreased in the patients with stroke. Dynamic CA was significantly reduced in patients with stroke compared with controls (strokes: ARI 3.8 (SD 2.2) and 3.2 (SD 2.0) for pressor and depressor stimuli respectively v controls: ARI 4.7 (SD 2.2) and 4.5 (SD 2.0) respectively (p<0.05 in all cases)). There was no difference between stroke and non-stroke hemispheres in ARI, which was also independent of severity of stroke, BP, BP variability, BRS, sex, and age.

Conclusion: Dynamic cerebral autoregulation, as assessed using spontaneous transient pressor and depressor BP stimuli, is globally impaired after acute ischaemic stroke and may prove to be an important factor in predicting outcome.

**********

Cerebral autoregulation (CA) is the ability of the brain to maintain relatively constant cerebral blood flow (CBF) despite changes in perfusion pressure. Before the development of transcranial Doppler ultrasound, static CA was assessed using steady state blood pressure (BP) changes and assessing the alteration in CBF without taking into account the speed at which the CBF recovers following a change in BP. Transcranial Doppler ultrasound (TCD) and non-invasive beat to beat BP monitors have allowed the dynamic relation between cerebral blood flow velocity (CBFV) and mean arterial pressure (MAP) to be quantified (changes in BP taking place over 5 to 10 seconds) giving a measure of dynamic CA (dCA). Dynamic CA may have different underlying pathophysiological control mechanisms to static CA. (1) Dynamic CA has been shown to be influenced differently from static CA in disease states such as stroke. (2)

Non-pharmacological manoeuvres to induce rapid perturbations in BP--for example, the sudden release of thigh cuffs or the Valsalva manoeuvre--have been used to assess dCA but are problematic. (3) They may be unacceptable or impractical for some patients and can induce changes in sympathetic nervous system activity, respiration, cardiac output, and carbon dioxide concentration, all of which may affect dCA directly or indirectly. These potential problems could be avoided by using spontaneous BP fluctuations in recordings made at rest.

A widely applicable method of measuring dCA in patients with acute stroke is needed to allow detailed investigation of the relation between altered cardiovascular homeostasis and outcome, and may ultimately be relevant in the treatment of BP in the acute stroke period.

After acute stroke normal cardiovascular homeostatic mechanisms are impaired and in the immediate postictal phase BP levels are often increased, tending to fall spontaneously over the subsequent 10-14 days. (4-6) Although hypertension is a major risk factor for primary stroke, its prognostic relevance in the acute poststroke period is uncertain. If CA is impaired after acute ischaemic stroke, then CBF flow becomes dependent on systemic BP and increasing BP may result in cerebral oedema or haemorrhagic transformation of the infarct, whereas reducing systemic BP could reduce flow to the ischaemic penumbra and increase infarct size.

Clinical studies reporting BP and outcome after acute stroke are at variance. (7-9) and have not clarified these diametrically opposed theoretical views as to the benefits of BP reduction after acute stroke and the role of CA has not been investigated. Beat to beat BP variability hyperperfusion is known to be increased in acute stroke (10) and associated with a worse prognosis in terms of death and disability, independently of MAP levels and stroke severity. (11) This adverse outcome associated with increased BP variability could be mediated by impairment in dCA, which could result in hyperperfusion and/or hypoperfusion of the ischaemic penumbra with spontaneous pressor and depressor BP changes. Cardiac baroreceptor sensitivity (BRS) is also reduced after stroke (12) and may account for the increased BP variability seen. It is therefore important to assess the relation between dCA, BP, and cardiac BRS, to understand how these parameters influence one another and their clinical significance.

The aims of this study were to assess if dCA is impaired after acute cerebral infarction, using spontaneous, rather than induced, transient changes in BP as the BP stimulus, and to study the relation between the changes in dCA after stroke with cardiac BRS and beat to beat BPV.

SUBJECTS AND METHODS

Methods

Fifty six patients with ischaemic stroke diagnosed by CT or MRI were recruited within 72 hours of ictus from the acute stroke units at Glenfield Hospital NHS Trust and Leicester General Hospital. Stroke types were classified using the Oxford Community Stroke Project (OCSP) classification (13) and functional severity was graded using the Barthel index. (14) Patients were …