Background A family history of premature coronary heart diseasehas long been thought to be a risk factor for coronary heartdisease. Using data from 26 years of follow-up of 21,004 Swedishtwins born between 1886 and 1925, we investigated this issuefurther by assessing the risk of death from coronary heart diseasein pairs of monozygotic and dizygotic twins.
Methods The study population consisted of 3298 monozygotic and5964 dizygotic male twins and 4012 monozygotic and 7730 dizygoticfemale twins. The age at which one twin died of coronary heartdisease was used as the primary independent variable to predictthe risk of death from coronary heart disease in the other twin.Information about other risk factors was obtained from questionnairesadministered in 1961 and 1963. Actuarial life-table analysiswas used to estimate the cumulative probability of death fromcoronary heart disease. Relative-hazard estimates were obtainedfrom a multivariate survival analysis.
Results Among the men, the relative hazard of death from coronaryheart disease when one's twin died of coronary heart diseasebefore the age of 55 years, as compared with the hazard whenone's twin did not die before 55, was 8.1 (95 percent confidenceinterval, 2.7 to 24.5) for monozygotic twins and 3.8 (1.4 to10.5) for dizygotic twins. Among the women, when one's twindied of coronary heart disease before the age of 65 years, therelative hazard was 15.0 (95 percent confidence interval, 7.1to 31.9) for monozygotic twins and 2.6 (1.0 to 7.1) for dizygotictwins. Among both the men and the women, whether monozygoticor dizygotic twins, the magnitude of the relative hazard decreasedas the age at which one's twin died of coronary heart diseaseincreased. The ratio of the relative-hazard estimate for themonozygotic twins to the estimate for the dizygotic twins approached1 with increasing age. These relative hazards were little influencedby other risk factors for coronary heart disease.
Conclusions Our findings suggest that at younger ages, deathfrom coronary heart disease is influenced by genetic factorsin both women and men. The results also imply that the geneticeffect decreases at older ages. .
During the past 20 years, the role of family history in early-onsetcoronary heart disease in men has been well established1,2,3,4,5,6,7,8,9,10,11,12,13,14.However, only a few prospective studies have investigated theinfluence of familial factors on this disease in women15,16.Furthermore, the effect of a family history of coronary heartdisease in older subjects, either men or women, has been examinedin only one recent study17.
The extent to which the familial occurrence of coronary heartdisease is due to genetic mechanisms can be assessed in twinor adoption studies. Early studies from the Swedish and Danishtwin registries18,19 found a genetic influence on the risk ofdeath from coronary heart disease in men by comparing concordancebetween monozygotic and dizygotic twins. A recent adoption study20showed a genetic influence of mortality due to all cardiovascularand cerebrovascular diseases. None of these studies, however,specifically investigated the extent to which the genetic riskof coronary heart disease varied according to age at death.This is important because in several other chronic diseases,an early age at onset and an early age at death have been suggestedto indicate genetic susceptibility21,22.
Using the Swedish Twin Registry, we performed a large prospectivestudy examining the influence of genetic factors on mortalitydue to coronary heart disease at different ages, among bothwomen and men.
Methods
Swedish Twin Registry
The cohort drawn from the Swedish Twin Registry for this studycontained 10,944 pairs of twins (21,888 twins) of the same sexwho were born between 1886 and 1925; both members of each pairwere alive in 196123. The details of the compilation of thetwin registry are presented elsewhere24.
The present study was based on a follow-up of mortality during26 years, from 1961 through 1987. The information in the twinregistry is matched annually with information about causes ofdeath obtained from death certificates and coded according tothe standards of the International Classification of Diseases(seventh, eighth, and ninth editions). Medical certificationis carried out by the attending physician or coroner, with useof both clinical records and autopsy reports25. In this study,the listing of the underlying cause of death was used to identifydeaths from coronary heart disease.
Study Population
The study population totaled 21,004 twins (10,502 pairs) afterthe exclusion of 439 pairs whose zygosity could not be determinedand 3 other pairs for whom information about the cause of deathwas missing. The final sample included 3298 monozygotic and5964 dizygotic male twins and 4012 monozygotic and 7730 dizygoticfemale twins.
Study Variables
Age at Death from Coronary Heart Disease
Since the twin registry is population-based and the study samplewas identified (in 1961) before any twin had died of coronaryheart disease, both twins of each pair were included as subjectsin this study. The age at which a subject died of coronary heartdisease was the primary variable used to predict the risk ofdeath from coronary heart disease in that person's twin. Ageat death was determined from the year of birth and year of deathlisted in the national population and death registries.
We divided the men who died of coronary heart disease into fiveage groups and the women into four groups, as shown in Table 1.All women who died of coronary heart disease before the ageof 66 were included in one age group because of the small numberof these subjects. In the survival analyses, the variable ofdeath from coronary heart disease in one's twin was categorizedaccording to age interval. The reference category for each variablewas defined as the group of subjects whose twins did not dieof coronary heart disease in that age interval.
Table 1. Mortality Due to Coronary Heart Disease among Twins in the Study Sample of the Swedish Twin Registry.
Other Risk Factors
Questionnaires had been sent to all twins in the study cohortin 1961 and 1963, to obtain information about their health statusand health-related habits. All risk factors assessed in thesequestionnaires and known to be associated with coronary heartdisease were chosen as covariates. These included cigarettesmoking, body-mass index, diabetes, hypertension, level of education,and marital status.
In the 1961 questionnaire, subjects were asked whether theysmoked then, had formerly smoked, or had ever smoked at all.Those who had never smoked served as the reference group insurvival analyses. Body-mass index (calculated by dividing theweight in kilograms by the square of the height in meters) wasdetermined from the weight and height listed on the 1963 questionnaire.This variable was categorized as less than 24, 24.0 to 27.9,and 28 or more.
The subjects' status with regard to hypertension and diabeteswas assessed from their own replies; these variables were regardedas dichotomous. Educational status was treated dichotomously,with a grade-school education serving as the reference category.With respect to marital status, subjects were categorized asunmarried, married, or divorced. Unmarried subjects served asthe reference group.
A variable for birth cohort was created for discrete-time survivalanalysis, with four birth periods: 1886 through 1895, 1896 through1905, 1906 through 1915, and 1916 through 1925. Finally, zygositywas included as a dichotomous variable, with monozygosity servingas the base line.
Statistical Analysis
Correction for Left Censoring
All analyses were corrected for the left truncation due to staggeringof the age at which each pair of twins was entered in the registry26.Furthermore, correcting for left truncation also adjusted forthe effect of left censoring inherent in the registry, whichwas due to the study requirement that both twins be alive in1961.
Life-Table Analysis
Life tables of mortality due to coronary heart disease wereused to construct survival curves in order to examine the riskof death from coronary heart disease among the subjects whosetwins had died of this disorder. Survival probabilities werecalculated separately according to the age interval in whichone's twin died of coronary heart disease.
The actuarial approach was used to estimate the cumulative probabilityof death from coronary heart disease, with correction for leftcensoring. This adjustment required staggered entry of the subjectsinto the life table according to their ages27.
Discrete-Time Survival Analysis
We performed a discrete-time survival analysis to obtain relative-hazardestimates for the effect of death from coronary heart diseasein one's twin. We chose this approach because it corrected forthe left censoring inherent in the registry, in addition toallowing for the effects of other covariates. Discrete-timesurvival analysis uses logistic regression to model hazard estimateswhen survival time is measured in discrete intervals28. Withthis method, the logarithm of the odds of death from coronaryheart disease during an interval, which is conditional on survivaluntil the beginning of that interval, is the dependent variable.The registry data were modified in a manner outlined by Hosmerand Lemeshow28 in order to use the model for discrete-time survival.The period of follow-up was 26 years; the earliest age at whicha subject was considered to be at risk was 36 years, and thelatest was 102 years. Survival analysis was performed for eachyear of risk for each subject.
Separate variables for the age at which one's twin died of coronaryheart disease were created for the monozygotic twins and thedizygotic twins. The relative-hazard estimates for these variablesin the monozygotic twins were then directly compared with theestimates in the dizygotic twins.
The covariates described above were also included in the discrete-timesurvival analyses. Since some information was lacking for eachrisk factor recorded in the registry, all multivariate analysesincluded only subjects for whom information about risk factorswas complete (7715 men and 7748 women). The analyses evaluatingthe effect of the age of death from coronary heart disease inone's twin were also performed in the reduced sample, withoutthe covariates; the results were very similar to those of theanalysis of the full sample.
To correct for the fact that deaths from coronary heart diseasein each pair of twins did not represent independent observations,the variances of the beta coefficients for the mortality-relatedvariables were doubled in all analyses. This approximated anapproach designed by Bonney29 for dependent observations inlogistic regression.
Results
Concordance
Among the 1649 pairs of monozygotic male twins, 114 were concordantand 335 were discordant for death from coronary heart disease,as compared with 164 concordant and 705 discordant pairs amongthe 2982 pairs of dizygotic male twins. Among the 2006 pairsof monozygotic female twins, 66 were concordant and 273 werediscordant for death from coronary heart disease, as comparedwith 99 concordant and 611 discordant pairs among the 3865 pairsof dizygotic female twins. There was thus a greater proportionof concordant pairs among the monozygotic twins than among thedizygotic twins in both men and women, suggesting a geneticcomponent to death from coronary heart disease in the SwedishTwin Registry.
Life-Table Analysis
The age-specific risks derived from the life-table analysispresented in Figure 1 demonstrate the influence of the age ofone's twin at death from coronary heart disease on the probabilityof death from this disease. Both male and female twins diedof coronary heart disease at earlier ages than did the wholepopulation of the twin registry if their respective twins haddied of this disease before the age of 76 years. Furthermore,the monozygotic twins died earlier of coronary heart diseasethan the dizygotic twins if their respective twins died in theearly age intervals. The fact that the influence of having amonozygotic twin who died of coronary heart disease was greaterthan that of having a dizygotic twin suggests that there maybe a genetic component to the risk that a twin may die of coronaryheart disease before the age of 76. As the age at death fromcoronary heart disease in one's twin increased, the differencebetween the survival probability of the monozygotic twins andthat of the dizygotic twins became smaller. This finding appliedto both men and women (Figure 1). Also, the probability of deathfrom coronary heart disease moved closer to that in the generaltwin population.
Figure 1. Age-Specific Probabilities of Death from Coronary Heart Disease in Subjects Whose Twins Died of the Disease.
The age categories of 36 to 55 years and 56 to 65 years were merged into the category of 36 to 65 years for women because of the small number of deaths.
If one's twin died after the age of 85 years, the probabilityof death from coronary heart disease was less than that in thegeneral twin population, most likely because this general populationincluded subjects whose twins had died at earlier ages.
Discrete-Time Survival Analysis
The results of the discrete-time survival analyses are presentedin Table 2 for both men and women. The relative hazard of deathfrom coronary heart disease for monozygotic male twins whoserespective twins had died of coronary heart disease when 36to 65 years old was approximately three times greater than thehazard for dizygotic twins. As the age at which one's twin diedof coronary heart disease increased, the relative hazards forboth the monozygotic and dizygotic twins decreased in magnitude.These results parallel the findings reflected by the survivalcurves.
Table 2. Relative Hazard of Death from Coronary Heart Disease in Subjects According to the Age of Their Twins at Death from Coronary Heart Disease.
The relative hazards for monozygotic and dizygotic male twinswhose respective twins had died of coronary heart disease when56 to 75 years old were significantly different from each other.The finding that there was no significant difference betweenthe estimates for monozygotic and dizygotic twins whose respectivetwins had died when 36 to 55 years old was most probably dueto the small number of deaths from coronary heart disease inthis age group, since the difference in the relative hazardin this group was the largest of such differences among allthe age groups.
Among women, the relative hazard for twins whose respectivetwins had died of coronary heart disease before the age of 66was 14.9 for monozygotic twins and 2.2 for dizygotic twins.As in the men, the hazards in both zygosity groups decreasedas the age at which the twin had died of heart disease increased.Among women whose twins had died of coronary heart disease at36 to 75 years of age, the relative hazard for monozygotic twinsdiffered significantly from the relative hazard for dizygotictwins.
We next examined the extent to which other standard risk factorsmeasured in the registry might confound the effect of earlydeath from coronary heart disease in one's twin (Table 3). Allcovariates shown by univariate analysis to be significant predictorsof death from coronary heart disease were included in a multivariateanalysis along with variables related to the age at death. Forthe men these covariates were hypertension, diabetes, smoking,birth cohort, body-mass index, marital status, and education,and for women they were hypertension, diabetes, smoking, birthcohort, and body-mass index. All these covariates were alsoshown to be significant predictors in the multivariate analysis(Table 3).
Table 3. Relative Hazard of Death from Coronary Heart Disease in Subjects According to the Age of Their Twins at Death from Coronary Heart Disease, with Control for Risk Factors.
Among the men, the relative hazard when one's twin died at 36to 55 years of age was reduced (from 13.4 to 8.1) only in themonozygotic twins, after other risk factors were included. Todetermine which variable most influenced this reduction in therelative hazard, each risk factor was individually includedin a separate analysis with the variable for the age at whichone's twin died of coronary heart disease. The reduction inrisk was most strongly influenced by control for the effectof the birth cohort, which probably reflected temporal trendsin mortality due to coronary heart disease among all subjectsin the Swedish Twin Registry. To a smaller degree, controllingfor diabetes also reduced the effect of having a twin who haddied of coronary heart disease before the age of 56 years.
Among the dizygotic male twins and all female twins, there waslittle reduction in the relative hazard according to the ageat which the first twin died of coronary heart disease whenthis variable was analyzed together with other covariates. Therefore,the effect of one's twin's death from coronary heart diseasewas largely uninfluenced by the other covariates.
Discussion
We found that among both women and men, death from coronaryheart disease at an early age in one's twin was a strong predictorof the risk of death from this disorder. This risk was greaterin monozygotic twins than in dizygotic twins and was largelyindependent of other personal risk factors for coronary heartdisease.
Both the Nurses' Health Study16 and the Framingham OffspringStudy17 found that a family history of coronary heart diseasewas an independent risk factor for coronary disease in women.The Danish Twin Concordance Study18 found that concordance forcoronary heart disease was higher among monozygotic than amongdizygotic twins, but the investigators did not stratify thesubjects according to age or examine the effects of other riskfactors. In our study, we have demonstrated that in both menand women a family history of early death from coronary heartdisease is associated with an increased risk of death from thedisease. Our data also suggest that this increased risk is,at least in part, genetic in nature.
We found that the difference in relative hazard between themonozygotic and dizygotic twins remained statistically significantexcept among subjects whose twins died of coronary heart diseaseafter the age of 75. Our findings also indicate that geneticsusceptibility to death from coronary heart disease becomesless pronounced in older age. The Danish Adoption Register study,20however, revealed a genetic component only in subjects whoseparents died of cardiovascular causes before the age of 50.The results of our study do not necessarily contradict thoseof the adoption study, since the larger size of our study populationand the long period of follow-up allowed us to detect theseassociations at later ages (up to age 75) more readily.
There were several risk factors for coronary heart disease thatwere not measured in this study. In interpreting our results,we cannot ignore the possibility that monozygotic twins sharedmore environmental risk factors, such as dietary variables andphysical inactivity, than the dizygotic twins. However, it isknown that at least one primary variable for coronary heartdisease, the total cholesterol level, is influenced in largepart by genetic mechanisms, as shown in a recent study of Swedishtwins reared apart30.
Since all the risk factors in the present study were determinedfrom the subjects' responses, some cases of hypertension anddiabetes mellitus may have been missed. Furthermore, informationabout risk factors was obtained only at the beginning of thefollow-up period; therefore, both misclassification and changesin status for risk factors could have led to underestimationof their effect. Nevertheless, the risk factors of smoking,hypertension, diabetes, unmarried status, limited education,and obesity were still predictive of death from coronary heartdisease.
One of the primary concerns in research into mortality is whethercauses of death have been reliably identified. A study of deathcertificates entered in the Swedish Twin Registry from 1970to 1975 found that they had a positive predictive value of 92percent for death from coronary heart disease31. The authorsof that study concluded that categorization of coronary heartdisease as a cause of death on death certificates was reliable.Other studies of death certificates in Sweden have also shownthe positive predictive value for such mortality to be morethan 90 percent32,33.
The high preponderance of monozygotic as compared with dizygotictwins among the pairs of twins who both died of coronary heartdisease at an early age suggests that multiple genetic factorsinteract to produce susceptibility to death from coronary disease34.The interaction may be due to the effects of several monogenicmechanisms, genes of small effect, or a combination of both.Since coronary heart disease has long been thought to have complexmultifactorial causes, it is not surprising that our resultssupport this view.
Many of the genetic mechanisms that predispose people to coronaryheart disease remain unknown. Most of the research leading toan understanding of the genetic factors underlying coronaryheart disease, which has been recently reviewed,35,36,37,38has focused on the genetic variability of quantitative traitsassociated with the disease. The candidate genes and defectsthat underlie abnormal levels of lipoprotein gene products foundin the plasma have also been carefully studied and reviewedin recent years39,40. It is unlikely, however, that abnormalitiesin lipoproteins account for all genetic risk of coronary heartdisease. It has been suggested35,36,38,40 that the geneticsof coronary heart disease would be better understood if studiesincluded factors directly related to the pathogenesis of atheroscleroticplaques, such as the reactivity of the blood-vessel wall toinjury, the role of scavenger cells, and the influence of theblood-clotting system. Also, specific polymorphisms in the geneencoding the angiotensin-converting enzyme may be involved41.
Our study suggests that it is important to identify both menand women whose first-degree relatives have died of coronaryheart disease at any age, particularly when young, so that theirmodifiable risk factors for coronary disease can be addressed.Further research is clearly needed to determine the molecularmechanisms that underlie genetic susceptibility to coronaryheart disease and how these mechanisms may vary with age.
Supported in part by the MacArthur Research Network on SuccessfulAging through a grant from the John D. and Catherine T. MacArthurFoundation, by a training grant (2-T32-MH-14235) from the NationalInstitute of Mental Health, by a grant (HG-00348) from the NationalInstitutes of Health, by a grant (09533) from the Medical ResearchCouncil of Sweden, by the Swedish Heart and Lung Foundation,and by King Gustav V and Queen Victoria's Foundation.
We are indebted to Drs. Nancy Pedersen and Larry Gall for theirvaluable input and to the Steering Committee of the SwedishTwin Registry for permitting us access to the registry.
Source Information
From the Departments of Epidemiology and Public Health (M.E.M., N.R., L.F.B.) and Genetics (N.R.), Yale University School of Medicine, New Haven, Conn.; and the Department of Environmental Hygiene, Karolinska Institute (B.F.), and the Division of Cardiovascular Medicine, Department of Internal Medicine, Karolinska Hospital, and Division of Epidemiology, Institute of Environmental Medicine, Karolinska Institute (U.F.), Stockholm, Sweden. Presented in part at the American Heart Association Cardiovascular Epidemiology Meetings, Memphis, Tenn., March 18-19, 1992.
Address reprint requests to Dr. Marenberg at the Department of Epidemiology and Public Health, Yale University School of Medicine, 60 College St., New Haven, CT 06510.
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