Cerebrovascular diseases, vascular risk factors and socioeconomic status

Cerebrovascular disease, has an enormous, and increasing, impact on global health. As well as causing clinical stroke, cerebrovascular disease is thought to be a major contributor to cognitive decline and dementia. Socioeconomic status (SES) is associated with risk of stroke. Those in the lowest SES group are estimated to be at twice the risk of stroke compared to those in the highest SES group. Those with low SES may also have a more severe stroke and a poorer outcome. It is imperative that the extent and mechanism of this association is clarified. This thesis aims to determine if the association between SES and stroke is explained by a greater prevalence of traditional vascular risk factors amongst those of low SES. It also explains the link with a novel risk factor, poor oral health. Lastly it addresses the long-term cognitive outcome in older people at risk of vascular disease. A systematic review and meta-analysis was undertaken to establish if vascular risk factors explain the association between SES and stroke incidence / post-stroke mortality. This demonstrated that lower SES was associated with an increased risk of stroke and that a greater burden of vascular risk factors in those with low SES explained about 50% of the additional risk of stroke. However this meta-analysis could not clarify what vascular risk factors are most critical. Low SES was also associated with increased mortality risk in those who have a stroke although study results were heterogeneous and this link was not readily explained by known vascular risk factors. A prospective study of 467 consecutive stroke and transient ischameic attack (TIA) patients from three Scottish hospitals was undertaken with the aim of establishing whether those with low SES carry higher levels of vascular risk factors, have a more severe stroke and have equal access to stroke care services and investigations. Stroke / TIA patients with low SES were younger and more likely to be current smokers but there was no association with other vascular risk factors /co-morbidity. Those who had lower SES had a more severe stroke. The lowest SES group were less likely to have neuroimaging or an electrocardiogram although differences were not significant on multivariate analysis. There was however equal access to stroke unit care. A secondary analysis of a prospective cohort study of 412 stroke patients was conducted. The aim was to explore oral health after acute stroke and assess if poor oral health explains the association between SES and stroke. Dry mouth amongst acute stroke patients was very common, however there was no association between oral health and low SES. There was an association of dry mouth with pre-stroke disability and Urinary Tract Infection. There was also a link with oral Candida glabrata colonisation, although the clinical relevance of this is uncertain. In the acute phase after stroke there was no convincing association of dry mouth with dysphagia or pneumonia. Therefore there was no association between SES and poor oral health as measured in this study but oral health may still be part of the explanation of the association between SES and acute stroke and this needs further investigation. Vascular disease is an important contributor to cognitive decline and dementia. Low SES may be associated with an increased risk of cognitive decline in later life and vascular disease may be a mediating factor. More effective prevention of vascular disease may slow cognitive decline and prevent dementia in later life, particularly in low SES groups. Lipid lowering with statins might be effective in preventing dementia but so far evidence from randomised control trials does not show benefit from statins in preventing cognitive decline and dementia. However the duration of follow-up in these trials was short and there may be benefit in the long-term. My aim was therefore to establish if long-term follow-up of the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER) study was feasible. I found that it was feasible to follow-up 300 elderly survivors from the Scottish arm of the PROSPER study and the methods could be extended to the whole group. As expected nearly half of the PROSPER participants were dead. Additionally a large proportion of traceable participants had significant cognitive impairment. Smoking cessation, control of blood pressure and management of other vascular risk factors should be made a priority in areas of low SES. Additionally further research is needed to fully clarify the association between SES and stroke incidence. Avenues for exploration might include the possibilities of poorer access to effective stroke care, reduced uptake of care and poorer oral health in lower SES groups. In addition public health campaigns regarding smoking cessation should be directed at lower SES groups. I have shown that a large scale follow-up of the PROSPER participants is feasible and may determine new and novel risk factors for dementia and assess the long-term effect of a period of treatment with pravastatin