Risk factors and cerebrovascular disease

Abstract

Worldwide stroke and other cerebrovascular diseases (CVD) are a leading cause of physical disability. They are the second commonest cause of mortality (accounting for 10.8 % of all deaths; WHO, 2011) and the primary reason for admission in a large proportion of hospital inpatients. As a result, it is perhaps not surprising that the financial and social costs arising from CVD, which predominantly relate to subsequent physical care needs, are substantial. The outlook is also far from encouraging, since incidence of CVD is highest in the elderly and the morbidity and costs associated with age-related disorders such as these are likely to continue to mount with the pattern of extended life expectancy observed in Western populations. Although recent attention has focused on the acute hospital treatment of CVD, and in particular intravenous thrombolysis, even the most effective immediate interventions for ischemic stroke have little impact on overall disability and dependency within the general population when compared to primary prevention. In order to apply primary prevention strategies more effectively and efficiently across relevant populations we need to improve our understanding of constituent disease phenotypes and individualized risk factors (genetic and environmental), so that risks are more comprehensively assessed and informed interventional programs developed. An example of how effective targeted primary prevention can be in ischemic stroke relates to atrial fibrillation (AF), where aspirin confers an approximately 22 % absolute risk reduction (ARR) for ischemic stroke, but warfarin confers a much greater (66 %) ARR, albeit with an increased risk of bleeding. The recently revised CHA2DS2-VASc score now enables straightforward stratification of stroke risk for patients with documented AF to balance the risk benefits for specific patients. Newer anticoagulants and left atrial appendage closure devices are now coming into more widespread clinical practice and may have less associated risks (e.g., bleeding), so that treatment options for AF continue to improve and expand. It is also widely considered that a significant proportion of the 25 % of strokes that are ‘‘unexplained’’ (cryptogenic) have undocumented AF as the primary etiology, but the management of this group of patients and how to identify them remains unclear. However, for the majority of patients, the etiology of their cerebrovascular disease is less well defined and although there have been successful campaigns tackling public understanding of stroke symptoms, to facilitate rapid treatment, perhaps the biggest challenge for the future will be to identify all at risk patients and apply effective individualized strategies to prevent these devastating disorders. In this month’s journal club we review some current concepts of the underlying etiologies of CVD. The first two of the three papers are retrospective studies that examine risk factors outside of those given mainstream attention (namely psycho-physical stress and genetic polymorphisms), while the third is a prospective study tackling the issue of sub-clinical AF and stroke. A common and timeless theme emerges from these studies, which is that if we are to be successful in unraveling the diverse causes of these disorders, clinical phenotyping will be an essential tool. J. T. Anderson N. P. Robertson (&) Department of Neurology, University Hospital of Wales, Cardiff, UK e-mail: robertsonnp@cardiff.ac.uk