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(Stroke. 1995;26:1145-1149.)
© 1995 American Heart Association, Inc.

Articles

The Geography of Stroke Mortality in the United States and the Concept of a Stroke Belt

Douglas J. Lanska, MD, MS Lewis H. Kuller, MD, DrPH

From the Departments of Neurology and Preventive Medicine and Environmental Health, and the Sanders Brown Center on Aging, University of Kentucky Medical Center, Lexington, and the Neurology Service, Veterans Affairs Medical Center, Lexington, Ky (D.J.L.); and the Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pa (L.H.K.).

Correspondence to Douglas J. Lanska, MD, Department of Neurology, Rm E124, Kentucky Clinic, University of Kentucky, Lexington, KY 40536-0284. E-mail djlansva@ukcc.uky.edu.

Key Words: cerebrovascular diseases • epidemiology • risk factors • geography • mortality

	Introduction

Top Introduction The Concept of a... References

 
Since at least 1940 there has been a consistent pattern of marked geographic variation in stroke mortality rates within the United States.^{1 2 3} Very high rates are reported in the Southeast, and particularly the southeast coastal plain, while very low rates are reported in the Mountain census division and along the northern Atlantic coast.^{1 2 3} These general patterns of geographic variation have been observed for both sexes and for whites and nonwhites, although stroke rates have been consistently declining in all geographic areas of the continental United States over this interval.¹ Comparable age-adjusted and race- and sex-specific data for earlier periods are not available because (1) tabulations of deaths are limited to the Death Registration Area, which did not include all of the coterminous United States until 1933,^{4 5 6} and (2) US mortality data were first cross-tabulated by age, race, sex, cause of death, and state in 1937. Nevertheless, age-adjusted stroke mortality rates for whites suggest that the current spatial distribution of stroke mortality was not in place in 1920; instead, the high-rate states were apparently concentrated in the northeastern United States.³ From 1920 through 1933, rates declined considerably in all states but particularly in the Northeast, shifting the distribution of excess stroke mortality southward. By 1940, rates had declined further but least in the Southeast, leaving this area with an excess of stroke mortality that has persisted for half a century.

The nonrandom distribution of stroke mortality across the United States; the persistence of the pattern over more than five decades; the similarity of the pattern for different age, race, and sex groups; the fact that the pattern is not delimited by county, state, or other political administrative boundaries; and the extreme magnitude of the differences between rates in high- and low-rate areas suggest that the geographic pattern of stroke mortality rates is not an artifact of different diagnostic and reporting practices.¹ Furthermore, in the 1960s, national cooperative studies confirmed the apparent large differences in stroke mortality rates between geographic areas in the United States.^{7 8} These large variations in mortality rates could not be explained by (1) differences in certification practices (such as the choice of underlying cause of death when multiple causes contributed to death), (2) the frequency with which clinical stroke diagnoses were listed on the certificates, (3) differences in the accuracy of diagnosis of stroke, or (4) variations in the standards of medical care.^{7 8 9 10 11} Furthermore, the large regional differences in stroke mortality parallel geographic differences in stroke incidence¹² and in hospital utilization rates for stroke.²

Nonartifactual variations in stroke mortality rates may theoretically arise from differences in stroke incidence, survival after stroke, or both.^{13 14 15} The geographic distribution of hospital usage for stroke follows closely the distribution of reported stroke mortality rates.^{1 16} Several factors contribute to the strong association between hospitalization rates for stroke and stroke mortality rates: (1) most patients with clinically recognized acute stroke presenting to a physician are hospitalized; (2) stroke is rapidly fatal in a significant and fairly uniform percentage (about a third are dead within 6 months)^{17 18 19 20} ; and (3) most deaths in the several months immediately following a stroke are attributed to stroke on the death certificate.^{19 21 22} In contrast, case-fatality rates show relatively little interstate variation, are not similarly clustered, and are much less strongly associated with stroke mortality rates. Together this information suggests that factors determining stroke occurrence and hospital utilization are more important than factors determining case fatality in explaining the long-standing geographic distribution of stroke mortality in the United States. Factors affecting only case fatality but not hospital utilization, such as the quality of medical care provided in the hospital, cannot explain the geographic distribution of stroke mortality in the United States.

The causes of the marked regional variation in stroke hospital utilization and stroke mortality within the United States remain unknown but are probably multifactorial.^{1 2} Some of the observed geographic variation may be due to variations in the distributions of stroke risk factors, the effects of selective migration, and variations in genetic- or host-susceptibility factors.

Regional variation in stroke risk factors (eg, prevalence of hypertension, diabetes, and cigarette smoking) has been documented by various US government health surveys, but none of the factors have been clearly related to the pattern of geographic variation in stroke morbidity and mortality.¹ Systematic attempts to investigate the geographic variation in stroke risk factors as an explanation of the geographic variation in stroke frequency have been few and the results inconsistent.^{1 23 24 25 26 27} Recognized stroke risk factors, including hypertension, apparently account for only a small fraction of the spatial variation in stroke mortality.^{1 27} Certainly, the spatial distributions of stroke risk factors, and the spatial distributions of nonstroke mortality associated with the risk factors, do not closely correlate with the spatial distribution of stroke mortality.² In addition, the magnitude of the interregional variation in recognized stroke risk factor prevalence as determined from national health surveys is probably insufficient to explain the marked and persistent variation in stroke mortality.² Furthermore, in many cases the geographic variation in stroke risk factor prevalence has not been consistent across studies or among the different race and sex groups.²

Although hypertension is strongly associated with both atherothrombotic brain infarction and intraparenchymal hemorrhage,²⁸ geographic variation in hypertension prevalence does not appear to account for the large variation in stroke occurrence and mortality.^{1 2 27} Available data on the geographic distribution of hypertension prevalence in the United States are inconsistent and generally show only minor regional differences.^{23 24 29 30 31 32} As part of cycle 1 of the National Health Examination Surveys, 6672 persons were examined from a national probability sample of 7710 persons during the period of 1959 through 1962. There were only minor differences in mean blood pressure levels between the various geographic regions.^{29 30} For all age groups, the rates for white men and white women were higher than expected for the age distribution of the population in the Northeast and lower than expected in the West, whereas the rates for blacks were lower than expected in the Northeast.³⁰ As part of cycle III of the National Health Examination Surveys, 6768 youths of ages 12 to 17 years were examined from a national probability sample of 7514 youths during the period 1966 through 1970; there were no consistent regional differences in blood pressure.³¹ As part of cycle I of the National Health and Nutrition Examination Surveys, 23 808 persons were examined from a national probability sample of 32 331 persons during the period 1971 through 1975.³² The mean age-adjusted, race- and sex-specific systolic blood pressures of those in the South tended to be somewhat higher than in other regions. However, for both white and black males the differences were of small magnitude and not statistically significant. For females there were modest statistically significant differences between the South and West for whites and between the South and Midwest and the South and Northeast for blacks. In contrast to the results of the National Health Examination Surveys and the National Health and Nutrition Examination Surveys, the National Health Interview Surveys have noted a higher prevalence of self-reported hypertension in the South.^{33 34}

Cigarette smoking is an important independent risk factor for both hemorrhagic and nonhemorrhagic stroke.^{35 36 37 38} The geographic patterns of cigarette smoking in the United States are similar to those for stroke: the southeastern United States has the highest rates of cigarette smoking and per capita cigarette consumption, while areas with low stroke mortality rates have corresponding low rates of cigarette consumption.² Although such ecological data are suggestive of an etiopathological relationship, Utah's low rates of cigarette smoking and cigarette consumption do not account for the persistently low stroke mortality rates in that state. Almost three fourths of the Utah population are Mormons (members of the Church of Jesus Christ of Latter-day Saints). Only about 10% of Mormons are regular smokers compared with approximately 40% for the non-Mormon white population of Utah and 35% for the general US population. Significantly, stroke mortality rates are low in both Mormons and non-Mormons in Utah,³⁹ presumably implicating some other protective factor.

Dietary factors have also been linked to stroke, particularly in Japanese populations that consume large quantities of rice and little meat.^{40 41 42 43 44} In the United States, there has been persistent (albeit diminishing) regional variation in dietary intake, with the traditional Southern diet being comparable in nutrient content to diets linked to stroke in other populations, ie, relatively high in grain-derived complex carbohydrates and low in animal protein, saturated fat, and cholesterol.² In this regard, it is of interest that the area of excess stroke mortality in the Southeast is contiguous with the pellagra belt of earlier in this century^{45 46} ; however, given the current wide distribution and consumption of prepared foods, it seems unlikely that a deficiency of a specific nutrient accounts for the excess stroke mortality in the Southeast. It is possible, however, that regional variations in food preparation or consumption patterns might affect the relative balance of certain nutrients, which in turn may influence stroke mortality directly or through their effects on recognized stroke risk factors.

Variations in dietary minerals (especially sodium and potassium) have been considered as possible direct and indirect (ie, through effects on blood pressure) modulators of stroke mortality.^{47 48 49 50 51 52 53 54 55} Epidemiological, clinical, and animal experimental data generally indicate positive associations between sodium consumption and both blood pressure and stroke mortality, particularly among subgroups of susceptible individuals, while potassium intake is generally negatively correlated with blood pressure and stroke mortality. The results have not been entirely consistent, however, and the precise role of these nutrients in the genesis of hypertension and stroke remain controversial. Methodological weaknesses of existing studies, large intraindividual variations in intake, and the high degree of intercorrelation among various dietary factors⁵⁶ have prevented clear separation of effects of individual nutrients in human populations and have contributed to the inconclusive and conflicting results published to date. In any case, it is unlikely that geographic variation in dietary intake of these minerals can explain the spatial variation in stroke mortality in the United States for the following reasons. (1) Established associations of dietary intake of these minerals with hypertension or stroke mortality are not strong enough to account for the magnitude of the spatial variation in stroke mortality.⁵⁷ (2) The effect on stroke mortality of variation in these nutrients would presumably be mediated largely by corresponding variation in hypertension prevalence, and a consistent geographic pattern of hypertension prevalence has not been demonstrated in national health examination surveys.^{1 2 23 24 29 30 31 32} (3) Previous attempts at relating overnight urinary sodium and potassium determinations with the spatial distribution of stroke mortality in the United States did not demonstrate consistent gradients of urinary excretion (as an index of intake) from low- to high-rate stroke areas.²⁴ (4) There is no similarity between the spatial distributions of stroke and stomach cancer mortality in the United States,^{1 58 59 60} despite the fact that an apparent geographic relationship between these conditions has been noted in several other countries^{61 62} and despite the fact that the spatial distributions of both conditions have been attributed to variations in salt intake.^{61 62}

Another factor that may explain at least some of the spatial variation in stroke hospital utilization and stroke mortality rates is selective migration. Although the overall large-scale spatial distribution of resident stroke mortality rates cannot be explained by migration effects,⁶³ some individual states have rates that are strongly influenced by migration.^{1 2 63} In particular, interstate migration by the elderly strongly influences both stroke hospital admission rates and mortality from stroke in certain Sunbelt retirement destination states, especially Florida.^{1 2 63} For more than four decades, Florida has been the leading destination of elderly interstate migrants, receiving up to a quarter of all elderly migrants: in-migrants to Florida make up a phenomenally high proportion (approximately 88%) of the resident elderly population of that state, with recent in-migrants (within the previous 5 years) accounting for about 20% of the elderly population. These in-migrants are almost exclusively white, and a large majority are healthy, independent, well educated, and financially secure. As a result of the selective in-migration of large numbers of healthy elderly whites, stroke mortality rates for white residents of Florida became significantly lower than the national rate after World War II and have remained low, in contrast to persistently significantly high rates among black residents of Florida and in contrast to persistently high rates among both whites and blacks in other South Atlantic states over this period.^{1 63} This migration-induced selection by health status also produced lower-than-expected stroke hospitalization rates in Florida but not in other South Atlantic states.¹

	The Concept of a Stroke Belt

Top Introduction The Concept of a... References

 
The first use of the "stroke belt" concept is now obscure, but the term was applied in the 1970s after the gradual recognition during the 1960s of the existence of a broad area of excess stroke mortality in the southeastern United States.^{45 64 65 66 67} Studies of the geographic distribution of stroke mortality in the United States had been conducted earlier, in fact as early as the late 1940s, but these studies downplayed the evident spatial variation in stroke mortality, especially in comparison with the apparently larger spatial variation in cardiovascular mortality.⁶⁸

The term "stroke belt" subsequently has been used variously to refer to either the broad area of excess stroke mortality covering much of the southeastern United States or, in a more selective way, to an area of extreme stroke mortality rates along the southeast Atlantic coastal plain. For example, the National Heart, Lung, and Blood Institute (NHLBI) has defined the stroke belt as those states that had a 1980 age-adjusted stroke mortality rate more than 10% above the average national rate⁶⁹ ; the NHLBI stroke belt therefore includes Alabama, Arkansas, Georgia, Indiana, Kentucky, Louisiana, Mississippi, North and South Carolina, Tennessee, and Virginia. In contrast, Howard and colleagues⁷⁰ in this issue of Stroke define the stroke belt somewhat arbitrarily as a group of contiguous counties along the coastal plains of Georgia and the Carolinas. This latter definition is not based directly on reported rates in those areas but is roughly consistent with some of the area of extreme rates among whites in corresponding state economic areas⁷¹ ; nevertheless, it includes some counties that do not have extreme rates, while it excludes other counties that do.⁷¹ Others have used different definitions of the stroke belt or simply used the term in vague reference to the areas of high stroke mortality rates in the Southeast.

The conceptual value of the term "stroke belt" as it has already been used is limited because (1) available definitions encompass wildly disparate areas, some of which are arbitrarily defined⁷⁰ ; (2) excess mortality is clustered in the southeastern United States for only some stroke types, but it is not clustered in the Southeast for subarachnoid hemorrhage or cerebral embolism⁶⁰ ; (3) even for those stroke types that are clustered in the Southeast, there is considerable variation in the distribution of excess mortality by stroke type⁶⁰ ; (4) the spatial distributions of stroke mortality rates have varied somewhat over time^{1 71} ; (5) although similar, the spatial distributions of stroke mortality rates differ somewhat by race and sex^{1 60 71} ; (6) confounding by race has not been adequately considered in some definitions such as the NHLBI definition, which defines the stroke belt on the basis of the age-adjusted rate for the total population⁶⁹ ; since blacks have much higher stroke mortality rates than whites and since the black population is highly concentrated in the Southeast, the NHLBI definition essentially defines the stroke belt as the area of the country with a high proportion of blacks, even though the distribution of high stroke mortality among whites is also concentrated in the Southeast; and (7) the effect of selective and highly channeled elderly interstate migration has been ignored, particularly in regard to Florida,⁶³ and as a result, Florida has been inappropriately excluded from current definitions of the stroke belt, at least when considering black and native nonmigrant white Floridians. In part because of such problems, various authors have questioned the extent of the boundaries of the stroke belt.^{72 73}

So how should the stroke belt be defined, or can it? "Belt" as applied by geographers and social scientists is in fact often a loose construct, referring to a broad, often imprecisely defined area that is characterized by some distinctive feature (eg, the manufacturing belt, the snow belt, the Sunbelt, etc). The stroke belt concept as applied so far has generally, but not universally,⁷⁰ followed this precedent. Any further attempts to apply the term—if it is going to have any lasting value—should at least be consistent. In addition, since "the stroke belt" could become a useful buzzword for raising public awareness of stroke and stroke prevention in high-rate areas, it seems preferable to target the entire broad area of excess stroke mortality across the southeastern United States than to limit use of the term to a relatively small geographic area with a total population of less than 2 million people. It seems reasonable, therefore, to apply the term "stroke belt" to the broad area of excess mortality encompassing much of the southeastern United States⁶⁹ and to refer to the southeastern coastal plain as the "extreme rate zone" of the stroke belt.

Within this broad framework, it must be recognized that the stroke belt could be defined in many different ways, each better for some purposes than for others. For etiologic investigations, for example, it may be preferable to define a number of stroke belts, each applicable to a specific stroke type and race-sex population group, rather than to define a single stroke belt on the basis of mortality from all types of stroke for the total population, as was done for the NHLBI definition.⁶⁹ In contrast, for public health purposes, a simpler definition of a single collective stroke belt is more practical and would be less confusing to the public toward which risk factor modification campaigns might be directed. In any case, the definitions used generally should be based directly on available data to reflect the dynamic spatial-temporal variation in stroke mortality; arbitrarily defined fixed geographic areas, such as in the definition of Howard and colleagues,⁷⁰ will not vary as rates in component or boundary areas change, and they may cease to have any meaning in terms of encompassing or even representing the areas of true excess mortality.

Geographic units smaller than states (eg, state economic areas or counties) could be used^{60 71} to more precisely define the boundaries of high-rate areas. However, a number of limitations must be considered with such data: (1) there has been no validation of the spatial variation in stroke mortality rates at this level, particularly within the area of high rates across the southeastern United States; (2) smaller geographic units are prone to markedly greater variability in the rate estimates because of the much smaller population sizes; (3) there is some suggestion that the boundaries of high-rate areas are becoming increasingly hard to define using smaller geographic units as stroke rates decline and previous areas of intense clustering begin to dissipate⁷¹ ; and (4) longitudinal studies will be limited by some shifts in county boundaries over time and by the lack of county- level data from before 1968.

In conclusion, while no single definition of the stroke belt will suit all purposes, the term "stroke belt" should generally be used to refer to the broad area of excess mortality encompassing much of the southeastern United States. For many purposes, it may be necessary to define a number of stroke belts, each applicable to a specific stroke type and a specific population group. Data-based definitions are generally preferable to arbitrary definitions based on geographic area. The geographic units used must conform to the purposes of the definition; the use of smaller geographic units will be constrained by a number of factors, including greater variability in rate estimates and concerns about the validity of apparent heterogeneity.

	Acknowledgments

 
This project was supported in part by a clinical investigator development award from the National Institutes of Health (1-K08-NS01549-01, Dr Lanska), by Research Advisory Group funding from the Office of Research and Development of the Department of Veterans Affairs (Dr Lanska), and by the philanthropic support of Jayne Bolotin (Dr Lanska).

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