ArticlesEstimation of contribution of changes in classic risk factors to trends in coronary-event rates across the WHO MONICA Project populations
Introduction
Routinely collected statistics on mortality rates from coronary heart disease (CHD) showed increases in the 1950s and early 1960s in most industrialised countries, but a decline started in the 1960s in the USA and Australia, followed by other countries.1 Key questions were raised at a conference on this decline, convened by the National Institutes of Health in Bethesda, MD, USA, in 1978. Were the mortality changes real, and if so, how much was attributable to change in incidence of coronary events, and how much to change in case fatality? Could the changes in coronary-event rates be related to population trends in the known coronary risk factors of cigarette smoking, blood pressure, and serum cholesterol? Could the changes in case fatality be related to trends in coronary care? These questions could not be answered because of a lack of basic information.2 Consequently, WHO invited investigators with an interest in what was happening to CHD in their own populations in many different countries, to collaborate in an epidemiological study that became the WHO Multinational Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) Project. Protocols, procedures, and quality-assurance methods were developed for collecting a standard set of data on trends in CHD mortality, non-fatal acute myocardial infarction, coronary care, and major coronary risk factors, in defined populations for men and women aged 35–64 years.3 Apart from fulfilling local needs, the data from the different populations were to be put together centrally to address the unanswered questions from the Bethesda meeting. (For objectives and outline protocol of the WHO MONICA Project see URL: www.ktl.fi/publications/monica/manual/part1/i-1.htm URN: NBN:fi-fe19981147)
In a previous paper, we confirmed the validity of the mortality trends and showed that, in populations in which mortality declined, coronary-event rates contributed two-thirds of the decline and one-third came from change in case fatality.4 The conclusion was that the main determinant of change in CHD mortality was whatever drives changes in rates of coronary events.
The two other questions from Bethesda are now addressed in separate papers. Here we address the first question, formulated for the 1983 protocol as a null hypothesis that for the population reporting units there is no relation between: 10-year trends in the major cardiovascular-disease risk factors of serum cholesterol, blood pressure, and cigarette consumption; and 10-year trends in incidence rate (fatal plus non-fatal attack rates) of CHD.
Relative bodyweight was not originally included in the study protocol for this analysis, but we have included it because of its perceived public-health importance.5
We address the second question, which relates changes in case fatality and other coronary endpoints to changes in coronary care, in another paper in this issue of The Lancet.6 Differences in definitions of populations and in timing of data on risk factors and coronary care inhibit an all-inclusive first analysis of the two questions.
Accumulated evidence of causality through the consistency, strength and reversibility of the classic coronary risk factors in individuals has increased substantially since 1983. The null hypothesis is, therefore, of less importance than estimating the size of the effect. We attempted to estimate the extent to which trends in classic risk factors are driving the change in coronary-event rates at population level. Since the units in this paper are populations, the analysis was ecological.7, 8
Section snippets
Study populations
Study populations consisted of residents of geographically defined areas aged 35–64 years. There was no follow-up of individuals beyond the 28-day duration of a coronary event. The 38 populations in 21 countries were mostly in Europe, but three were in Asia, three in Australasia, and two in North America (table 1). Short descriptions of the populations have been published elsewhere.9 The populations are almost the same as in our previous paper on coronary events,4 except for six that cover
Trends in coronary-event rates and risk factors
The average annual coronary-event rates in the last 5 years of event registration, the means of the risk factors, the risk score in the final survey, and the trends in these are shown in Table 2, Table 3. An average annual change in daily cigarette smoking of 0·5% means that over 10 years, the prevalence of smoking increased by 5 percentage points; likewise an average annual change of systolic blood pressure of −0·69 mm Hg means that, over 10 years, the mean systolic blood pressure of a given
Rationale for the study
From the 1950s onwards, epidemiological studies, led by Framingham in the USA,24 identified personal characteristics as risk factors for the development of premature CHD in previously healthy people. Of these modifiable factors, distinct from age and sex, cigarette smoking, blood pressure, and total blood cholesterol were most consistently and powerfully implicated.25, 26, 27 In the Seven Countries study,28 investigators showed these risk factors to be important within populations in different
Conclusion
The apparent contribution of the classic risk factors to the trends in CHD over 10 years across the WHO MONICA Project populations has been less precisely estimated than had been hoped. Estimates for women were less reliable than those for men because of greater imprecision in the estimation of trends in event rates. Estimates are low, with perhaps 15% in women and 40% in men of the variability of trends in coronary-event rates being “explained” by trends in the major risk factors. How much of
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Participating centres of the MONICA Project listed at end of paper