344
representing about 15% of all acute events in a 1-year period, have residual difficulties with caring for themselves. 18 Apart from death, it is difficult to compare most outcome measures following stroke because of variable definitions of handicap and disability. Most epidemiological studies have tended to concentrate on handicap-ie, the disadvantage experienced as a result of impairment or disability resulting from stroke. However, many elderly people are already handicapped before their stroke and in institutional care; between 10 and 40% of all patients die before hospital admission can be arranged or are cared for in the
community. Hospital care in the acute phase after stroke is the most costly component of the care of stroke patients. The lengthy hospital stay of a small proportion of patients explains the high use and disproportionate share of hospital resources. The increasing burden of health care of stroke patients in the future will be in the acute stages rather than in the long-term management of elderly patients because first-ever stroke often kills people who have been handicapped by other causes, especially if they are elderly.19 Institutional care for about 20% of survivors likewise contributes to the costs. Nevertheless, the bulk of long-term care of stroke patients falls on family members and community services.18 The best measure of the total burden of stroke is prevalence, which provides information about the number of people at any one time in the population who have had a stroke, but reliable estimates of prevalence are especially difficult to come by. For health service planning and for the allocation of resources to help families cope with strokeimpaired survivors, we urgently need accurate information about the prevalence of stroke and about the prevalence of stroke disability. Total prevalence of stroke is estimated to be 5-8 per 1000 population over the age of 25 years.2o Unless a decline in stroke incidence can be achieved, the absolute numbers of stroke victims will rise significantly as the age of the population increases. The 1970s and 1980s were a time of expansion of stroke incidence studies, encouraged by WHO. Since 1984, about fifteen countries have registered stroke events in selected populations according to a standard protocol as part of the WHO MONICA projectand data collection will continue for 10 years. This collaborative effort will shed light on the changes in incidence because it is linked to studies of trends in risk factor levels in the same populations. REFERENCES
Molyneaux A, Warlow C. Value of computerised tomography in patients with stroke: the Oxfordshire Community Stroke Project. Br Med J 1985; 290: 193-97. 2. WHO MONICA Project, Principal Investigators. The World Health Organisation MONICA Project (monitoring trends and determinants in cardiovascular disease): a major international collaboration. J Clin Epidemiol 1988; 41: 105-14. 3. Allen CMC. Clinical diagnosis of the acute stroke syndrome. Q J Med
8. Bonita
R, Beaglehole R, North JDK. Event, incidence and case-fatality
of cerebrovascular disease in Auckland, New Zealand. Am J Epidemiol 1984; 120: 236-43. 9. Broderick JP, Phillips SJ, Whisnant JP, et al. Incidence rates of stroke in the eighties: the end of the decline in stroke? Stroke 1989; 20: 577-82. 10. Terent A. Increasing incidence of stroke among Swedish women. Stroke rates
1988; 19: 598-603. 11. World Health Statistics Annual 1989. Geneva: WHO, 1989. 12. Bamford J, Dennis M, Sandercock P, et al. The frequency, causes and timing of death within 30 days of a first stroke: the Oxfordshire Stroke Project. J Neural Neurosurg Psychiatry 1990; 53: 824-29. 13. Terent A. Survival after stroke and transient ischemic attacks during the 1970s and 1980s. Stroke 1989; 20: 1320-26. 14. Bonita R, Ford M, Stewart AW. Predicting survival after stroke: a three-year follow-up. Stroke 1988; 19: 669-73. 15. Ueda K, Omai T, Hirota Y, et al. Decreasing trend in incidence and mortality from stroke in Hisayama residents, Japan. Stroke 1981; 12: 154-60. 16. Tuomilehto J, Bonita R, Stewart AW, et al. Hypertension, cigarette smoking, and the decline in stroke incidence in eastern Finland. Stroke 1991; 22: 7-11.
Garroway W, Whisnant J, Drury I. The continuing decline in the incidence of stroke. Mayo Clin Proc 1983; 58: 520-23. 18. Bonita R, Anderson A, North JDK. The pattern of management after stroke. Age Ageing 1987; 16: 29-34. 19. Malmgren R, Bamford J, Warlow C, et al. Projecting the number of patients with first ever strokes in patients newly handicapped by stroke in England and Wales. Br Med J 1989; 298: 656-60. 20. Christie D. Prevalence of stroke and its sequelae. Med J Aust 1981; ii: 17.
182-84.
Primary prevention of stroke We do not clearly understand the most dramatic feature of the epidemiology of stroke-the striking decline in mortality that has been observed in many countries (see Bonita, p 342). Nevertheless, reductions in stroke mortality will probably continue; whether or not from our actions will be debatable. It is tempting to invoke dietary changes, with or without consequent alterations in blood pressure,’ or vigorous treatment of hypertension. Secular changes in average blood pressure are hard to document, not least because of the technical difficulties of conducting comparisons over time; and the reduction in stroke mortality was underway well before antihypertensive drugs were widely and successfully used. Such doubts do not detract from the body of knowledge that suggests that we can prevent stroke, and that preventive measures are worth trying. This article reviews what is known about risk factors for stroke and discusses possible strategies for prevention.
1. Sandercock P,
1983; 52: 515-23. 4. Bamford J, Sandercock P, Dennis M, et al. A prospective study of acute cerebrovascular disease in the community: the Oxfordshire Community Stroke Project 1981-1986. 1. Methodology, demography and incidence cases of first-ever stroke. J Neurol Neurosurg Psychiatry 1988; 51: 1373-80. 5. Ward G, Jamrozik K, Stewart-Wynn E. Incidence and outcome of cerebrovascular disease in Perth, Western Australia. Stroke 1988; 19: 1501-06. 6. Bonita R, Stewart AW, Beaglehole R. International trends in stroke mortality: 1970-1985. Stroke 1990; 32: 989-92. 7. Malmgren R, Warlow C, Bamford J, Sandercock P. Geographical and secular trends in stroke incidence. Lancet 1987; ii: 1196-2000.
Stroke is
preventable
Three types of evidence suggest that stroke is, in principle preventable. First, time trends: much of the rapid change in stroke mortality is likely to have resulted from change in incidence rates, so factors determining onset of disease must have changed. Second, there are large international ADDRESSES Department of Epidemiology and Public Health, University College and Middlesex School of Medicine, London, UK (Prof M G Marmot, FFPHM, N. R Poulter, MRCP); Department of Epidemiology and Population Sciences, London School of Hygiene and Tropical Medicine (Prof M G. Marmot); and Department of Clinical Pharmacology, St Mary’s Hospital Medical School, London (N. R Poulter). Correspondence to Prof M G Marmot, Department of Epidemiology and Public Health, University College and Middlesex School of Medicine, 66-72 Gower Street, London WC1 E 6EA, UK.
345
differences in stroke mortality, but these are not fixed, as shown by the experience of migrants. For example, Japan has high rates of stroke and low rates of coronary heart disease (CHD) whereas men of Japanese ancestry living in the USA have lower rates of stroke and higher rates of CHD.2 Third, the data that have amassed on causes of stroke strongly suggest that (a) many of them can be avoided, and (b) although they exert their effect over decades, this effect is at least partly reversible in a few years. One study suggested that 50% of cerebrovascular deaths in patients under 70 years might be preventable by application of
existing knowledge.3 Risk factors for stroke Causes, risk factors, and variations in The
term
occurrence
risk factor is used in various ways. The
following distinctions among risk factors for stroke are worth making: inherent biological traits such as age and sex that cannot themselves be altered; physiological characteristics that predict future occurrence of stroke (eg, blood pressure, serum cholesterol concentration, fibrinogen, weight/height, blood sugar); behaviours (eg, diet, smoking, alcohol consumption, oral contraceptive use) that may be associated with stroke because of their links with characteristics such as blood pressure or serum cholesterol, or via other mechanisms; social characteristics such as social class or ethnic group that mark out differences in rate of occurrence of disease without telling us the reason, whether due to differences in behaviour, to other social and cultural factors, or to genes; and environmental features that may be
physical (eg, temperature) psychosocial, or biological. These risk factors have different implications for prevention. A physiological characteristic such as blood pressure may be lowered by drugs irrespective of the determinants of high blood pressure Or the intervention point could be behaviour-eg, tobacco smoking or changes in diet that affect blood pressure. If risk factors differ by social characteristic, prevention should deal with the social distribution of the factors. An appropriate response to an environmental cause such as cold will be to protect against it; the response to an adverse psychosocial environment might be to change the environment. Ethnic and social variations in
occurrence
of stroke
are pronounced ethnic differences in stroke Rates are high in Afro-Caribbeans in the UK,4 as mortality. in blacks in the USA. The high rates accord with the are they levels of blood pressure seen in Afro-Caribbeans.5 high has no one shown that these higher average Nevertheless, are sufficient to account for the high levels blood pressure
There
stroke class
rates.
Stroke, like CHD, shows considerable social
variation-higher class/less stroke. This class difference, like the geographic difference in the UK, may be related to differences in diet;6 it may also, like CHD, be related to measures of social deprivation.7 Individual risk factors The three main classes of stroke that concern us are ischaemic stroke, intracerebral haemorrhage, and subarachnoid haemorrhage. Although blood pressure is related to each of these types, other risk factors are not shared. Lumping all strokes together-an unfortunate necessity in large studies because there are no reliable methods of distinguishing stroke type-may account for the conflicting findings from different investigations. Blood pressure-the table shows data from the 350 977 men screened for the Multiple Risk Factor Intervention Trial (MRFIT).8 The major risk factor for stroke, whether haemorrhagic or not, is high blood pressure. Another way of expressing these data is to say that about 40% of strokes can be attributed to systolic blood pressure of more than 140.9 Serum cholesterol-the relation between serum cholesterol and stroke is not as clear cut. 10 The table shows a possible reason. Serum cholesterol concentration is strongly related to death from non-haemorrhagic stroke, but not from intracerebral or subarachnoid haemorrhage. Men in the lowest category of serum cholesterol, (
representing about 15% of all acute events in a 1-year period, have residual difficulties with caring for themselves. 18 Apart from death, it is difficult to compare most outcome measures following stroke because of variable definitions of handicap and disability. Most epidemiological studies have tended to concentrate on handicap-ie, the disadvantage experienced as a result of impairment or disability resulting from stroke. However, many elderly people are already handicapped before their stroke and in institutional care; between 10 and 40% of all patients die before hospital admission can be arranged or are cared for in the
community. Hospital care in the acute phase after stroke is the most costly component of the care of stroke patients. The lengthy hospital stay of a small proportion of patients explains the high use and disproportionate share of hospital resources. The increasing burden of health care of stroke patients in the future will be in the acute stages rather than in the long-term management of elderly patients because first-ever stroke often kills people who have been handicapped by other causes, especially if they are elderly.19 Institutional care for about 20% of survivors likewise contributes to the costs. Nevertheless, the bulk of long-term care of stroke patients falls on family members and community services.18 The best measure of the total burden of stroke is prevalence, which provides information about the number of people at any one time in the population who have had a stroke, but reliable estimates of prevalence are especially difficult to come by. For health service planning and for the allocation of resources to help families cope with strokeimpaired survivors, we urgently need accurate information about the prevalence of stroke and about the prevalence of stroke disability. Total prevalence of stroke is estimated to be 5-8 per 1000 population over the age of 25 years.2o Unless a decline in stroke incidence can be achieved, the absolute numbers of stroke victims will rise significantly as the age of the population increases. The 1970s and 1980s were a time of expansion of stroke incidence studies, encouraged by WHO. Since 1984, about fifteen countries have registered stroke events in selected populations according to a standard protocol as part of the WHO MONICA projectand data collection will continue for 10 years. This collaborative effort will shed light on the changes in incidence because it is linked to studies of trends in risk factor levels in the same populations. REFERENCES
Molyneaux A, Warlow C. Value of computerised tomography in patients with stroke: the Oxfordshire Community Stroke Project. Br Med J 1985; 290: 193-97. 2. WHO MONICA Project, Principal Investigators. The World Health Organisation MONICA Project (monitoring trends and determinants in cardiovascular disease): a major international collaboration. J Clin Epidemiol 1988; 41: 105-14. 3. Allen CMC. Clinical diagnosis of the acute stroke syndrome. Q J Med
8. Bonita
R, Beaglehole R, North JDK. Event, incidence and case-fatality
of cerebrovascular disease in Auckland, New Zealand. Am J Epidemiol 1984; 120: 236-43. 9. Broderick JP, Phillips SJ, Whisnant JP, et al. Incidence rates of stroke in the eighties: the end of the decline in stroke? Stroke 1989; 20: 577-82. 10. Terent A. Increasing incidence of stroke among Swedish women. Stroke rates
1988; 19: 598-603. 11. World Health Statistics Annual 1989. Geneva: WHO, 1989. 12. Bamford J, Dennis M, Sandercock P, et al. The frequency, causes and timing of death within 30 days of a first stroke: the Oxfordshire Stroke Project. J Neural Neurosurg Psychiatry 1990; 53: 824-29. 13. Terent A. Survival after stroke and transient ischemic attacks during the 1970s and 1980s. Stroke 1989; 20: 1320-26. 14. Bonita R, Ford M, Stewart AW. Predicting survival after stroke: a three-year follow-up. Stroke 1988; 19: 669-73. 15. Ueda K, Omai T, Hirota Y, et al. Decreasing trend in incidence and mortality from stroke in Hisayama residents, Japan. Stroke 1981; 12: 154-60. 16. Tuomilehto J, Bonita R, Stewart AW, et al. Hypertension, cigarette smoking, and the decline in stroke incidence in eastern Finland. Stroke 1991; 22: 7-11.
Garroway W, Whisnant J, Drury I. The continuing decline in the incidence of stroke. Mayo Clin Proc 1983; 58: 520-23. 18. Bonita R, Anderson A, North JDK. The pattern of management after stroke. Age Ageing 1987; 16: 29-34. 19. Malmgren R, Bamford J, Warlow C, et al. Projecting the number of patients with first ever strokes in patients newly handicapped by stroke in England and Wales. Br Med J 1989; 298: 656-60. 20. Christie D. Prevalence of stroke and its sequelae. Med J Aust 1981; ii: 17.
182-84.
Primary prevention of stroke We do not clearly understand the most dramatic feature of the epidemiology of stroke-the striking decline in mortality that has been observed in many countries (see Bonita, p 342). Nevertheless, reductions in stroke mortality will probably continue; whether or not from our actions will be debatable. It is tempting to invoke dietary changes, with or without consequent alterations in blood pressure,’ or vigorous treatment of hypertension. Secular changes in average blood pressure are hard to document, not least because of the technical difficulties of conducting comparisons over time; and the reduction in stroke mortality was underway well before antihypertensive drugs were widely and successfully used. Such doubts do not detract from the body of knowledge that suggests that we can prevent stroke, and that preventive measures are worth trying. This article reviews what is known about risk factors for stroke and discusses possible strategies for prevention.
1. Sandercock P,
1983; 52: 515-23. 4. Bamford J, Sandercock P, Dennis M, et al. A prospective study of acute cerebrovascular disease in the community: the Oxfordshire Community Stroke Project 1981-1986. 1. Methodology, demography and incidence cases of first-ever stroke. J Neurol Neurosurg Psychiatry 1988; 51: 1373-80. 5. Ward G, Jamrozik K, Stewart-Wynn E. Incidence and outcome of cerebrovascular disease in Perth, Western Australia. Stroke 1988; 19: 1501-06. 6. Bonita R, Stewart AW, Beaglehole R. International trends in stroke mortality: 1970-1985. Stroke 1990; 32: 989-92. 7. Malmgren R, Warlow C, Bamford J, Sandercock P. Geographical and secular trends in stroke incidence. Lancet 1987; ii: 1196-2000.
Stroke is
preventable
Three types of evidence suggest that stroke is, in principle preventable. First, time trends: much of the rapid change in stroke mortality is likely to have resulted from change in incidence rates, so factors determining onset of disease must have changed. Second, there are large international ADDRESSES Department of Epidemiology and Public Health, University College and Middlesex School of Medicine, London, UK (Prof M G Marmot, FFPHM, N. R Poulter, MRCP); Department of Epidemiology and Population Sciences, London School of Hygiene and Tropical Medicine (Prof M G. Marmot); and Department of Clinical Pharmacology, St Mary’s Hospital Medical School, London (N. R Poulter). Correspondence to Prof M G Marmot, Department of Epidemiology and Public Health, University College and Middlesex School of Medicine, 66-72 Gower Street, London WC1 E 6EA, UK.
345
differences in stroke mortality, but these are not fixed, as shown by the experience of migrants. For example, Japan has high rates of stroke and low rates of coronary heart disease (CHD) whereas men of Japanese ancestry living in the USA have lower rates of stroke and higher rates of CHD.2 Third, the data that have amassed on causes of stroke strongly suggest that (a) many of them can be avoided, and (b) although they exert their effect over decades, this effect is at least partly reversible in a few years. One study suggested that 50% of cerebrovascular deaths in patients under 70 years might be preventable by application of
existing knowledge.3 Risk factors for stroke Causes, risk factors, and variations in The
term
occurrence
risk factor is used in various ways. The
following distinctions among risk factors for stroke are worth making: inherent biological traits such as age and sex that cannot themselves be altered; physiological characteristics that predict future occurrence of stroke (eg, blood pressure, serum cholesterol concentration, fibrinogen, weight/height, blood sugar); behaviours (eg, diet, smoking, alcohol consumption, oral contraceptive use) that may be associated with stroke because of their links with characteristics such as blood pressure or serum cholesterol, or via other mechanisms; social characteristics such as social class or ethnic group that mark out differences in rate of occurrence of disease without telling us the reason, whether due to differences in behaviour, to other social and cultural factors, or to genes; and environmental features that may be
physical (eg, temperature) psychosocial, or biological. These risk factors have different implications for prevention. A physiological characteristic such as blood pressure may be lowered by drugs irrespective of the determinants of high blood pressure Or the intervention point could be behaviour-eg, tobacco smoking or changes in diet that affect blood pressure. If risk factors differ by social characteristic, prevention should deal with the social distribution of the factors. An appropriate response to an environmental cause such as cold will be to protect against it; the response to an adverse psychosocial environment might be to change the environment. Ethnic and social variations in
occurrence
of stroke
are pronounced ethnic differences in stroke Rates are high in Afro-Caribbeans in the UK,4 as mortality. in blacks in the USA. The high rates accord with the are they levels of blood pressure seen in Afro-Caribbeans.5 high has no one shown that these higher average Nevertheless, are sufficient to account for the high levels blood pressure
There
stroke class
rates.
Stroke, like CHD, shows considerable social
variation-higher class/less stroke. This class difference, like the geographic difference in the UK, may be related to differences in diet;6 it may also, like CHD, be related to measures of social deprivation.7 Individual risk factors The three main classes of stroke that concern us are ischaemic stroke, intracerebral haemorrhage, and subarachnoid haemorrhage. Although blood pressure is related to each of these types, other risk factors are not shared. Lumping all strokes together-an unfortunate necessity in large studies because there are no reliable methods of distinguishing stroke type-may account for the conflicting findings from different investigations. Blood pressure-the table shows data from the 350 977 men screened for the Multiple Risk Factor Intervention Trial (MRFIT).8 The major risk factor for stroke, whether haemorrhagic or not, is high blood pressure. Another way of expressing these data is to say that about 40% of strokes can be attributed to systolic blood pressure of more than 140.9 Serum cholesterol-the relation between serum cholesterol and stroke is not as clear cut. 10 The table shows a possible reason. Serum cholesterol concentration is strongly related to death from non-haemorrhagic stroke, but not from intracerebral or subarachnoid haemorrhage. Men in the lowest category of serum cholesterol, (
