(Stroke. 1997;28:284-290.)
© 1997 American Heart Association, Inc.
Articles |
the Department of Community and Preventive Medicine, University of Rochester Medical Center, NY (W.H.B.); and the Kaiser Permanente Center for Health Research, Portland, Ore (J.P.M.).
| Abstract |
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Methods We conducted a retrospective analysis of three successive period cohorts (1967 through 1971, 1974 through 1978, and 1981 through 1985) of persons
65 years of age enrolled in a large group model HMO in a metropolitan community. All new hospitalized and a sample of nonhospitalized strokes were ascertained, and samples of first-ever strokes were studied. Incidence, case-fatality rates, survival times, and comorbidities were compared across cohorts.
Results There was no significant change in stroke incidence over time; however, 1-month case fatality declined dramatically from 33% in 1967 through 1971 to 18% in 1981 through 1985 (P<.01); median survival increased from 213 to 1092 days. Indices of reduced severity included declines in coma from 27% to 12% (P<.01) and in wheelchair- or bed-bound status from 40% to 30% (P=.067). Cases with and without CT scan in 1981 to 1985, when this procedure became widely available in the health plan, were similar in severity, thereby reducing the possibility of ascertainment bias.
Conclusions In this well-defined older population, stroke has become a less lethal and disabling though no less common disease. This finding fails to support the "compression of morbidity" hypothesis while supporting a model of delayed progression for stroke in this age group.
Key Words: aging epidemiology incidence mortality
| Introduction |
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The present study specifically analyzes secular trends in stroke incidence rate, case-fatality rate, clinical severity, and functional outcome and their correlates in a large well-defined elderly population during the period of 1967 through 1985. The study takes into account two important potential sources of bias that may have limited other stroke trend studies: (1) we included nonhospitalized as well as hospitalized cases and (2) we directly assessed the possibility that widespread use of CT scans in the early 1980s altered case ascertainment in favor of finding milder cases of stroke disease.7 17 18
| Subjects and Methods |
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Design
For purposes of analyzing stroke trends, we used a historical cohort study design, comparing three successive period cohorts of older members, each of which was followed for up to 5 years. The cohorts, identified from health-plan computerized membership records, consisted of all members who were
65 years old at the beginning of the first year of each of the following 5-year study periods: 1967-1971 (period 1); 1974-1978 (period 2); and 1981-1985 (period 3). Total persons and person-years of observation increased over time as increasing numbers of health-plan members reached age 65: 7117 persons and 30 513 person-years in period 1, 11 190 and 48 132 in period 2, and 16 960 and 72 503 in period 3, with a grand total of 151 148 person-years of observation. Individual subjects were eligible to contribute person-years to more than one of the successive 5-year study periods.
Study Samples
Case finding to identify samples of first-ever acute strokes for inclusion in the study involved several steps. First, computerized discharge records available for 100% of hospitalizations were searched for any mention of ICDA codes for cerebrovascular disease among all listed discharge diagnoses for all hospitalizations within the respective 5-year study periods. (See "Appendix" for cerebrovascular disease ICDA 7-9 codes.) To ascertain nonhospitalized strokes, medical records on 20% simple random samples of the study populations were reviewed by trained research nosologists to identify any mention of stroke or cerebrovascular disease in outpatient notes during the respective 5-year study periods. A total of 7790 outpatient records were reviewed for the three periods. Confirmed hospitalized and nonhospitalized strokes were those that met the widely used WHO definition: a new-onset focal neurological abnormality lasting at least 24 hours that is not attributable to a noncerebrovascular cause.21 22 A total of 1783 hospitalized and 131 nonhospitalized possible acute stroke patients were identified, and medical records were reviewed for confirmation of the diagnosis using the WHO definition: 1377 of the former (77%) and 43 of the latter (33%) were confirmed. Old strokes and transient ischemic attacks accounted for over 90% of exclusions.
To identify first-ever (incident) strokes, chart reviews were conducted for simple random samples of total confirmed hospitalized strokes in each study period and for all 43 confirmed nonhospitalized strokes. The goal for hospitalized cases was to randomly select samples of 300 to 350 confirmed strokes per period and to review medical records to identify first-ever strokes and exclude recurrent strokes. The sampling goal was readily attained for periods 2 and 3 but not for the earliest period, which had the smallest cohort and only 249 total confirmed strokes. As summarized in Table 1
, this process yielded study samples of 196, 247, and 275 hospitalized and 7, 17, and 16 nonhospitalized first-ever strokes for periods 1, 2, and 3, respectively. Other strokes were classified as recurrent on the basis of medical-record documentation of previous stroke and were excluded from analyses. Among the hospitalized patients for the respective periods, 8%, 8%, and 7% were nursing home residents at the time of stroke occurrence, whereas none of the nonhospitalized patients in periods 1 and 2 and only one patient in period 3 was a nursing home resident.
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For purposes of comparing incidence rates over time, the total number of first-ever hospitalized strokes for each period was estimated by dividing the observed number (H) by the sampling proportion (f) for the respective periods (ie, 0.92, 0.69, and 0.51). The total number of first-ever nonhospitalized strokes was estimated by dividing the observed number (n) by the 0.20 sampling fraction. The period incidence rates (r) of first-ever strokes were estimated by dividing the estimated total hospitalized and nonhospitalized cases by the person-years of observation during the respective study period: r=(H/f±n/0.20)/total person-years. Assuming a Poisson incidence distribution, the standard error of a period incidence rate was estimated by:
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Data
Age, sex, date of occurrence of stroke, and vital status for a 5-year follow-up period were obtained for the first-ever strokes in the study samples for use in calculating incidence rates, case-fatality rates, and survival. Data on deaths and death dates during the 5-year follow-up period were obtained from medical records and from matching study subjects against vital status records for the states of Oregon and Washington. Detailed medical record reviews were conducted to identify trends in clinical factors that might contribute to differences in case fatality. These included measures of clinical severity of acute stroke, prevalence of comorbidities, life-threatening medical events occurring at the time of stroke, and selected medical management and diagnostic practices. Trained research nosologists at the CHR conducted the medical record reviews using explicit abstracting instructions, which were in large part derived from a validated system developed by the Rand Corporation for retrospective study of stroke.23
Neurological manifestations of acute stroke documented within the first 48 hours from onset included level of consciousness (coma, confusion, alert), loss of motor function of one or more extremities, and speech, swallowing, and visual impairment. The medical record for 12 months before stroke was reviewed for evidence of treatment for the following comorbid conditions: hypertension, diabetes, coronary heart disease (myocardial infarction, angina, or other), other forms of heart disease, atrial fibrillation, and transient ischemic attack. The most recent blood pressure recorded during the year before stroke was used to classify hypertension control status according to Joint National Committee24 criteria that were in effect in the 1970s and early 1980s; those subjects with systolic or diastolic pressure above 160 or 95 mm Hg, respectively, were classified as uncontrolled. Diagnostic studies that were ascertained included cerebrospinal fluid examination, carotid angiography, and CT scans of the brain. Potentially life-threatening acute medical complications during the first 30 days after stroke included recurrent stroke, seizure, myocardial infarction, congestive heart failure, cardiac arrest with resuscitation, diabetic acidosis, pulmonary embolism, pneumonia, and urinary tract infection. Measures of medical management consisted of the time interval between onset of stroke symptoms and receipt of medical care; admission to the intensive care unit; and provision of physical, occupational, and speech therapy. Mobility status before stroke and within 1 month after stroke was classified from information in the hospital record as follows: walks independently, with cane, with walker, wheelchair-bound, and bed-bound. Data on other indices of disability (dependency status in dressing, eating, bathing, and transferring) were not consistently available in medical records.
Statistical Analyses
Estimated stroke incidence rates per 100 000 person-years for each of the three study periods were analyzed for homogeneity and for linear secular trends.
2 Tests of homogeneity of incidence rates were performed within age (65 to 74, 75 to 84, and 85+ years) and sex groups.25
Period incidence rates are transformed to approximate normal variates, z=(r-r)/SE, squared, and summed over the three periods. Standard errors of period incidence rates were estimated using the formula given above. The weighted mean of the incidence rates, where the weights are the reciprocal of the squared standard errors, was calculated as r. This homogeneity test statistic has a
2 distribution with 2 df.
Linear trends in incidence rates were tested within age and sex groups by weighted regression. The linear trend of period incidence rates over time (t) was estimated as b=(
wi ti ri)/(
wi ti2), where ti is the midpoint of the ith period. Dividing b2 by variance (b)=(
[wi ti]2 [SEi]2)/(
wi ti2)2 gives an approximate
2 test statistic within 1 df.
Age- and sex-specific cumulative case-fatality rates at 7 days, 30 days, 6 months, and 1 year after stroke were compared across the three study periods using the Mantel-Haenszel
2 test for linear trends. Period-specific survival functions were estimated using the Kaplan-Meier product limit method, and log rank statistics were used to test for period differences in poststroke survival. Cox proportional hazards models were used to test for period effects, as well as for effects of demographic and clinical characteristics on short- and long-term mortality.26 27 Case-fatality, survival, and proportional hazards analyses were based on first-ever hospitalized strokes.
| Results |
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2 Homogeneity tests and
2 tests for linear trends in stroke incidence were not significant for any of the age-sex groups.
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Case Fatality and Survival
Over a 1-year period of follow-up, there were 315 deaths among the 718 individuals with first-ever strokes who were hospitalized and 2 deaths among the 40 first-ever stroke patients who were not hospitalized (1 in period 2 and 1 in period 3). Because so few deaths occurred among nonhospitalized cases, analyses of case fatality and survival were limited to the 718 hospitalized cases. A highly significant decreasing trend in fatality among hospitalized strokes at 1 week, 1 month, 6 months, and 1 year occurred between period 1 and period 3 (Table 3
). In subgroup analyses, these declining trends were observed among 65- to 74-year-old and 75- to 84-year-old male and female patients but not among those
85 years of age among whom poststroke fatality rates were unchanged over time. The Figure
depicts 5-year survival curves following hospitalized stroke for the respective periods, with close correspondence to the constant separation of a proportional hazards model. Median survival times increased some fourfold to fivefold, from 213 (95% CL, 94 to 404) days in period 1 to 474 (95% CL, 252 to 696) days in period 2 and 1092 (95% CL, 792 to 1372) days in period 3.
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Clinical Characteristics
Table 4
summarizes major neurological manifestations documented within the first 48 hours of stroke presentation in each of the three study periods and compares these manifestations among those cases with and without brain CT scan in period 3. While motor deficit of the extremities was present in a comparable 77% to 81% of cases among the three study periods, there was a significant decrease in coma from 27% to 12% and increase in percentage with documented visual or speech deficits in period 3. CT scan, which became routinely available in the health plan only in the late 1970s, was performed in 132 of the cases (48%) in period 3. The spectrum of neurological manifestations of cases with and without CT scan was essentially identical, with specifically no evidence that CT scans increased the detection of milder strokes.
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Table 5
compares the prevalence of preexisting comorbidities, occurrence of potentially life-threatening medical complications, and selected aspects of medical management among the incident hospitalized strokes across the three study periods. There were statistically significant trends toward a greater proportion of cases with a history of hypertension under medical treatment (P
.05) and lower mean systolic and diastolic blood pressures (P
.001). The prevalence of hypertensive heart disease declined from 6% to 2% (P
.05), and the prevalence of angina increased from 10% to 16% (P
.05). Prevalence of other listed comorbidities did not change significantly over time. One or more potentially serious medical complications during hospitalization were documented in a similar 24% to 26% of cases. With respect to medical management, the time interval from stroke onset to medical attention was similar; the proportion of patients admitted to an ICU and receiving various rehabilitation therapies increased significantly over time.
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A number of Cox regression models, which incorporated age, sex, study period, and acute neurological manifestations, comorbidities, medical complications, admission to ICU, and rehabilitation variables shown in Table 5
, were constructed to explain the observed decline in poststroke mortality across the study periods. For the models, blood pressure status at the most recent prestroke medical visit was classified as uncontrolled hypertension, no blood pressure recorded, or blood pressure in control range, with the latter serving as reference. As seen in Table 6
, major heart disease and particularly coma, both of which decreased over time, were significantly associated with fatality at 1 month. The same two factors plus older age and medical complications at time of stroke hospitalization were associated with worse survival at 1 year. There was no independent association between uncontrolled hypertension and death at 1 month or 1 year. Improved stroke survival over time is largely explained by decreased frequency of coma and major heart disease among incident strokes, although there did appear to be a small independent effect on death at 1 year for period 1.
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Mobility Outcome
Among persons discharged alive from the hospital, the proportion who became newly wheelchair-dependent or bed-bound decreased from 38% to 29% (P=.067), while the proportion of newly walker-dependent and the proportion who retained independent ambulation remained unchanged (Table 7
).
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| Discussion |
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65 years old, the widely observed decline in stroke mortality in recent decades is attributable to decrease in poststroke fatality rate but not decrease in stroke incidence. Both clinical severity of acute stroke and degree of impairment in poststroke mobility decreased and survival time increased severalfold among incident cases between the late 1960s and early 1980s.
These composite observations suggest a shift in the natural history of stroke toward a less lethal and less disabling though no less common disease in this elderly population. As an alternative explanation, changing management or diagnostic practices over time might have introduced bias favoring the detection of milder strokes in the latter period, thus giving a spurious appearance of sustained frequency of new strokes and declining case-fatality rates. This possibility has been addressed in several ways. First, the widely accepted WHO clinical criterion for confirming incident acute stroke was used consistently in all three study periods. Second, we included nonhospitalized and hospitalized cases to avoid the possible effect of changing practices regarding location of stroke management, a well-recognized limitation of the many stroke trend studies restricted to hospitalized cases.7 28 29 With the exception of some incident strokes that occurred in subjects residing in nursing homes and that may not have been documented in health-plan medical records, we feel that ascertainment of new strokes was quite complete. Such missing data from nursing home occurrences would have been largely confined to persons >85 years of age as noted elsewhere30 and would limit generalization of our findings for this age group. Finally, our comparison of cases with and without CT scan of the brain in study period 3 (Table 4
) found no difference in clinical severity between groups, thereby excluding the possibility that scanning was selectively associated with detection of mild cases that would not have been detected in the earlier prescanning study periods.17 18 We cannot, however, completely exclude the possibility that increased physician interest might have led to some patients being given the diagnosis of stroke in the latter time period who would not have received this diagnosis in the earlier period.
A number of other observational studies have been conducted in the United States and elsewhere to document and explain the accelerated decline in stroke mortality in the 1970s and 1980s. Earliest among these was a community-based study from Olmsted County, Minnesota, reporting evidence of declining new-stroke rate and case-fatality rate in the 1970s.5 30 A more recent study from the same setting reported increasing stroke rates with continued decreasing case-fatality rates in the 1980s.31 With the exception of the early Olmsted County study and studies from Japan, Finland, and Hawaii,32 33 34 virtually all other population-based investigations have reported either stable or increasing stroke rates and significant decrease in case fatality, similar to the present study.8 9 10 11 12 13 14 The majority of other studies, however, have been limited to hospitalized strokes. Several have discussed the possibility of detection bias from widespread use of CT scan in the late 1970s and 1980s9 11 12 18 ; however, no other studies have empirically tested this possibility by comparing clinical manifestations among cases with and without CT scan as was done in the present study.
Decline in case fatality in our study is most clearly attributable to the observed sharp decrease in occurrence of coma among stroke cases in the 1980s. Decreases in neurological severity of acute stroke in association with improved survival during the 1970s and early 1980s have also been reported from a community-based series of incident strokes among younger cohorts in the Framingham study12 and from several sequential series studies of hospitalized strokes.9 10 11 In addition to the major role of decrease in coma, our data indicate that secular decline in prevalence of hypertensive heart disease among new stroke cases may have contributed to the reduction in case fatality.
The contribution of widespread hypertension treatment to the accelerated decline in stroke mortality in the 1970s and early 1980s has been debated.3 35 36 37 38 39 40 41 The failure to find evidence of decreased occurrence of incident strokes during this period is at variance with general expectations based on results of clinical trials of hypertension treatment, including those involving the elderly, which consistently found reductions in expected numbers of new strokes.42 43 Alternatively, it may be speculated that hypertension control efforts have contributed to stroke mortality decline by reducing the severity of acute stroke.44 45 In line with this argument, both the present study (unpublished data) and the Minneapolis study46 observed significantly lower blood pressures in their respective communities, reflecting national trends,47 as well as among incident strokes over time. Because lethal hypertension-related strokes are typically massive intracerebral hemorrhages, the hypothesized shift to a less severe form of hypertension-related stroke might represent smaller hemorrhagic strokes or a true reduction in hemorrhagic strokes, compensated for by an increase in thrombotic strokes. Such phenomena have been observed in clinical,30 48 epidemiological,8 49 and experimental50 studies and hence seem fully plausible. Because retrospective studies from chart review are notoriously inadequate in distinguishing between hemorrhagic and nonhemorrhagic stroke,22 51 the present study is unable to further elucidate the matter.
From a public health perspective, the observed secular trend toward increased stroke survival time, with stroke rate unchanged, translates into increased prevalence of this major chronic condition in the older population. This finding fails to support the "compression of morbidity" hypothesis, which postulates delayed time of onset and decreased duration of chronic disease before death,15 and supports an alternative model that postulates an unchanging time of onset but delayed progression of chronic disease.16 This would potentially result in increased needs for health and health-related services to care for stroke patients who live longer.
The anticipated impact on service needs may, however, be lessened because of the trend toward decreased degree of disability among stroke survivors as manifest, albeit somewhat crudely, in the lower proportion of survivors with major limitations in mobility. Such a finding for stroke, one of the most common disabling chronic conditions of old age, represents a microcosm of the recently observed general pattern of decreasing levels of chronic disability among the aging population in the United States.52
| Selected Abbreviations and Acronyms |
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| Acknowledgments |
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| Footnotes |
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| Appendix |
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ICDA 8, 1/70 to 12/78
ICDA 9, 1/79 to Present
Received September 4, 1996; revision received October 31, 1996; accepted October 31, 1996.
| References |
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|
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2.
Soltero I, Liu K, Cooper R, Stamler J, Garside D. Trends in mortality from cerebrovascular diseases in the United States, 1960-1975. Stroke. 1978;9:549-558.
3.
Klag MJ, Whelton PK, Seidler AJ. Decline in US stroke mortality: demographic trends and antihypertensive treatment. Stroke. 1989;20:14-21.
4.
Bonita R, Stewart A, Beaglehole R. International trends in stroke mortality. Stroke. 1990;21:989-992.
5. Garraway WM, Whisnant JP, Furlan AJ, Phillips AH, Kurland LT, O'Fallon WM. The declining incidence of stroke. N Engl J Med. 1979;300:449-452.[Abstract]
6. Why has stroke mortality declined? Lancet. 1983;1:1195-1196. Editorial.[Medline] [Order article via Infotrieve]
7. Malmgren R, Bamford J, Warlow C, Sandercock P. Geographical and secular trends in stroke incidence. Lancet. 1987;2:1196-1200.[Medline] [Order article via Infotrieve]
8.
Kramer S, Diamond EL, Lilienfeld AM. Patterns of incidence and trends in diagnostic classification of cerebrovascular disease in Washington County, Maryland, 1967-1971 to 1974-1976. Am J Epidemiol. 1982;115:398-411.
9.
Howard G, Toole JF, Becker C, Lefkowitz DS, Truscott L, Rose L, Evans GW. Changes in survival following stroke in five North Carolina counties observed during two different periods. Stroke. 1989;20:345-350.
10.
Ahmed OI, Orchard TJ, Sharma R, Mitchell H, Tallot E. Declining mortality from stroke in Allegheny County, Pennsylvania: trends in case fatality and severity of disease, 1971-1980. Stroke. 1988;19:181-184.
11.
McGovern PG, Burke GL, Sprafka JM, Xue S, Folsom AR, Blackburn H. Trends in mortality, morbidity, and risk factor levels for stroke from 1960 through 1990: the Minnesota Heart Survey. JAMA. 1992;268:753-759.
12.
Wolf PA, Agostino RB, O'Neal A, Sytkowski P, Kase CS, Belanger AJ, Kannel W. Secular trends in stroke incidence and mortality: the Framingham Study. Stroke. 1992;23:1551-1555.
13.
Modan B, Wagener DK. Some epidemiological aspects of stroke: mortality/morbidity trends, age, sex, race, socioeconomic status. Stroke. 1992;23:1230-1236.
14. Bonita R, Broad JB, Beaglehole R. Changes in stroke incidence and case-fatality in Auckland, New Zealand, 1981-91. Lancet. 1993;342:1470-1473.[Medline] [Order article via Infotrieve]
15. Fries JF. Aging, natural death and the compression of morbidity. N Engl J Med. 1980;303:130-135.[Abstract]
16. Manton KG, Patrick CH, Stallard E. Mortality model based on delays in progression of chronic diseases: alternative to cause elimination model. Public Health Rep. 1980;95:580-588.[Medline] [Order article via Infotrieve]
17. Liebson C, Ballard DJ, Whisnant JP, Melton LJ. The compression of morbidity hypothesis: promise and pitfalls of using record-linked data bases to assess secular trends in morbidity and mortality. Milbank Q. 1992;70:127-154.[Medline] [Order article via Infotrieve]
18.
Drury I, Whisnant JP, Garraway WM. Primary intracerebral hemorrhage: impact of CT on incidence. Neurology. 1984;34:653-657.
19. Oregon Department of Human Resources. Oregon Vital Statistics Report for Calendar Year 1985. 1986:56-57.
20. Greenlick MR, Freeborn DK, Pop CR, eds. Health Care Research in an HMO. Baltimore, Md: John Hopkins University Press; 1988.
21. World Health Organization MONICA Project (monitoring trends and determinants in cardiovascular disease): a major international collaboration. J Clin Epidemiol. 1988;41:105-114.[Medline] [Order article via Infotrieve]
22. Walker AE, Robins M, Weinfeld FD. The National Survey of Stroke: clinical findings. Stroke. 1981;12(suppl I):I-13-I-34.
23. Rubinstein LV, Kosecoff J, Kahn KL. Medical Record Abstraction Forms and Guidelines for Assessing Quality of Care for Hospitalized Patients With Cerebrovascular Accident. Santa Monica, Calif: RAND Corp; 1988.
24.
1980 Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med. 1980;140:1280-1285.
25. Draper NR, Smith H. Applied Regression Analysis. New York, NY: John Wiley & Sons; 1966.
26. SAS Institute Inc. SAS User's Guide: Version 6 Edition. Cary, NC: SAS Institute; 1990.
27. Kalbfleisch JD, Prentice RL. The Statistical Analyses of Failure Time Data. New York, NY: John Wiley & Sons; 1980.
28. Anderson CS, Jamrozik KD, Burvill PW, Chakera TM, Johnson GA. Ascertaining the true incidence of stroke: experience from the Perth community stroke study, 1989-1990. Med J Aust. 1993;158:80-84.[Medline] [Order article via Infotrieve]
29.
Garraway WM, Whisnant JP, Drury I. The changing pattern of survival following stroke. Stroke. 1983;14:699-703.
30. Brown RD, Whisnant JP, Sicks JD, O'Fallon WM, Wiebers DO. Stroke incidence, prevalence, and survival: secular trends in Rochester, Minnesota, through 1989. Stroke. 1996;27:373-380.
31.
Broderick JP, Philips SJ, Whisnant JP, O'Fallon WM, Bergstralh EJ. Incidence rates of stroke in the 80s: the end of the decline in stroke? Stroke. 1989;20:577-582.
32.
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.
33.
Tuomilehto J, Bonita R, Stewart AW, Salonen JT. Hypertension, cigarette smoking, and the decline in stroke incidence in eastern Finland. Stroke. 1991;22:7-11.
34. Kagan A, Popper J, Reed D, McLean CJ, Grove TS. Trends in stroke incidence and mortality in Hawaiian Japanese men. Stroke. 1994;25:1170-1175.[Abstract]
35.
Whisnant JP. Decline of stroke. Stroke. 1984;15:160-168.
36.
Hachinski V. Decreased incidence and mortality of stroke. Stroke. 1984;15:376-378.
37. Whelton PK. Declining mortality from hypertension and stroke. South Med J. 1982;75:33-38.[Medline] [Order article via Infotrieve]
38. 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-69-I-73.
39.
Casper M, Wing S, Strogatz D, Davis CE, Tyroler HA. Antihypertensive treatment and US trends in stroke mortality, 1962-1980. Am J Public Health. 1992;82:1600-1606.
40.
Kannel WB, Wolf PA. Inferences from secular trend analysis of hypertension control. Am J Public Health. 1992;82:1593-1595.
41.
Whisnant JP. Effectiveness versus efficacy of treatment of hypertension for stroke prevention. Neurology. 1996;46:301-307.
42. MacMahon SW, Cutler JA, Neaton JD. Relationship of blood pressure to coronary and stroke morbidity and mortality in clinical trials and epidemiological studies. J Hypertens. 1986;4(suppl 6):S14-S17.
43.
SHEP Cooperative Research Group. Prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension. JAMA. 1991;265:3255-3264.
44. Rabkin SW, Mathewson FA, Tate R. The relation of blood pressure to stroke prognosis. Ann Intern Med. 1978;89:15-20.
45.
Palmer AJ, Bulpitt CJ, Fletcher AE, Beevers DG, Coles EC, Ledingham JG, O'Riordan PW, Petrie JC, Rajagopalan BE, Webster J, Dollery CT. Relation between blood pressure and stroke mortality. Hypertension. 1992;20:601-605.
46.
McGovern PG, Pankow JS, Burke GL, Shahar E, Sprafka JM, Folsom AR, Blackburn H. Trends in survival of hospitalized stroke patients between 1970 and 1985. Stroke. 1993;24:1640-1648.
47.
Dannenberg AL, Drizd T, Horan MJ, Haynes SG, Leaverton PE. Progress in the battle against hypertension: changes in blood pressure levels in the United States from 1960 to 1980. Hypertension. 1987;10:226-233.
48.
Schuetz H, Dommer T, Boedecker R, Damian M, Krack P, Dorndorf W. Changing pattern of brain hemorrhage during 12 years of computed axial tomography. Stroke. 1992;23:653-656.
49. Katsuki S, Hiroto Y. Recent trends in incidence of cerebral hemorrhage and infarction in Japan. Jpn Heart J. 1966;7:26-34.[Medline] [Order article via Infotrieve]
50.
Fujii K, Weno BL, Baumbach GL, Heistad DD. Effect of antihypertensive treatment on focal cerebral infarction. Hypertension. 1992;19:713-716.
51.
Thrift AG, Dannon GA, McNeil JJ. Epidemiology of intracerebral hemorrhage. Epidemiol Rev. 1995;17:361-381.
52. Manton KG, Corder LS, Stallard E. Estimates of change in chronic disability and institutional incidence and prevalence rates in the US elderly population from the 1982, 1984 and 1989 national long-term care survey. J Gerontol. 1993;48:S153-S166.[Abstract]
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H. Numminen, M. Kaste, K. Aho, O. Waltimo, and M. Kotila Decreased Severity of Brain Infarct Can in Part Explain the Decreasing Case Fatality Rate of Stroke Stroke, March 1, 2000; 31(3): 651 - 655. [Abstract] [Full Text] [PDF] |
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M. Nicolaou, A. L. DeStefano, I. Gavras, L. A. Cupples, A. J. Manolis, C. T. Baldwin, H. Gavras, and L. A. Farrer Genetic Predisposition to Stroke in Relatives of Hypertensives Stroke, February 1, 2000; 31(2): 487 - 492. [Abstract] [Full Text] [PDF] |
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W. D. Rosamond, A. R. Folsom, L. E. Chambless, C.-H. Wang, P. G. McGovern, G. Howard, L. S. Copper, and E. Shahar Stroke Incidence and Survival Among Middle-Aged Adults : 9-Year Follow-Up of the Atherosclerosis Risk in Communities (ARIC) Cohort Stroke, April 1, 1999; 30(4): 736 - 743. [Abstract] [Full Text] [PDF] |
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P. Duncan, L. Richards, D. Wallace, J. Stoker-Yates, P. Pohl, C. Luchies, A. Ogle, and S. Studenski A Randomized, Controlled Pilot Study of a Home-Based Exercise Program for Individuals With Mild and Moderate Stroke Stroke, October 1, 1998; 29(10): 2055 - 2060. [Abstract] [Full Text] [PDF] |
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L. Zhu, L. Fratiglioni, Z. Guo, H. Aguero-Torres, B. Winblad, and M. Viitanen Association of Stroke With Dementia, Cognitive Impairment, and Functional Disability in the Very Old : A Population-Based Study Stroke, October 1, 1998; 29(10): 2094 - 2099. [Abstract] [Full Text] [PDF] |
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M. Peltonen, B. Stegmayr, and K. Asplund Time Trends in Long-term Survival After Stroke : The Northern Sweden Multinational Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) Study, 1985–1994 Stroke, July 1, 1998; 29(7): 1358 - 1365. [Abstract] [Full Text] [PDF] |
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M. Prencipe, F. Culasso, M. Rasura, A. Anzini, M. Beccia, M. Cao, F. Giubilei, and C. Fieschi Long-term Prognosis After a Minor Stroke : 10-Year Mortality and Major Stroke Recurrence Rates in a Hospital-Based Cohort Stroke, January 1, 1998; 29(1): 126 - 132. [Abstract] [Full Text] [PDF] |
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W. H. Barker, J. P. Mullooly, and K. L. P. Linton Trends in Hypertension Prevalence, Treatment, and Control In a Well-Defined Older Population Hypertension, January 1, 1998; 31(1): 552 - 559. [Abstract] [Full Text] [PDF] |
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G D PERKIN Aging J. Neurol. Neurosurg. Psychiatry, October 1, 1997; 63(4): 417 - 418. [Full Text] [PDF] |
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