European Heart Journal (2001) 22, 136–144doi:10.1053/euhj.2000.2179, available online at http://www.idealibrary.com on

Optimal risk factors in the population: prognosis,prevalence, and secular trends

Data from Goteborg population studies

A. Rosengren, A. Dotevall, H. Eriksson and L. Wilhelmsen

Section of Preventive Cardiology, Sahlgrenska University Hospital/O} stra, Goteborg, Sweden

Aims To assess the prognosis and prevalence of optimalrisk factors in the population.

Methods and Results Data from several Goteborg popu-lation studies were used. Optimal risk factors were definedas serum cholesterol <5 mmol . l�1, blood pressure <140/90 without treatment and being a non-smoker. In a 20-yearfollow-up of 7130 men aged 47 to 55 at baseline a group of117 men who were optimal with respect to cholesterol,blood pressure and smoking were identified. In this groupthere was only one death from coronary disease, corre-sponding to 0·4 deaths per 1000 years, whereas the overallrisk of coronary death in the study was 4·8 per 1000 years.Among men and women aged 25 to 34 in the GoteborgMONICA study 1995, less than half were optimal on allthree scores, and in men and women aged 55 to 64, only 7%and 6%, respectively, were optimal. If body mass indexbelow 25 was included only 34% and 37%, respectively, ofmen and women aged 25 to 34 were optimal, and 11% and

0195-668X/01/220136+09 $35.00/0

22% among men and women aged 35 to 44. In an analysisof secular trends over 30 years in four successive cohorts ofmen aged 50 the prevalence of optimal risk factors withrespect to cholesterol, blood pressure and smoking in-creased from 1963 to 1993 but was still only 11% in 1993.

Conclusions As expected, optimal risk factors with re-spect to serum cholesterol, blood pressure and smokingconfers a very low risk of coronary death. However, theprevalence of optimal risk factor status in the Swedishpopulation is still low.(Eur Heart J 2001; 22: 136–144, doi:10.1053/euhj.2000.2179)� 2001 The European Society of Cardiology

Key Words: Coronary disease, risk factors, smoking,cholesterol, blood pressure, population study.

See page 105 for the Editorial comment on this paper

Introduction

Coronary heart disease is largely preventable. The hugevariations in this disease between populations as well asover time bear ample witness to this. As populationcharacteristics change, so do coronary heart incidenceand mortality. The geographical variation is wellknown[12]. A recent development is the increasing inci-dence in the developing countries[3]. Ischaemic heartdisease is estimated to be the leading cause of lostlife-years until at least 2020[4].

In the established market economies the last decadeshave seen important decreases in the incidence of myo-cardial infarction and coronary mortality. Swedish fig-ures for coronary heart disease are in the middle range

of the European countries[2], and the average annualdecrease in coronary heart disease incidence between1987 and 1996 in men and women aged 30 to 89 hasbeen 2·2% and 1·8%, respectively[5]. Similar changeshave been noted in men and women in Goteborg sincethe beginning of the 1980s[6]. Changes in the cardio-vascular risk factor pattern seem to account for this[7–10].The decrease in incidence in men below 65 years of agecorresponds well to the decreasing levels of the threemain risk factors[10]. However, rates of coronary diseasein Sweden are still disturbingly high.

Comprehensive action for the prevention of coronaryheart disease has to include a population strategy inaddition to individual secondary prevention and pri-mary prevention in high risk men and women. Riskfactor goals for prevention in subjects with knowncoronary disease and in healthy high risk subjects arebased on solid scientific evidence derived from a multi-tude of experimental and observational studies, whichhave been summarized in the second joint task force of

Revision submitted 17 March 2000, and accepted 21 March 2000.

Correspondence: Annika Rosengren, MD, professor, Departmentof Medicine, Sahlgrenska University Hospital/O} stra, SE-416 85Goteborg, Sweden.

� 2001 The European Society of Cardiology

Data from Goteborg 137

European and other societies on coronary prevention[11].In this document, the ideal goals for prevention ofcoronary diseases and other atherosclerotic diseaseshave been defined as a diet compatible with ideal weight,and a plasma total cholesterol level of less than5 mmol . l�1, regular exercise, the avoidance of allforms of tobacco, and a blood pressure of less than140/90 mmHg. Levels of risk factors in various popula-tions are known from a large number of studies[8,9,12–19],usually in terms of mean levels and prevalence ofpre-defined high levels. However, the prevalence ofoptimal risk factors is rarely described. In Goteborg,prospective and cross-sectional studies of representativepopulation samples have been carried out since 1963. Inthe present investigation, we used data from several ofthese samples to identify low risk subjects, and todescribe prognosis, prevalence, and secular trends withrespect to optimal risk factor status.

Methods

For the prospective part of the study, data were takenfrom the multifactor primary prevention study whichstarted in Goteborg in 1970 and included all men inthe city who had been born between 1915 and 1925,except those born in 1923[20]. The intervention groupof 10 000 men comprised a random third of the men inthe trial, with two control groups of 10 000 men each.At follow-up, after 11·8 years, there were no significantdifferences in risk factor levels or in outcome withrespect to cardiovascular, cancer or all-cause mortalitybetween the intervention or any of the controlgroups[20], and we consider the study group to bereasonably representative of the background popula-tion in the city. The present study deals only with theparticipant men in the intervention group with com-plete data and no prior infarction or diabetes (n=7130out of a total of 7495 participant men), aged 47 to 55(mean 51) years at baseline. A first screening examina-tion took place between January 1970 and March1973. Data on smoking habits, diabetes, and history ofmyocardial infarction were collected by a postal ques-tionnaire which was sent to all subjects along with aninvitation to the study. Screening examinations wereperformed in the afternoon. Weight and height weremeasured. Blood pressure was measured to the nearest2 mmHg after 5 min rest with the subject seated. Be-cause blood pressure was generally high in the after-noon a systolic reading of 140 or of diastolic of 90 wasincluded in the normotensive group. Serum cholesterolconcentration (from a sample taken after fasting forat least 2 h) was determined according to standardlaboratory procedures.

All subjects in the multifactor primary preventionstudy were followed until 31 December 1993 (mean 19·7years). The Swedish national register on deaths due tospecific causes from the years 1970 to 1993 was matchedagainst a computer file of the men in the study. In 1987,

there was a change from the 8th to the 9th revision of theInternational Classification of Diseases, but for thebroad groupings used in the present study this will havemade no difference. Coronary death was defined as ICDcodes 410-414. During the first 11·8 years of thefollow-up there were 329 first non-fatal myocardialinfarctions registered by the Goteborg MyocardialRegister in the study population[20]. As this register onlyrecords events in persons younger than 65 years of agethere were no data concerning non-fatal events duringthe latter part of the follow-up.

The MONICA study population and survey methodshave been described[8]. Random population samples ofmen and women aged 25 to 64 years were sent a postalquestionnaire, and on returning the questionnaire theywere invited to a screening examination in 1995. Partici-pation rates were 64% and 63% for men and women,respectively. All examinations were done in the morning.Blood pressure was measured in the sitting position,after 5 min rest, with a random zero mercury sphygma-nometer. Weight and height as well as waist circumfer-ence were measured with the subject in light indoorclothing, without shoes. All blood samples were takenafter an overnight fast. Serum cholesterol and triglycer-ides were determined according to WHO MONICAcriteria. LDL cholesterol was calculated according toFriedewald’s formula. Systolic and diastolic (Korotkoffphase V) pressure was always measured before veni-puncture according to the WHO MONICA standardafter at least 5 min rest with the subject in the sittingposition. Before the examination, all participants hadcompleted a postal questionnaire dealing with smokinghabits.

For the study of secular trends, data from the studyof men born in 1913, 1923, 1933 and 1943 were used.Starting in 1963 and with ten year intervals, fourpopulation samples of men aged 50 and living in thecity of Goteborg, Sweden, have been examined withrespect to cardiovascular risk factors[9]. In 1963 all menborn in 1913 on dates divisible by three were invited.Of the 973 invited men, 855 took part in the study(88%). For the 1973 study all men born in 1923 on the3rd, 15th and 27th day of each month were invited,providing a sample of 292, of which 226 (77%) partici-pated. For the 1983 and 1993 studies, a randomsample of half of all men in the city born in 1933 and1943 were invited; 776 (76%) and 798 (55%), respect-ively, took part[9]. All examinations were done in themorning after an overnight fast. Blood pressuremeasurements were done in the sitting position by aphysician (except in 1983 when measurements weredone by a nurse) using a standard cuff and a mercurymanometer. Only Korotkoff phase 4 was available in1963. In 1993 both phase 4 and phase 5 were regis-tered. The mean difference (2 mm) was deducted fromthe 1963 diastolic readings when creating categoricalblood pressure variables. Data on smoking habits werecollected by a postal questionnaire. Fasting serumcholesterol and triglyceride measurements were deter-mined according to standard laboratory procedures.

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138 A. Rosengren et al.

Statistical methods

We used the SAS statistical package (version 6.12). Inthe prospective study, proportional hazards analyseswere used to adjust for age. Four categories of risk werecreated: (1) optimal: total cholesterol <5 mmol . l�1,and blood pressure <140/90 without treatment, andnon-smoker; (2) Low risk: non-smoker and (total chol-esterol 5–6·5 mmol . l�1 and/or blood pressure 141-160/91-95 without treatment); (3) Moderate risk: smoker or(total cholesterol �6·5 mmol . l�1 and/or blood pres-sure >160/95 or treatment) (4) High risk: total choles-terol >6·5 mmol . l�1 and blood pressure >160/95 ortreatment, and smoker. Three dummy variables werecreated, with moderate risk as a reference, as threequarters of the population in the primary preventionstudy were in that category. In the MONICA studysimple correlation tests were used to assess relationshipsbetween age and continuous or graded variables. For theanalysis of secular trends, the respective cohorts wereassigned numbers from one to four and correlation testswere used to assess relationships between the cohortnumber and continuous variables. Mantel–Haenszeltests were used to assess the statistical significance of

Eur Heart J, Vol. 22, issue 2, January 2001

differences between the cohorts with respect to gradedvariables.

Results

In a first step we analysed the impact on coronary andtotal mortality of total serum cholesterol, blood pressureand smoking in 7130 men aged 47 to 55 (mean 51) yearsand followed for 20 years (Table 1). All relationshipswere in the expected direction and magnitude. A smallgroup of 117 men (2% of the population) were charac-terized by low levels of both blood pressure and serumcholesterol and were also non-smokers. In this groupone coronary death occurred over 2414 observationyears, corresponding to 0·4 deaths per 1000 years. Theoverall risk of coronary death over the 20-year follow-upwas 4·8 deaths per 1000 observation years. In compari-son with the majority of the population, who were eithersmokers and/or had total cholesterol of 6·5 mmol . l�1

or above, and/or blood pressure >160/95 but not allthree, the age-adjusted relative risk was 0·09, albeit withwide confidence intervals (0·01–0·64). The group ofmen with optimal risk factors also had low all-causemortality.

Table 1 Outcome according to serum cholesterol, smoking, and hypertension and combined risk factors in menexamined in 1970–72 and followed until 1993

Number of men(% of total)

Observationyears

CHD deaths(number))

Per 1000observation

years

All deaths(number)

Per 1000observation

years

Total cholesterol<5·0 mmol . l�1 701 (10) 13 729 53 3·9 212 15·45·0–6·49 mmol . l�1 3198 (45) 63 083 240 3·8 894 14·0�6·50 mmol . l�1 3231 (45) 63 166 384 6·1 1045 16·5

Blood pressure<140/90, no treatment 2168 (30) 43 846 119 2·7 507 11·6140-160/90-95, no treatment 1407 (20) 28 113 104 3·7 379 13·5Treatment, or SBP >160, or DBP <95 3555 (50) 68 799 454 6·6 1265 18·4

Smoking habits at baselineNon-smoker 3610 (51) 73 784 242 3·3 793 10·7Smoker 3520 (49) 66 794 435 6·5 1358 20·3

Risk factor status at baseline1

Optimal 117 (2) 2414 1 0·4 19 7·9Low risk 894 (13) 18 720 30 1·6 124 6·6Moderate risk 5310 (74) 104 958 497 4·7 1631 15·5High risk 809 (11) 14 666 149 10·2 377 25·7

Relative risk by risk factor statusat baseline

Age-adjustedRR of CHD

95%confidence interval

Age-adjustedRR of death

95%confidence interval

Optimal 0·09 (0·01–0·64) 0·51 (0·33–0·80)Low risk 0·34 (0·24–0·49) 0·42 (0·35–0·51)Moderate risk 1·00 — 1·00 —High risk 2·22 (1·85–2·66) 1·72 (1·54–1·92)

All relationships between events/deaths and risk factors P<0·001.1Optimal: total cholesterol <5 mmol . l�1, and blood pressure <140/90 without treatment, and non-smoker; Low risk: non-smoker and(total cholesterol 5–6·5 mmol . l�1 and/or blood pressure 141–160/91–95 without treatment); Moderate risk: smoker or (total cholesterol�6·5 mmol . l�1 and/or blood pressure >160/95 or treatment); High risk: total cholesterol >6·5 mmol . l�1 and blood pressure >160/95or treatment, and smoker.CHD=coronary heart disease; SBP/DBP=systolic/diastolic blood pressure.

Data from Goteborg 139

We also calculated the ten-year risk of a coronaryheart disease event over the first 12 years of the study,where we had data on non-fatal events (Table 2). Theten-year risk of a coronary heart disease event in thelow-risk group was 0·8%. In the group with the mostadverse risk factor profile (smoker, blood pressureabove 160/95 or treatment, serum cholesterol above6·5 mmol . l�1) the ten-year risk was 17·9%, and in thetotal study group the ten-year risk was 6·1%.

Data from the 1995 MONICA survey show compara-tively favourable risk factor levels in the youngest group,men and women aged 25 to 34 (Table 3), but asexpected, overall risk factor profiles deteriorated withage in both men and women. At ages 35 to 44, less thanhalf had serum cholesterol below 5 mmol . l�1. In thehighest age group 18% of the men and 16% of thewomen had serum cholesterol below 5 mmol . l�1, and39% and 46%, respectively, were normotensive. Themajority at all ages were non-smokers.

If very strict criteria were used to define optimalrisk factors (total cholesterol <5 mmol . l�1, LDL<3 mmol . l�1, HDL >1 mmol . l�1, triglyceride<2 mmol . l�1, waist <94 cm (women <80 cm), bloodpressure <140/90 mmHg without treatment, non-smoker, normal weight (body mass index <25) few, evenamong the youngest age group, were optimal, 27%among the men and 35% among the women (Table 4).Among men and women aged 55 to 64 this combinationwas almost non-existent. Applying less rigid criteria,based on total cholesterol, blood pressure, smoking andbody mass index only (total cholesterol <5 mmol . l�1,blood pressure <140/90 without treatment, non-smoker,normal weight (body mass index <25)) did not, however,yield very different results. With these less rigid criteria,34% and 37%, respectively, of the youngest men andwomen were optimal, and 3% and 4% of men andwomen aged 55 to 64.

In a further step, we defined a set of optimal riskfactors, based on serum cholesterol, systolic blood press-ure and smoking only, without the weight criterion, inaccordance with the risk charts[11]. Of the men and womenaged 25–34, 46% and 47%, respectively, had total choles-terol <5 mmol . l�1, blood pressure <140/90 withouttreatment, and were non-smokers. Corresponding figuresfor men and women aged 55 to 64 were 7% and 6%.

In a final analysis (Table 5) we investigated thedistribution of optimal risk factors over a period of 30years in four cohorts of men who were 50 years whenthey were examined in 1963, 1973, 1983 and 1993. Theproportion of men with serum cholesterol below5 mmol . l�1 increased from 9%–22%, and the pro-portion of men who were normotensive (below 140/90without treatment) increased from 45%–61%. In 1963less than half of the men, or 44%, were non-smokers,whereas in 1993, 69% did not smoke. Very few men, or2%, in 1963 had optimal levels of all three risk factors. In1993, the proportion had increased, but was still only11%. Rates of overweight and obesity increased over theperiod[9]. If normal body weight was added to thecriteria only 6%, or 45 men overall, were optimal.

Discussion

In the prospective part of the study, we found essentiallywhat we expected. An optimal risk factor profile carriesa very low risk of coronary death and myocardialinfarction. If this pattern were to prevail, this wouldmean pronounced changes in the panorama of disease.We also found, however, that even though the riskfactor profile today is generally better than 30 years ago,optimal levels are still rare, particularly in the middle-aged and older population. Also, obesity is increasing[9],with associated metabolic disturbances and diabetes.

Table 2 Outcome with respect to fatal and non-fatal events according to serum cholesterol, smoking, and hypertensionand combined risk factors in men examined in 1970–72 and followed until 1983

Number of men(% of total)

Observationyears

CHD events(fatal andnon-fatal)

(n)

Per 1000observation

years

All deaths(n)

Per 1000observation

years

Risk factor status at baselineOptimal 117 (2) 1283 1 0·8 6 4·6Low risk 894 (13) 9853 19 1·9 39 3·9Moderate risk 5310 (74) 57 243 316 5·5 480 8·2High risk 809 (11) 8101 145 17·9 139 16·1

Relative risk by risk factorstatus at baseline1

Age-adjustedRR of CHD

95 per centconfidence interval

Age-adjustedRR of death

95 per centconfidence interval

Optimal 0·14 (0·02–1·02) 0·55 (0·25–1·23)Low risk 0·37 (0·23–0·59) 0·50 (0·36–0·70)Moderate risk 1·00 — 1·00 —High risk 3·08 (2·56–3·75) 1·94 (1·60–2·34)

1See legend to Table 1.

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140 A. Rosengren et al.

Table 3 Risk factors by age and sex in men and women aged 25 to 64 in the Goteborg MONICA study

Age group 25–34 35–44 45–54 55–64

Men (n) (151) (184) (189) (217)Total cholesterol, mmol . l�1, mean (SD) 4·86 (0·89) 5·36 (1·08) 5·78 (1·11) 5·89 (1·08)% (n)

<5·0 mmol . l�1 59 (89) 38 (69) 25 (47) 18 (38)5·0–6·49 mmol . l�1 37 (56) 48 (88) 52 (99) 57 (124)�6·50 mmol . l�1 4 (6) 15 (27) 23 (43) 25 (55)

LDL cholesterol, mmol . l�1, mean (SD) 3·01 (0·83) 3·38 (0·98) 3·73 (1·03) 3·80 (0·99)% (n)

<3·0 mmol . l�1 56 (84) 39 (72) 29 (55) 18 (39)3·0–4·99 mmol . l�1 42 (64) 55 (101) 60 (114) 73 (158)�5·0 mmol . l�1 2 (3) 6 (11) 11 (20) 9 (20)

HDL cholesterol, mmol . l�1, mean (SD) 1·23 (0·27) 1·23 (0·31) 1·27 (0·37) 1·28 (0·38)% (n)�1·0 mmol . l�1 83 (125) 80 (147) 81 (153) 79 (171)

Serum triglyceride, mmol . l�1, mean (SD) 1·38 (0·66) 1·74 (1·16) 1·82 (1·25) 1·84 (1·23)% (n) �2·0 mmol . l�1 86 (130) 73 (134) 73 (138) 72 (157)

Body mass index, kg�m�2, mean (SD) 24·4 (2·9) 26·1 (4·1) 25·9 (3·8) 26·7 (3·9)% (n)

<25 62 (94) 38 (70) 46 (86) 35 (75)25–30 33 (50) 50 (92) 41 (78) 51 (110)>30 5 (7) 12 (22) 13 (25) 15 (32)

% (n) waist circumference <94 cm 81 (122) 60 (110) 60 (113) 43 (93)Blood pressure, mmHg, mean (SD)Systolic 122 (12) 128 (15) 134 (17) 144 (20)Diastolic 78 (9) 83 (10) 87 (11) 88 (11)% (n)

<140/90, no treatment 85 (129) 68 (126) 55 (103) 39 (84)140-160/90-95, no treatment 11 (17) 21 (38) 24 (45) 22 (47)Treatment, or SBP >160, or DBP >95 3 (5) 11 (20) 22 (41) 40 (86)

% (n) current non-smokers 81 (122) 73 (135) 67 (127) 66 (143)

Women (n) (181) (220) (242) (223)Total cholesterol, mmol . l�1, mean (SD) 4·70 (0·89) 5·09 (0·91) 5·61 (1·08) 6·05 (0·96)% (n)

<5·0 mmol . l�1 67 (122) 49 (107) 32 (77) 16 (35)5·0–6·49 mmol . l�1 30 (54) 45 (98) 50 (122) 52 (117)�6·50 mmol . l�1 3 (5) 7 (15) 18 (43) 32 (71)

LDL cholesterol, mmol . l�1, mean (SD) 2·66 (0·75) 3·03 (0·87) 3·40 (0·97) 3·77 (0·89)<3·0 mmol . l�1 72 (130) 54 (119) 38 (91) 22 (48)3·0–4·99 mmol . l�1 28 (50) 44 (96) 56 (135) 70 (157)�5·0 mmol . l�1 1 (1) 2 (5) 7 (16) 8 (18)

HDL cholesterol, mmol . l�1, mean (SD) 1·53 (0·34) 1·54 (0·38) 1·59 (0·41) 1·60 (0·40)% (n) �1·0 mmol . l�1 97 (175) 96 (211) 95 (230) 95 (211)

Serum triglyceride, mmol . l�1, mean (SD) 1·13 (0·47) 1·16 (0·50) 1·38 (0·75) 1·47 (0·75)% (n) �2·0 mmol . l�1 96 (173) 91 (201) 90 (217) 85 (189)

Body mass index, kg�m�2, mean (SD) 23·2 (3·4) 23·8 (3·5) 25·1 (4·2) 26·3 (4·5)% (n)

<25 77 (139) 68 (150) 56 (136) 47 (105)25–30 18 (33) 26 (58) 33 (79) 36 (81)>30 5 (9) 5 (12) 11 (27) 17 (37)

% (n) waist circumference <80 cm 77 (139) 65 (144) 51 (123) 41 (91)Blood pressure, mmHg, mean (SD)Systolic 116 (10) 120 (13) 131 (18) 142 (21)Diastolic 76 (8) 77 (9) 83 (10) 85 (9)% (n)

<140/190, no treatment 93 (168) 88 (193) 67 (163) 46 (102)140-160/90-95, no treatment 6 (11) 6 (13) 15 (37) 28 (63)

Treatment, or SBP >160, or DBP >95 1 (2) 6 (14) 17 (42) 26 (58)% (n) current non-smokers 75 (136) 67 (147) 74 (179) 78 (173)

All relationships between age and risk factors P<0·001, except smoking in women (P=0·22) and HDL cholesterol (P=0·02 in men and0·03 in women).

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Data from Goteborg 141

Risk prediction in the Primary Preventionstudy

Compared to the risk charts used in the Europeanrecommendations[11] the absolute risk in the men of theprimary prevention study appeared to be lower. The riskcharts were developed using Framingham data that maynot be wholly applicable to Swedish populations. How-ever, a 12-year follow-up study of middle-aged men andwomen from eastern Finland examined in the 1970sdemonstrated risks that were not dramatically different

from those found in the primary prevention study[21]. Arecent study compared the Framingham risk model forcoronary heart disease mortality rates with two nationalsamples from the U.S. population and found a fairlyaccurate rank ordering while the prediction of absoluterisk was less precise[22]. From a clinical point of view,prediction of absolute risk is essential, as treatmentdecisions will be based on the individual clinician’sconception of risk in an individual patient[23].

Limitations of the present study are that there wereonly single measurements of the relevant risk factors,and that risk factor status may have changed during

Table 4 Optimal risk factors by age and sex in men and women aged 25 to 64 in the Goteborg MONICA study.Figures are percentages (n)

Age group 25–34 35–44 45–54 55–64

Men (n) (151) (184) (189) (217)All risk factors optimal1 27 (41) 10 (18) 3 (5) 2 (4)Optimal including body mass index <25 34 (51) 11 (21) 5 (9) 3 (7)Optimal 46 (69) 23 (43) 10 (19) 7 (15)Low risk 30 (45) 34 (62) 29 (54) 24 (52)Moderate risk 25 (37) 42 (78) 60 (114) 67 (145)High risk 0 1 (1) 1 (2) 2 (5)

Women (n) (181) (220) (242) (223)All risk factors optimal1 35 (63) 19 (42) 12 (28) 3 (6)Optimal including body mass index <25 37 (67) 22 (49) 14 (34) 4 (9)Optimal 47 (85) 30 (67) 21 (50) 6 (14)Low risk 25 (46) 27 (60) 31 (75) 36 (80)Moderate risk 28 (50) 42 (92) 48 (115) 55 (123)High risk 0 0 (1) 1 (2) 3 (6)

1All risk factors optimal: total cholesterol <5 mmol . l�1, LDL <3 mmol . l�1, HDL>1, triglyceride <2 mmol . l�1, waist 94 cm (80 cmin women), pressure <140/90 without treatment, non-smoker, normal weight (body mass index <25), no diabetes.

Table 5 Distribution of risk factors 1963 to 1993 in 50-year old men in Goteborg

Men bornin 1913

Men bornin 1923

Men bornin 1933

Men bornin 1943

Men (number) (855) (225) (765) (794)Total cholesterol, mmol . l�1, mean (SD) 6·42 (1·12) 6·46 (1·34) 6·12 (1·12) 5·88 (1·04)% (n)<5·0 mmol . l�1 9 (81) 12 (26) 12 (130) 22 (177)5·0–6·49 mmol . l�1 45 (382) 46 (103) 48 (367) 49 (386)�6·50 mmol . l�1 46 (392) 43 (96) 35 (268) 29 (231)Blood pressure, mmHg, mean (SD)

Systolic 138·2 (20·9) 137·4 (22·1) 134·0 (16·9) 128·7 (17·1)Diastolic [90·6 (12·5)]1 89·9 (14·1) 86·2 (10·6) 84·4 (10·6)% (n)<140/90, no treatment 45 (386) 40 (90) 51 (388) 61 (482)140-160/90-95, no treatment 26 (223) 22 (50) 22 (168) 19 (150)Treatment, or SBP >160, or DBP >95 29 (246) 38 (85) 27 (209) 20 (162)

% (n) current non-smokers 44 (375) 47 (103) 63 (483) 69 (548)Risk factor status2

Optimal 2 (17) 3 (6) 7 (51) 11 (84)Low risk 30 (257) 28 (63) 28 (211) 33 (261)Moderate risk 65 (552) 67 (151) 62 (471) 54 (432)High risk 3 (29) 2 (5) 4 (32) 2 (17)

All trends P<0·001.Missing data in 1, 11 and 4 men, respectively, in the three youngest cohorts.1Korotkoff phase IV.2See legend to Table 1.

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142 A. Rosengren et al.

follow-up, which could have attenuated associations. Inparticular, there were changes in smoking status[20], butthe approximately twofold increase in risk is similar tothe relative risk of 1·7 found in the most recent coronaryprediction model from Framingham[24]. Risk factorlevels in the primary prevention study were generallyhigh. Blood pressure levels were high, probably due tothe fact that the screening sessions were conductedduring the afternoon. As a consequence, the group withoptimal risk factor levels identified was very small, 2% ofthe entire group. Nevertheless, in the cohorts born in1913 and 1923, where the men were examined in themorning, the proportion of men with optimal riskfactors was very similar, at about 2% to 3%. Measure-ments of several other relevant factors were not avail-able in this study, which was designed in the late 1960s,such as serum triglycerides, HDL cholesterol, waist tohip ratio, plasma fibrinogen, insulin or blood glucose.

Risk factors in the population

In general, risk factor levels in the general population inSweden are fairly high, from a global perspective.Among the MONICA populations, Goteborg rankedamong the middle with respect to serum cholesterol, andsmoking in men, but among the highest with respect tosmoking in women[12]. Means of body mass index forboth men and women were among the lowest among theMONICA populations. With respect to blood pressure,Goteborg ranked comparatively low, chiefly due to lowpressure, among the youngest study participants[25].

With the exception of the MONICA study, compara-bility with other studies is difficult, not only becausemethodology varies from study to study, but also be-cause of different ages, and presentation of age adjustedmeans or proportions. Both serum cholesterol and bloodpressure increased substantially with age. In theMONICA study, Goteborg had among the highestincreases with age in men[25]. But increasing bloodpressure with age may not be a natural phenomenon. Ina study of a Tanzanian, a Brazilian and an Italianpopulation, blood pressure was correlated with age onlyin the latter two[16]. In the African population, whoconsumed a low salt ‘fish and vegetable’ diet, bloodpressure did not increase with age.

We have been able to identify few studies that describethe prevalence of optimal risk factors in the population,but this, however, is an area that is difficult to reviewfully because of the wealth of information available. Oneanalysis, very similar in design to our study was done inthe population of the Chicago Heart Association Detec-tion Project in Industry[26]. Using cut-off levels whichwere only slightly different from those used in our study,5% of the men and 7% of the women were found to haveno risk factors, and a very low risk of coronary deathover 22 years of follow-up, 1·3 and 0·7 per 1000,respectively, in men and women. Another cross-sectional analysis of optimal risk factor status wascarried out in a southern Korean population in 1990 to

Eur Heart J, Vol. 22, issue 2, January 2001

1992[17]. Korea is a low risk country with respect tocoronary disease but age-adjusted ischaemic heart dis-ease mortality has increased dramatically since 1981according to national statistics. About 60% of the menand women in the sample had serum cholesterol below200 mg . dl�1 (5·2 mmol . l�1). The prevalence ofhypercholesterolaemia, defined as 240 mg . dl�1

(6·2 mmol . l�1) or more, increased sharply with age inwomen but not in men. With a cut-off of 240 mg . dl�1

for serum cholesterol but otherwise the same criteria fornormotension and smoking, more than four out of fiveKorean women aged 35–44, and 41% of those aged55–59, had optimal risk factor status with respect toblood pressure, serum cholesterol and smoking. Theestimate in Korean men was much lower, due to theirvery high rates of smoking.

Disturbingly, but concomitant with the high rates ofcoronary heart disease in Sweden, the oldest cohort inGoteborg, those 55–64 years old, comprised very fewsubjects with optimal risk factor status, even if onlyserum cholesterol, blood pressure and smoking habitwere used to define optimal risk factors. If ideal levels ofbody mass index were included to define optimal riskfactor status, this group dwindled to almost nothing, or3%–4%. In the youngest group aged 25 to 44, only aboutone third had optimal risk factor status. In the next agestratum, men and women aged 35–44, only 11% of themen and 22% of the women had ideal risk factor status.

Secular trends

With respect to serum cholesterol, smoking and hyper-tension decreasing trends were seen for all three duringthe period 1963–1993 in men[9]. Several studies havereported declines in population levels of serumcholesterol[27–32], usually against a background ofdecreasing incidence of coronary disease. In easternFinland the rate of death from coronary disease hasdecreased to less than half of its previous level[33] andabout half of the observed decrease in mortality ratecould be explained by a decrease in cholesterol level inthe population. As the atherosclerotic process starts at afairly young age, the contribution of a decrease in serumcholesterol levels to the decline in coronary mortalityrate may be even greater than that estimated frommeasurements of cholesterol in middle age[30]. The mostlikely explanation for the decrease in serum cholesterollevels in Sweden, as well as in other countries, is dietarychanges, such as the introduction of low-fat dairy prod-ucts and oil-based soft margarine. Decreasing levels ofhypertension have also been reported from a largenumber of MONICA populations[32,34].

In Goteborg, coronary heart disease incidence inmiddle-aged men has decreased 30%–40% since 1975[6],concomitant with similar decreases in risk factorstatus[10], and similar decreases have been reported withrespect to mortality on a national level[35]. However,official statistics show that the decrease in incidence of

Data from Goteborg 143

myocardial infarction in women and in men above 65years of age has been less pronounced than in men below65[5]. At the same time, also according to nationalstatistics, admissions for angina, without a diagnosis ofmyocardial infarction have increased. Possibly, the im-provement seen in risk factor status has led to a lateronset of the disease or to a milder form, or both. Withbetter survival and increased life expectancy, the preva-lence of the disease is likely to increase, demanding moreresources in the near future.

From a clinical point of view, the concept of riskfactors is useful and distinguishes between people athigh and at low risk so that the most intensive interven-tion may be used in those in greatest need of reduction inrisk. Patients with established coronary disease andhealthy individuals at high risk of developing coronaryheart disease should be targeted for intervention by themedical profession. However, as the majority of eventsoccur in persons at moderate risk this will influence ratesof coronary disease in the population only to a compara-tively small extent. In order to achieve important reduc-tions in coronary heart disease incidence and mortality,intervention aimed at shifts in the distribution of bloodlipids and blood pressure as well as to a reversal in thetrend in increasing obesity in the population and lesssmoking must be a health policy priority.

This study was supported by the Swedish Medical ResearchCouncil, the Bank of Sweden Tercentenary Fund, the SwedishHeart and Lung Foundation, the Swedish Labour MarketInsurance Company, and the Inga-Britt and Arne LundbergFoundation.

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