a Department of Public Health and Hygiene, Oita Medical University, Oita, Japan.
b Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, MN, USA.
c Chuo Public Health Center, Oita Prefectural Government, Beppu, Japan.
Reprint requests to: Isao Saito, Department of Public Health and Hygiene, Oita Medical University, Idaigaoka, Hasama-machi, Oita 8795593, Japan. E-mail: saitoi{at}oita-med.ac.jp
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Abstract |
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MethodsPopulation-based fatal CHD data were compared between the Oita Cardiac Death Survey, Japan and the Atherosclerosis Risk in Communities (ARIC) Study, USA. Both studies (population: Oita City 198 093; the ARIC comunities 286 820) identified possible fatal CHD events (International Classification of Diseases, Ninth Revision [ICD-9]: 410414, 250, 401402, 427429, 440, and 798799) among residents aged 3574 years during 19921993. Comparable criteria for classifying cause of death were applied. Sex-specific, age-adjusted mortality rates of CHD were calculated by place of death.
ResultsIn all, 330 deaths in Oita and 1398 in the ARIC communities had eligible ICD-9 death certificate codes; CHD codes (ICD-9 410414) comprised 30.6% of investigated deaths in Oita and 58.6% in ARIC. For men, the non-validated rate ratio for CHD deaths (ARIC:Oita City) was 5.9 (95% CI : 4.28.5), which fell to 4.7 (95% CI : 3.56.4) with validation and inclusion of sudden deaths within one hour of onset as fatal CHD. For women, the overall non-validated rate ratio was 4.6 (95% CI : 2.87.6), which fell to 3.9 (95% CI : 2.46.3) with validation and but there was little further change when the sudden deaths were added.
ConclusionsOur results suggest that differences in fatal CHD rates between Japanese and Americans were not as large as suggested by vital statistics when events were validated and sudden deaths were included.
Keywords Coronary disease, vital statistics, mortality, sudden death
Accepted 24 March 2000
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Introduction |
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In parallel with declining CHD mortality in Japan, mortality rates for heart failure as an underlying cause of death have steadily increased.1 In Japan, physicians consider the term heart failure to not just reflect congestive heart failure, but it can include sudden deaths or the mode of dying in the end stages of stroke or cancer.12 Therefore, it has been suggested that CHD deaths may be hiding under the heart failure rubric in Japanese vital statistics.13 In support of this hypothesis, we recently showed that age-adjusted rates of validated CHD mortality plus sudden deaths in Oita City remained stable from 19871988 to 19921993 in men (37.8/100 000 to 38.3/100 000) and increased from 11.2/100 000 to 17.3/100 000 in women, whereas CHD vital statistics decreased over the 5 years in both sexes.12,14
It has been well-known from vital statistics that age-adjusted CHD mortality rates for Americans are much higher than those for Japanese.15 Coronary heart disease mortality occurs at an earlier age in Americans than in Japanese, with vital statistics indicating that 63% of Japanese CHD deaths occur after the age of 75 years.1 However, in consideration of both the unfavourable serum cholesterol trend and the unclear trend in vital statistics for CHD in Japan, we believed that the difference in age-adjusted CHD mortality rates between Japan and the US may not be as great as vital statistics have indicated.
Others have argued that vital statistics are insufficient to compare fatal CHD between different cultures because of substantial diagnostic differences.16,17 There are few contemporary epidemiological data comparing fatal CHD between Japan and the US. We therefore compared validated fatal CHD rates in the Oita Cardiac Death Survey (OCDS)14 and the Atherosclerosis Risk in Communities (ARIC) Study.18
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Methods |
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The population aged 3574 years was 198 093 in Oita City and 286 820 in the ARIC communities in 19921993. Although Washington County, Maryland is also one of the ARIC communities, it was excluded because data on out-of-hospital deaths were not available. Oita City has only ethnic Japanese and the ARIC communities a majority of whites. The percentage of African Americans in the three ARIC communities was 25% overall (approximately 25% in Forsyth County, 50% in Jackson, and 1% in suburban Minneapolis).
All death certificates were reviewed, and deaths were selected if they had the following International Classification of Diseases, Ninth Revision (ICD-9) codes as underlying causes of death: diabetes mellitus (ICD-9: 250), essential hypertension (401), hypertensive heart disease (402), acute myocardial infarction (AMI) (410), other ischaemic heart disease (411414), cardiac dysrythmias (427), heart failure (428), ill-defined descriptions and complications of heart disease (429), atherosclerosis (440), sudden death, cause unknown (798), and other ill-defined and unknown causes of morbidity and mortality (799). In the OCDS, 100% of these deaths were investigated. In ARIC, 50% of deaths coded as 250, 401402, 427429 (except for 429.2), 440, and 798799 were investigated and 100% of the other codes were investigated.19
The Oita Cardiac Death Survey (OCDS)
The OCDS was performed to identify fatal CHD in Oita City residents who died from heart disease and other CHD-related diseases according to death certificates.12 Briefly, trained investigators recruited eligible deaths using medical records, physician interview, or police records when needed. We were able to get some information for validation in 97.6% of all eligible deaths. Only 2.4% were not investigated, for privacy reasons. Location of death (in-hospital or out-of-hospital) was verified. Deaths occurring in a nursing home or dead on arrival were considered to be out-of-hospital deaths. The elapsed time was defined as the time from onset to collapse, not the end of unsuccessful attempts at resuscitation. Death certificates were reviewed by a co-author (TY), as part of an investigation for the Oita Public Health Center to examine vital statistics in communities. It was permitted by the Community Health Act of Japan.
Information on chest pain, enzymes, electrocardiogram, autopsy, and previous CHD history was obtained, and the death was classified into one of five categories based on the World Health Organization (WHO) Monitoring Trends and Determinants in Cardiovascular Disease (MONICA) project's criteria:20 (1) definite fatal acute myocardial infarction (AMI), (2) possible fatal AMI or CHD death, (3) sudden death, (4) non-CHD death, and (5) insufficient data. The first two categories followed the MONICA criteria exactly. Sudden death comprised deaths within 24 hours of the onset of acute symptoms without reports of typical or atypical chest pain defined by the MONICA criteria,20 and without clear signs suggesting another cause. Diagnostic information was independently categorized by two physicians. When they disagreed, the cases were reviewed again, and a final classification was made.
The Atherosclerosis Risk in Communities (ARIC) Study
The ARIC Study included community-based surveillance of CHD to document incidence, case-fatality rates, and mortality rates.18,19 In addition, prospective cohorts randomly selected among residents of the four ARIC communities were set up to examine relationships between the cardiovascular disease occurrence and its risk factors. In brief, the surveillance data included standardized abstractions of medical records, physician questionnaires, next-of-kin interviews, and coroner records. Place of death and time to death were determined by abstractors. Deaths in nursing homes or emergency rooms and deaths on arrival were regarded as out-of-hospital deaths.
The ARIC Study classified events into five categories:18 (1) definite fatal MI, (2) definite fatal CHD, (3) possible fatal CHD, (4) non-CHD death, and (5) unclassifiable. Out-of-hospital deaths were classified by two physicians on the ARIC Mortality and Morbidity Classification Committee, and disagreements were adjudicated by a third physician. Many in-hospital deaths were classified by a computerized diagnostic algorithm, with certain events requiring physician review.18
Categorization and comparability
In order to compare rates between the OCDS and ARIC Study, CHD events were re-classified into the following five equivalent categories: (1) fatal CHD, (2) sudden death within one hour of onset (SD1h), (3) sudden death within 124 h (SD>1h,
24h), (4) non-CHD death, and (5) unknown. Definite fatal AMI plus possible fatal AMI or CHD death in the OCDS was defined comparably to definite fatal MI plus definite fatal CHD in the ARIC Study. These therefore comprised fatal CHD. For cases in which there was no evidence suggesting fatal CHD or another cause of death, we created two sudden death categories according to the time interval to death (
1 h, or >1
24 h), because we believed such deaths, especially within one hour, were possibly due to CHD.2123 Non-CHD death was classified based on the categorization of each study when a diagnosis other than CHD was made by physicians. The category of unknown included deaths for whom the time interval was unknown or was over 24 hours and there was no evidence to assign another cause of death.
Autopsy findings were excluded in ARIC surveillance to avoid an influence of differing autopsy rates among the ARIC communities.18 The OCDS used autopsy data, but autopsies were rare (n = 8).
Statistical methods
Annual mortality rates for both non-validated and validated CHD, and corresponding 95% CI, were calculated after adjustment for age by the direct method using the standard world population. Population size was the average of 1992 and 1993 in each study community. As certain ICD-9 codes on death certificates were sampled in the ARIC Study, we estimated the actual number of deaths for these causes by accounting for the sampling fraction. We also calculated rates for fatal CHD plus SD1h or SD>1h,
24h, because such sudden deaths were often presumed to be CHD deaths.
To compare CHD mortality rates between Oita City and the US communities, age-standardized mortality rate ratios and their 95% CI were also computed based on the non-validated and validated CHD mortality rates.24 The 95% CI were calculated from the weighted, age-stratified data using the normal approximation of the Poisson distribution. The rate ratios were recomputed after SD1h or SD>1h,
24h was added to validated fatal CHD.
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Results |
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The underlying causes of death were validated using criteria comparable between studies and classified into five categories by place of death (Table 2). In Oita City, 84.8% of AMI, 78.6% of other CHD, and 9.1% of other codes were assigned to validated fatal CHD for in-hospital deaths. Similarly, 86.6%, 81.2%, and 36.0%, respectively, were assigned in the ARIC communities. More validated CHD deaths among other codes in ARIC could result from frequent use of ICD code 429.2 (arteriosclerotic cardiovascular disease) as CHD on death certificates in Jackson. For out-of-hospital deaths, 60.6% of AMI, 75.0% of other CHD, and 10.8% of other codes were classified into fatal CHD in Oita City, versus 61.0%, 63.6%, and 34.0% in the ARIC communities. Although few sudden deaths occurred in-hospital, 25.1% of out-of-hospital deaths in Oita City were classified as SD
1h and 18.7% were SD>1h,
24h. These percentages were 12.3% and 13.1% in the ARIC communities, significantly lower than in Oita City (P = 0.001).
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Discussion |
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For men, rate ratios for validated fatal CHD comparing ARIC to Oita were similar to non-validated ones; however, they were lower after the addition of the sudden deaths to validated fatal CHD. We believe many sudden deaths in Oita City men were certified as heart failure on the official record rather than CHD. Furthermore, since the difference in CHD mortality rates decreased in the younger age group of men after adding SD1h (Figure 3
), younger men seemed more likely than older men to be assigned heart failure as a cause when they died suddenly. For women, the validated rate ratios were lower than the non-validated ones, but did not change much after adding sudden deaths. Thus, even though the CHD mortality was much higher in ARIC than Oita, the validated fatal CHD difference was smaller than the non-validated difference.
Limitations of this study warrant consideration. Although the OCDS and ARIC studies used comparable investigation procedures and criteria for the categorization of fatal CHD, some factors could cause bias because the studies were not designed to be compared. For example, the next-of-kin interview was conducted for out-of-hospital deaths only in the ARIC Study. Yet, it is unclear whether having the next-of-kin data would lead to overestimation or underestimation of the OCDS-ARIC difference in fatal CHD out-of-hospital. In addition, differences in the use of diagnostic procedures for CHD, such as coronary angiography, or medical systems including coronary care units or emergency rooms, might also affect comparability of fatal CHD diagnosis across communities. Indeed, the large observed difference in rates of CHD mortality, especially out-of-hospital (Figure 1), may be partly due to differences in data availability. That is, even though the timing of the onset of symptoms was frequently missing in both Oita and ARIC, many ARIC cases were classified as fatal CHD based on cardiac pain or previous CHD history from the next-of-kin interview. These cases in Oita City, with less information, were classified as sudden death. Additional limitations of this study include the relatively small number of events in Oita and the low response rate from next-of-kin.
The category of sudden death was defined because autopsy studies indicate that a high proportion of sudden deaths are CHD.2123,25 For example, autopsy data in Japan showed that approximately 50% of unexpected deaths within 24 hours of onset were due to CHD.25 Most deaths that we categorized as sudden deaths in Oita City had been assigned by vital statistics to other causes of death (e.g. heart failure). By contrast, more than half of sudden deaths in the ARIC communities had been assigned CHD as the underlying cause. These results imply that CHD was underestimated by vital statistics in Oita City. The percentage of sudden deaths in OCDS was similar to that found in another validation study, done in Suita City, Osaka, Japan in 19861988.26 The misuse of heart failure in Japan as an underlying cause for sudden deaths and other non-specific causes has been pointed out.27
The Seven Countries Study first reported large fatal CHD differences between the Japanese and the US populations.28,29 Japanese subjects had the lowest CHD mortality rates linked with the lowest mean total cholesterol among the seven countries. The Ni-Hon-San Study confirmed the relation between low CHD mortality rates and low total cholesterol levels among three Japanese cohorts living in Japan, Hawaii, and the US.30 These studies consistently indicated that the low average serum cholesterol level was the key to the low CHD mortality rates in Japan. Recently, however, lipid profiles have changed appreciably among both Japanese and Americans. For example, the National Cardiovascular Survey in Japan reported a 10 mg/dl increase between 1980 and 1990, with 1990 mean cholesterol levels approaching 200 mg/dl;6 in contrast, the third National Health and Nutrition Examination Surveys (NHANES III) reported an 8 mg/dl decrease (to 205 mg/dl) in serum cholesterol for all adults aged 20 years during the same period.9 Japanese living in Akita, Japan had more favourable total and low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol profiles than ARIC participants.31 Other studies have confirmed less dyslipidaemia in Japanese than Americans,32,33 but inter-country differences in serum total cholesterol appear to be smaller than a few decades ago.
We examined CHD mortality and did not attempt to ascertain CHD incidence or case-fatality rates in the OCDS. Comparisons of incidence rates and case-fatality based on CHD surveillance in a large population might help explain the mortality differences. Such epidemiological data in Japan are very scarce, because large sample sizes are needed to measure them. Japanese cohort data have indicated that CHD incidence did not change,34 or increased slightly among urban populations35 between the 1960s and 1980s. It has been suggested that the duration of exposure to high cholesterol levels has been too short to raise CHD mortality rates in Japan.36 If true, CHD mortality rates in Japan may eventually increase as the result of higher chol-esterol levels.
Our results suggest that differences in age-adjusted fatal CHD rates between Japan and the US may not be as large as vital statistics suggest, although the OCDS and ARIC population are not representative of the whole countries. Of interest is whether cholesterol levels in Japan may eventually exceed those in the US and whether CHD mortality differences may shrink in the future. For the Japanese, the recent rise in cholesterol is an unfavourable trend. In addition, smoking remains high in Japanese men. Continued epidemiological studies of CHD will play an important role both to document future CHD trends and to guide primary and secondary prevention efforts against CHD in Japan.
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Acknowledgments |
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References |
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