(Stroke. 1996;27:1055-1059.)
© 1996 American Heart Association, Inc.
Articles |
From the Departments of Neurology, Preventive Medicine and Environmental Health, and Statistics, and the Sanders Brown Center on Aging, University of Kentucky Medical Center, Lexington, and the Neurology Service, Veterans Affairs Medical Center, Lexington, Ky.
Correspondence to Douglas J. Lanska, MD, Department of Neurology, Rm L412, Kentucky Clinic, University of Kentucky, Lexington, KY 40536-0284.
| Abstract |
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Methods National Center for Health Statistics and Bureau of the Census data were used to assess regional-level temporal trends of underlying-cause stroke mortality rates in the United States for 1979 through 1989. Both additive and multiplicative models were fit to the data.
Results Underlying-cause stroke mortality rates have declined fairly steadily in all regions of the United States and for all race-sex groups, although there was significant regional variation in the rate of decline during the period 1979 through 1989. The South, which initially had the highest rates, had the most rapid decline for all race-sex groups when either additive or multiplicative models were used.
Conclusions From 1979 through 1989 there was significant geographic variation in the rate of decline of stroke mortality rates, with the most rapid rates of decline in the South. As a result, there has been a decrease in interregional variation in stroke mortality rates.
Key Words: cerebrovascular disorders epidemiology mortality risk factors
| Introduction |
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Recently, there has been some indication that the dense concentration of excess stroke mortality in the southeastern United States is dissipating.1 5 6 7 With the overall decline in stroke mortality rates, there has been a convergence (decrease in variability) of age-adjusted state stroke mortality rates overall and within the various race-sex groups.1 6 7 In addition, at the level of state economic areas, the dense concentration of excess stroke mortality along the South Atlantic coastal plain has dissipated considerably since the early 1960s.5 6
Although geographic variation in the decline of stroke mortality rates may be an important contributor to the changing geographic distribution of stroke mortality in the United States,7 some concern has been raised that this phenomenon may be model dependent.8 The present study evaluates the geographic variation in the decline of regional stroke mortality rates with the use of both additive and multiplicative models.
| Methods |
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Population data tabulated by state, race, sex, and age were obtained from published data of the US Bureau of the Census for 1970, based on the population enumerated as of April 1. The racial classification used for data collected in the 1980 and 1990 censuses, however, differs from the racial classification used for vital statistics data and for data from previous censuses. To maintain comparability with the racial designations used in the vital statistics mortality data, we used Census Bureau modified-race estimates of the 1980 and 1990 US population by age, race, and sex.14 15 16 17 18 19
Since the Census Bureau has no state- or regional-level intercensal estimates based on age, sex, and race (personal communication, US Bureau of the Census, 1996), population data for intercensal years were estimated by linear interpolation from decennial census data for each population group. Most of the fluctuation in intercensal estimates is due to changes in births and labor-force migration. For the population older than age 55, ie, the population most susceptible to stroke, significant deviations of age-, race-, sex-, and region-specific intercensal population estimates from the actual (unmeasured) values are unlikely (personal communication, US Bureau of the Census, 1996).
Age-, race-, and sex-specific rates were calculated by region for deaths with stroke listed as the underlying cause of death (underlying-cause rates). The states in each region are listed in the Appendix. Annual age-adjusted stroke mortality rates (per 100 000 population) by race and race-sex groups were computed by the direct method, that is, by applying the age-specific death rates for stroke to the standard population distributed by age. The reference population used was the total US population enumerated on April 1, 1980.
Two different models were fitted to the annual age-adjusted stroke
mortality rates. A linear or additive model was fit by linear
regression of stroke mortality rates on calendar year, ie,
rate=ßyear+
.20 21 The average annual rate of change
in regional or state age-adjusted stroke mortality rates was
measured as the slope of the regression of these rates on year. An
exponential decay or multiplicative model (ie,
rate=
eßyear) was fit by linear
regression of ln-transformed rates on calendar year, since
rate=
eßyear is equivalent to
ln(rate)=ßyear+
'.20 21 The average annual percent
change in regional age-adjusted stroke mortality rates was measured
as a function of the slope of the regression of ln-transformed
rates on year [average annual percent
change=100(1-eß)]. With both models,
comparison of slopes between regions was achieved by considering an
expanded linear model with either the mortality rates or
ln-transformed mortality rates as a function of both year and
region. A significant interaction effect between year and region
indicates a significant difference in absolute change or percent change
across regions. Goodness of fit of the models was assessed with the use
of the square of the sample correlation coefficient
(r2), which may be interpreted as the
proportion of total variability in the dependent or response
variable that is explained by the independent or explanatory
variable.20
| Results |
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Both additive and multiplicative models generally fit the data
extremely well (Table 3
). The relationship between
stroke rates and year was approximately linear within the study period;
analyses of residuals in the additive models revealed no marked
departures from linearity. Indeed, r2
values for the additive models ranged from .927 to .975 for the various
race-sex groups in the national models and from .904 to .981 for
whites and .595 to .963 for blacks in the regional models. The
relationship between ln-transformed stroke rates and year was also
approximately linear within the study period; analyses of
residuals in the multiplicative models revealed no marked departures
from linearity. r2 values for the
multiplicative model ranged from .943 to .987 for the various
race-sex groups in the national models and from .927 to .992 for
whites and .581 to .971 for blacks in the regional models. The
relatively poor fit for both models among blacks in the West reflects
the erratic rates due to the small number of blacks in that region.
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| Discussion |
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Although the causes of the long-standing regional variation in stroke mortality in the United States are unknown, the nonrandom distribution of stroke mortality across the United States, the large magnitude of the difference between high and low rate areas, the persistence of the pattern over more than four decades, the similarity of the distribution for different race-sex groups, and the lack of delimitation by administrative or political boundaries suggest that the pattern of excess stroke mortality is not an artifact of different diagnostic and reporting practices.1 2 4 7 In addition, in the 1960s, national cooperative studies confirmed the apparent large differences in stroke mortality rates among geographic areas in the United States23 25 ; these large variations in mortality rates could not be explained by differences in certification practices (such as choice of underlying cause of death when multiple causes contributed to death), the frequency with which clinical stroke diagnoses were listed on the certificates, differences in the accuracy of the diagnosis of stroke, or variations in the standards of medical care.23 24 25 26 27 Furthermore, the large regional differences in stroke mortality parallel geographic differences in stroke incidence28 and in hospital utilization rates for stroke.2 29
The present results demonstrate that the regional
heterogeneity of temporal changes in stroke mortality
rates is not simply a function of the additive models initially used to
help understand and interpret the regional trends.7
Without recourse to any modeling whatsoever, it is evident (see the
Figure
) that (1) stroke mortality rates have decreased for all regions
and for all race-sex groups over the study period; (2) the
magnitude of interregional differences has declined; and (3) while the
South initially had the highest rates, the rates dropped most quickly
in the South, and for whites crossed over other trend lines so that by
1989 the South no longer had the highest rates for white males or
females. Moreover, both additive and multiplicative models are
consistent in (1) providing extremely good fits to the data and
(2) indicating that the South had the most rapid (absolute or relative)
decline in stroke mortality rates during the study period.
The results of the present study support the previous suggestion5 6 7 that the long-standing excess of stroke mortality in the southeastern United States is beginning to dissipate. The South experienced the greatest declines in stroke mortality over the period from 1979 through 1989. Stroke mortality rates in the South now much more closely reflect the national experience than they did in previous decades. Although areas of very high stroke mortality rates still persist,1 2 they are becoming fewer and more isolated,5 6 especially when examined on a smaller geographic scale, and the magnitudes of the differences between high-rate areas and low-rate areas have lessened dramatically.1 7
The results of the present study are not accounted for by regional variation in the diffusion of CT. While the advent of CT has significantly improved the diagnosis of stroke types,30 31 32 in some cases affecting trend estimates for individual types of stroke,31 the impact of this technology on aggregate stroke mortality estimates is probably small. In most cases, clinical diagnostic errors identified by CT were in the diagnosis of the stroke type rather than in recognition of the presence or absence of cerebrovascular disease32 ; correction of these diagnostic errors by use of CT did not result in significant changes in estimates of the number of individuals with a stroke of any type. Furthermore, the regional per capita availability of this and related MRI technology33 34 35 36 and regional trends in the use of CT37 parallel neither the regional stroke mortality rates nor the regional rate of decline in stroke mortality rates.
| Acknowledgments |
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| Appendix 1 |
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Received October 9, 1995; revision received February 27, 1996; accepted February 27, 1996.
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