The haemorheology of transient ischaemic attacks

Rogers, Paul Noel (1987) The haemorheology of transient ischaemic attacks. MD thesis, University of Glasgow.

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Abstract

Stroke is a frequent cause of death and disability in Western society for which therapy has little to offer. The limitations of therapy for completed stroke has placed great emphasis on stroke prevention and this is manifested mainly by the elimination and control of previously identified risk factors, of which hypertension is the prime example. The occurrence of a transient ischaemic attack (TIA) is an important risk factor because, although only a minority of strokes are preceded by such an attack, the incidence of completed stroke following a TIA is high, particularly if the attack occurs in the carotid territory. In a majority of patients who experience a TIA the cause of the attack is identified; thromboembolic disease is the commonest aetiology and extracranial arterial disease is the source of emboli in most of these patients. In a minority of patients the cause of their symptoms remains undiscovered, often in spite of extensive investigation. The studies in this thesis set out to determine if TIAs of unknown aetiology shared the poor prognosis of thromboembolic attacks, and if so whether haemorheological abnormalities could explain these attacks. A retrospective follow-up study of patients with carotid distribution TIAs, in whom no embolic source had been identified by routine screening procedures, indicated that the stroke risk in this group is almost as high as that observed in studies of the natural history of TIA. In the light of this finding it was felt important to attempt to discover the cause of the symptoms in this group of patients with a view to developing a rational management policy. TIAs are the result of focal cerebral perfusion failure which may theoretically be due to inadequate perfusion pressure, diminished vessel radius or increased blood viscosity. Each of the first two mechanisms has been previously implicated in the pathogenesis of TIA. Consequently it seemed reasonable to investigate the possible role of increased blood viscosity in unexplained TIAs. A prospective study of whole blood viscosity, and its determinants, in carotid territory TIA revealed that there are no differences in whole blood viscosity between patients with unexplained attacks and those with presumed thromboembolic disease, identified by Doppler carotid scanning. Plasma fibrinogen levels were significantly higher in patients with carotid disease compared to those without detectable carotid disease. A study to compare haemorheological parameters in TIA patients with a normal age and sex-matched control group, demonstrated that although whole blood viscosity was the same in both groups plasma viscosity and plasma fibrinogen were both significantly higher in the TIA group. Further studies revealed that these changes in plasma viscosity and fibrinogen are similar in magnitude to those found in peripheral arterial disease patients, who have well documented blood viscosity abnormalities. Elevations in plasma fibrinogen levels may occur for many reasons. With regard to cerebrovascular disease the most relevant chronic influences on the plasma fibrinogen level are the presence of hypertension and cigarette smoking, both of which may cause it to rise. The possibility that the elevated fibrinogen levels in TIA patients, particularly those with carotid disease, were due to an increased prevalence of smoking and hypertension in these groups was considered. Sub-group analysis revealed that the influence of clinically evident arterial disease, manifested either by symptoms or positive Doppler carotid screening, outweighed the effect of smoking and hypertension. In conclusion, TIA patients who do not have a detectable embolic source are at a risk of stroke and cardiovascular morbidity comparable to other patients with TIA, and therefore merit continued review and/or repeated or more extensive investigation. Viscosity abnormalities do not account for symptoms in these patients. However, fibrinogen levels are elevated in all TIA patients, most notably those with carotid disease. In view of the association between raised plasma fibrinogen and arterial disease it is possible that patients with unexplained symptoms have undetected arterial disease which acts as a source of emboli. It is accepted that fibrinogen is a risk factor for ischaemic heart disease and stroke, and these studies now show that it is associated with TIA and the degree of detectable carotid disease. The relationship between raised fibrinogen and atheroma may be causative, consequential or merely coincidental. If increases in fibrinogen follow the development of arterial lesions or are produced by common stimuli then fibrinogen levels act only as markers of disease. If however, raised fibrinogen levels promote atheroma production or predispose to thrombosis in relation to pre-existing atheroma then defibrinogenation therapy may be beneficial in individuals at risk from arterial disease. Studies on the efficacy of such therapy must await the development of more suitable drugs than are available at present.

Item Type: Thesis (MD)
Qualification Level: Doctoral
Keywords: Medicine, Physiology
Date of Award: 1987
Depositing User: Enlighten Team
Unique ID: glathesis:1987-76690
Copyright: Copyright of this thesis is held by the author.
Date Deposited: 19 Nov 2019 13:53
Last Modified: 19 Nov 2019 13:53
URI: http://theses.gla.ac.uk/id/eprint/76690

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