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The Enigma of the Decline in Stroke Deaths in the United States

1996; Lippincott Williams & Wilkins; Volume: 27; Issue: 3 Linguagem: Inglês

10.1161/01.str.27.3.370

ISSN

1524-4628

Autores

Ruth Bonita, Robert Beaglehole,

Tópico(s)

Stroke Rehabilitation and Recovery

Resumo

HomeStrokeVol. 27, No. 3The Enigma of the Decline in Stroke Deaths in the United States Free AccessResearch ArticleDownload EPUBAboutView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticleDownload EPUBThe Enigma of the Decline in Stroke Deaths in the United States The Search for an Explanation Ruth Bonita and Robert Beaglehole Ruth BonitaRuth Bonita From the University Geriatric Unit, Department of Medicine (R. Bonita), and the Department of Community Health (R. Beaglehole), School of Medicine, University of Auckland (New Zealand). and Robert BeagleholeRobert Beaglehole From the University Geriatric Unit, Department of Medicine (R. Bonita), and the Department of Community Health (R. Beaglehole), School of Medicine, University of Auckland (New Zealand). Originally published1 Mar 1996https://doi.org/10.1161/01.STR.27.3.370Stroke. 1996;27:370–372Approximately 1 in 12 of all deaths worldwide are due to stroke; the majority occur in poorer countries.1 From the limited data on national cause of death (available for only about one quarter of the world's population), it is clear that there are striking variations among countries in both stroke death rates and their direction and rate of change. Age-standardized death rates in central and eastern European countries are four to five times greater than the rates in the United States and are increasing.2 Stroke death rates have been declining in the United States at least since the 1950s, with an increase in the rate of decline since the early 1970s. This decline, which has also occurred in many other industrialized countries, is real and has contributed to the increasing life expectancy of middle-aged and older people. Stroke is also a leading cause of disability, with poor countries carrying much of the global burden of stroke disability.3 With the aging of all populations, the global burden of stroke will inevitably increase. Well-designed studies, which prospectively measure the incidence and case fatality of stroke in large, well-defined populations, are required to understand the reasons for these trends. The change in death rates could be due to a decline (or an increase) in incidence as a consequence of the success (or the failure) of primary preventive efforts, to an improvement (or a deterioration) in case fatality as a consequence of treatment, or to a change in the natural history of the disease. Unraveling these competing explanations is a major challenge for epidemiologists. The decline in incidence rates is the most likely explanation for the striking declines in stroke mortality over most of the last four decades because in this period there have been few advances in the acute treatment of stroke that are widely applicable. The evidence is, however, inconsistent. Some studies have shown a decline in stroke incidence for different time periods,4567 others show no overall change89 or an in-crease in incidence,101112 and the trends are not always consistent for all age groups or for both men and women. Other studies point to improved case fatality as the more likely explanation for the trends.68913The best known of the long-term studies comes from Rochester, Minn, where stroke rates have been monitored since 1955. The strengths of the Rochester study are due to the well-established medical records and record-linkage system at the Mayo Clinic and the affiliated medical institutions that allow retrieval of the records of residents of Rochester with a stroke diagnosis. However, this population is not entirely typical of the population of the United States; the residents of Rochester are more educated, more homogeneous, more affluent, and younger on average than the US population, and they have greater access to a sophisticated health system. Stroke mortality rates in Rochester are lower than elsewhere in the United States, and the mortality decline has been more rapid than in the United States as a whole.14Until the end of the 1970s, successful primary prevention (declining incidence of stroke) was the explanation for the reduction in mortality from stroke in the Rochester population.15 Although this was attributed to improvements in the treatment of persons with hypertension,1617 the majority of strokes occurred in those in the middle range of the blood pressure distribution.18 The lack of further reduction in incidence in the early 1980s, despite continuing efforts to improve the treatment of individuals with high blood pressure with newer and more costly drugs, suggests that the impact of antihypertensive medication on population blood pressure levels may have been minimal.19Since the apparent end of the decline in the incidence of stroke in the Rochester population at the beginning of the 1980s was noted,20 an update has been eagerly awaited for the light it might shed on explanations for the decline in stroke deaths. The article published in this issue reporting stroke incidence rates and case fatality in Rochester for the quinquennial period of 1985 through 1989 suggests that the early leveling off of incidence rates has continued and rates are now as high, if not higher, than 10 years previously.21 These results, together with a lack of evidence of any improvement in early case fatality, are sobering and, if real, disturbing. They also present an enigma: they offer little understanding of the substantial improvement (around 5% each year) in stroke mortality rates that has occurred in the United States since the beginning of the 1970s. There are a number of reasons that might explain an apparent increase in incidence rates in the 1980s. First, the population of Rochester is small: fewer than 100 stroke events are registered each year, and precise estimates of incidence rates are difficult. Although not stated in the article, extrapolation from data provided in Table 1 suggests that the average annual population in the 1985 to 1989 quinquennium was 67 000, only 10% of whom were over the age of 65 years. Second, although essentially based on clinical criteria, definitions appear to have changed during the time period, reflecting increasing access to neuroimaging techniques. Trends in subtypes are particularly difficult to measure in a meaningful manner when diagnostic capability has changed so dramatically over the study period. Third, changes in case finding are likely to have increased the number of mild stroke patients identified. For example, the increase in the number and proportion of all events in women in the oldest age group (85 years and over) may have been a consequence of the expanded Medical Index and greater access to CT; in 1985 through 1989, one third of all events in women registered were in this age group, compared with only 17% in 1975 through 1979, despite the fact that there was little population increase during this time. An increase in the proportion of stroke patients receiving CT scans (from 6% in the early 1970s to over 80% in the 1980s) will have had an impact on case finding, especially because of the reliance on retrospective assessment of medical records. A decline in autopsy rates may also have had an impact on case finding because in earlier years autopsy reports that confirmed a diagnosis of stroke were included, regardless of the presence or absence of clinical signs. So where does this leave us? There has been a welcome increase in the number of population-based registers in many countries in recent years. These studies have been accompanied by improvements in design, with much more attention paid to the use of standardized data.22 However, only a few are able to report comparable data over time, and many of the new stroke registers are not based on sufficiently large populations to provide trend data with any confidence. It is regrettable that the Rochester study is the only long-term study of stroke trends in North America. Perhaps the most promising effort to understand the decline in stroke mortality, and to link this with changes in stroke risk factors, is the World Health Organization MONICA Project, which has investigated 21 populations in 12 countries, mostly European, over a 10-year period beginning in the early 1980s.23 In addition to monitoring incidence and case fatality with strict definitions and guidelines, all official mortality data are validated against the stroke registers. The study shows that geographical differences are real; the variation in mortality rates between countries is also reflected in incidence rates,24 indicating the enormous potential for prevention. The trend data from the MONICA Project are yet to come. We need to build on the best of the existing population-based studies of stroke that are of sufficient size for incidence rates to be estimated with confidence. Parallel studies monitoring changes in risk factor levels in the population are equally important. Lessons from earlier studies, including the Rochester study, need to be incorporated into new initiatives; adherence to strict criteria and standardized methods will be essential. Because most strokes occur in low- and middle-income countries, documenting changes in the stroke profile must become an international effort, with researchers in the wealthy countries assisting those in the poorer countries. Without this effort, the enigma will remain. The recent results from the Rochester study serve as a timely warning. If it is true that stroke incidence rates are no longer declining, it is a clear signal that primary prevention is failing. If it is also true that there is no improvement in survival in the acute phase, it suggests that the widespread adoption of neuroimaging techniques has not improved outcomes. The results from the Rochester study suggest that the efforts currently directed at secondary prevention have been at the expense of attempts to prevent strokes from occurring in the first place. Primary prevention strategies need greater emphasis. The high-risk approach should focus only on individuals at highest absolute risk of stroke,2526 but the greatest gains will come from the population strategy that aims to reduce the average level of risk in entire populations. The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.FootnotesCorrespondence to Ruth Bonita, MPH, PhD, University Geriatric Unit, North Shore Hospital, PB 93-503, Takapuna, Auckland 9, New Zealand. References 1 Murray CJL, Lopez AD. Global and regional cause-of-death patterns in 1990. Bull WHO.1994; 72:447-480. MedlineGoogle Scholar2 Bonita R, Beaglehole R, Asplund K. The worldwide problem of stroke. Curr Opin Neurol Neurosurg.1994; 7:5-10. CrossrefGoogle Scholar3 Murray CJL, Lopez AD, Jamison DT. The global burden of disease in 1990: summary results, sensitivity analysis and future directions. Bull WHO.1994; 72:495-509. MedlineGoogle Scholar4 Ueda K, Omae T, Hirota Y, Takeshita M, Katsuki S, Tanaka K, Enjoji M. Decreasing trend in incidence and mortality from stroke in Hisayama residents, Japan. Stroke.1981; 12:154-160. CrossrefMedlineGoogle Scholar5 Sarti C, Tuomilehto J, Sivenius J, Kaarsalo E, Narva EV, Salmi K, Torppa J, Salomaa V. Declining trends in incidence, case-fatality and mortality of stroke in three geographic areas of Finland during 1983-1989: results for the FINMONICA Stroke Register. J Clin Epidemiol.1994; 47:1259-1269. CrossrefMedlineGoogle Scholar6 Stegmayr B, Asplund K, Wester PO. Trends in incidence, case-fatality rate, and severity of stroke in Northern Sweden, 1985-1991. Stroke.1994; 25:1738-1745. CrossrefMedlineGoogle Scholar7 Feigin VL, Wiebers DO, Whisnant JP, O'Fallon WM. Stroke incidence and 30-day case-fatality rates in Novosibirsk, Russia, 1982 through 1992. Stroke.1995; 26:924-929. CrossrefMedlineGoogle Scholar8 Harmsen P, Tsipogianni A, Wilhelmsen L. Stroke incidence rates were unchanged, while fatality rates declined, during 1971-1987 in Göteborg, Sweden. Stroke.1992; 23:1410-1415. CrossrefMedlineGoogle Scholar9 Bonita R, Broad JB, Beaglehole R. Changes in stroke incidence and case-fatality in Auckland, New Zealand, 1981 to 1991. Lancet.1993; 342:1470-1473. CrossrefMedlineGoogle Scholar10 Terent A. Increasing incidence of stroke among Swedish women. Stroke.1988; 19:598-603. CrossrefMedlineGoogle Scholar11 Jorgensen HS, Plesner AM, Hubbe P, Larson K. Marked increase of stroke incidence in men between 1972 and 1990 in Frederiksberg, Denmark. Stroke.1992; 23:1701-1704. CrossrefMedlineGoogle Scholar12 Eisenblatter D, Heinemann L, Claben E. Community-based stroke incidence trends from the 1970s through the 1980s in East Germany. Stroke.1995; 26:919-923. CrossrefMedlineGoogle Scholar13 Wolf PA, D'Agostino RB. Secular trends in stroke in the Framingham Study. Ann Epidemiol.1993; 3:471-475. CrossrefMedlineGoogle Scholar14 Anderson GL, Whisnant JP. A comparison of trends in mortality from stroke in the United States and Rochester, Minnesota. Stroke.1982; 13:804-809. CrossrefMedlineGoogle Scholar15 Garraway WM, Whisnant JP, Drury I. The continuing decline in the incidence of stroke. Mayo Clin Proc.1983; 58:520-523. MedlineGoogle Scholar16 Whisnant JP. The decline of stroke. Stroke.1984; 15:160-168. CrossrefMedlineGoogle Scholar17 Garraway WM, Whisnant JP. The changing pattern of hypertension and the declining incidence of stroke. JAMA.1987; 258:214-217. CrossrefMedlineGoogle Scholar18 Beard TC, Heller RF. Relevance of the salt-hypertension hypothesis to the community control of hypertension. Med J Aust.1987; 147:29-38. MedlineGoogle Scholar19 Bonita R, Beaglehole R. Increased treatment of hypertension does not explain the decline in stroke mortality in the United States 1970-1980. Hypertension. 1989;13(suppl I):I-169-I-173. Google Scholar20 Broderick JP, Phillips SJ, Whisnant JP, O'Fallon WM, Bergstralh EJ. Incidence rates of stroke in the eighties: the end of the decline in stroke? Stroke.1989; 20:577-582. CrossrefMedlineGoogle Scholar21 Brown RD, Whisnant JP, Sicks JR, O'Fallon WM, Wiebers DO. Stroke incidence, prevalence, and survival: secular trends in Rochester, Minnesota, through 1989. Stroke.1996; 27:373-380. MedlineGoogle Scholar22 Malmgren R, Warlow C, Bamford J, Sandercock P. Geographical and secular trends in stroke incidence. Lancet.1987; 2:1196-1200. CrossrefMedlineGoogle Scholar23 Asplund K, Bonita R, Kuulasmaa K, Rajakangas AM, Feigin V, Schaedlich H, Suzuki K, Thorvaldsen P, Tuomilehto J, for the WHO MONICA Project. Multinational comparisons of stroke epidemiology: evaluation of case ascertainment in the WHO MONICA Stroke Study. World Health Organization Monitoring Trends and Determinants in Cardiovascular Disease. Stroke.1995; 26:355-360. CrossrefMedlineGoogle Scholar24 Thorvaldsen P, Asplund K, Kuulasmaa K, Rajakangas AM, Schroll M. Stroke incidence, case fatality, and mortality in the WHO MONICA project. World Health Organization Monitoring Trends and Determinants in Cardiovascular Disease. Stroke.1995; 26:361-367. CrossrefMedlineGoogle Scholar25 Jackson R, Barham P, Bills J, Birch T, McLennan L, MacMahon S, Maling T. The management of raised blood pressure in New Zealand: a discussion document. BMJ.1993; 307:107-110. CrossrefMedlineGoogle Scholar26 Cook RJ, Sackett DL. The number needed to treat: a clinically useful measure of treatment effect. BMJ.1995; 310:452-454.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Shrivastava A, Srivastava T and Saxena R (2016) CT Angiographic Evaluation of Pattern and Distribution of Stenosis and its Association with Risk Factors Among Indian Ischemic Stroke Patients, Polish Journal of Radiology, 10.12659/PJR.897039, 81, (357-362) Ahmed I, Jibawi A, Barkat M, Sakka K and Yusuf S (2011) Management of carotid artery disease in the elderly, Aging Health, 10.2217/ahe.11.16, 7:2, (321-333), Online publication date: 1-Apr-2011. Schievink W, Maya M, Moser F, Tourje J and Torbati S (2007) Frequency of spontaneous intracranial hypotension in the emergency department, The Journal of Headache and Pain, 10.1007/s10194-007-0421-8, 8:6, (325-328), Online publication date: 1-Dec-2007. Bainbridge N, Davie M and Haddaway M (2006) Bone loss after stroke over 52 weeks at os calcis: influence of sex, mobility and relation to bone density at other sites, Age and Ageing, 10.1093/ageing/afj045, 35:2, (127-132), Online publication date: 1-Mar-2006. Wolf P and Kannel W (2006) Epidemiology of Cerebrovascular Disease Vascular Medicine, 10.1016/B978-0-7216-0284-4.50035-X, (411-432), . Mouradian M, Hussain M, Lari H, Salam A, Senthilselvan A, Dean N and Shuaib A (2014) The Impact of a Stroke Prevention Clinic in Diagnosing Modifiable Risk Factors for Stroke, Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques, 10.1017/S0317167100004509, 32:4, (496-500), Online publication date: 1-May-2005. Camargo E, Bacheschi L and Massaro A (2005) Stroke in Latin America, Neuroimaging Clinics of North America, 10.1016/j.nic.2005.07.002, 15:2, (283-296), Online publication date: 1-May-2005. Wolf P (2004) Epidemiology of Stroke Stroke, 10.1016/B0-44-306600-0/50005-5, (13-34), . Wolf P (2002) Mortality in Patients with Stroke Long-Term Effects of Stroke, 10.1201/9780203908884.ch5, Online publication date: 21-Jun-2002. Carrozzella J and Jauch E (2002) Emergency Stroke Management, Nursing Clinics of North America, 10.1016/S0029-6465(03)00081-1, 37:1, (35-57), Online publication date: 1-Mar-2002. Bednar M, Gross C, Howard D, Russell S and Ellenberger C (2013) The effect of vasodilators on aspirin-induced antagonism of t-PA thrombolysis, Neurological Research, 10.1179/016164101101199117, 23:7, (745-750), Online publication date: 1-Oct-2001. Bednar M, Gross C, Russell S, Fuller S, Ahern T, Howard D, Falck J, Reddy K and Balazy M (2000) 16(R)-Hydroxyeicosatetraenoic Acid, a Novel Cytochrome P450 Product of Arachidonic Acid, Suppresses Activation of Human Polymorphonuclear Leukocytes and Reduces Intracranial Pressure in a Rabbit Model of Thromboembolic Stroke, Neurosurgery, 10.1097/00006123-200012000-00029, 47:6, (1410-1419), Online publication date: 1-Dec-2000. Czlonkowska A, Hier D, Mendel T and Ryglewicz D (2000) Heart disease contributes to high stroke mortality in Poland, Journal of Stroke and Cerebrovascular Diseases, 10.1053/jscd.2000.0090076, 9:2, (76-78), Online publication date: 1-Mar-2000. Orencia A and Biller J (1997) Prevention of Primary Event, Neurosurgery Clinics of North America, 10.1016/S1042-3680(18)30320-6, 8:2, (165-178), Online publication date: 1-Apr-1997. Gale C and Martyn C (2017) The Conundrum of Time Trends in Stroke, Journal of the Royal Society of Medicine, 10.1177/014107689709000307, 90:3, (138-143), Online publication date: 1-Mar-1997. Wolf P (1997) Epidemiology and Risk Factor Management Primer on Cerebrovascular Diseases, 10.1016/B978-012743170-3.50185-0, (751-757), . March 1996Vol 27, Issue 3 Advertisement Article InformationMetrics Copyright © 1996 by American Heart Associationhttps://doi.org/10.1161/01.STR.27.3.370 Originally publishedMarch 1, 1996 Advertisement

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