JACC Vol. 12. Xo. 5
November 19RR: 127; 8o
E PIDE MIOL OGIC STUDIE S
Risk Factors in Siblings of People Wit
DIANE M. BECKER, ScD, MPH,* LEWIS C. EECKER, MD, FACC,t
THOMAS A. PEARSON, MD, PHD.*$ DAN J. FINTEL, MD, FAX,? DAVID M. LEVINE MD,*
PETER 0. KWITEROVICI-I, MD4
Prior studies of the contribution of coronary disease risk
factors to familial aggregation of premature coronary dis-
ease may have underestimated risk factors by relying on
self-reported risk factor prevalence levels or, when risk
factors have been measured, by using cut points in excess of
the 9Otb percentile. To determine the actual prevalence of
hyperlipidenda, hypertension and diabetes, and the aware-
ness of these coronary risk factors in unaffected family
members, 150 apparently coronary disease-free sibling of
86 people who had documented coronary dise@e before 60
years uf age were studii. LUI subjects participated in a I
day screetig preceded by a self-administered risk factor
questhnmaire and a m
both the b&x patients
and sibtings exceeded 86%.
With the use of nationally established recommendations
for bbod pressure and lipids, which are based on coronary
dii risk curves, scmning revealed that 48% of broth-
ers and 41% of sisters were hypertensive, 45% of brothers
and 22% of sbters bad a lipid abnormality, 38% of siblings
interview. Participation of
were current cigarette smokers and 4,?‘% were d&&tic.
Two or more risk factors were present in 42% of bro&ers
and 25% of sisters. More than 75% of siblings had ooe or
more risk factors that woukl require iatervent&L
compared with a race-, gender- and age-matched referem
population from the Lipid Research Clinks Prevateace
Study, distributiows for b&d presses and for tetal &HI
low density lipoproteb~ cb&steral were Mgber for the
Gbliags in every gender SHI age group. !Sibli&gs were
of hypertensive siblii and 27% of si
abnormalities were aware of these risk factors.
PreGously u&tected risk factors were highly prevatent
in sibiiigs of pe@e witb premature comzary d&ease.
These data support cnrreH naGonal recommer&lat&msfor
comprehensive risk factor screen& io this fSs@ i&?&i.
able high risk fw group.
(J An Cdl Cardial 19&?;12:1273-80)
Coronary heart disease has long been shown to cluster
significantly within families. First degree relatives of pro-
bands who had coronary heart disease events before 60
years of age exhibit a risk of premature
is 2 to 12 times that of the general population (I-6). Consid-
erable controversy exists concerning the relative indepen-
coronary disease that
Fmm the Divisions of ??
Medicine; flhe Lipid Research Clinics. Department of Pediatrics; and Uhe
Deoartment of Euidcmioloav. The J ohns Hookins Medical Institutions, Bal-
tin&e. Maryland. This study was supported in part by Preventive CardioIagy
Academ;: Award No. KO7HLOI 13 and Grant No. RRllUOJ5 CLINFO
Computational assWnce) from the National Institutes of Health, Bethesda,
Maryland and a @nant
from the DuPont Corporation. North Bilkrica, Massa-
Manuscript received J anuary 8,1988; revised
1988, accepted J une 3, 1988.
A&&&r@& Diane M. Reeker, ScD. MPH, Preventive Cardiol-
ogy Promms, The J ohns Hopkins Hospital, 1830 East Monument Street.
lntemaI Medicine and tCardioloav. Department of
manuscript received May 5.
01988 by the Americnn College of Cardiology
dent contribution of unexplained genetic factors and known
coronary heart disease risk factors that aggregate within
families. Many investigators (7-11) contend that a positive
family history remains the most important independent
predictor for premature coronary heart disease, whereas a
few (12,131 suggest that the major portion of familjai-
clustered coronary heart disease can be attributed to in,‘ler-
ited and environmental risk factors. A recent review of
methodologic issues in family studies (14) nu!ed that one
problem in the majority of prior studies is the reliance on
self-reporting or reporting by other relatives of the presence
or absence of risk factors in family members of coronary
heart disease probands. Another common problem in prior
studies is the use of blood pressure and lipid cut points that
exclude values that have been shown fo be associated with
increased risk of coronary disease.
The existing studies, focusing predominantly on epidemi-
BECKGR El AL.
JACC Vol. 12. No. 5
Novcmbcr 1988: 1271-80
RISK FACTORS IN FP ‘LIES
ologic issues, may leave the clinical community confused
about the importance of screening for remediable risk factors
in families. The objectives of this study were I) to determine
the true prevalence of modifiable coronar)’ heart disease risk
factors including hypertension, hyperlipidcmia,
cigarette smoking using contemporary
determine the awareness of the presence of potentially
modifiabie risk factors in apparently healthy aduk siblings of
people with documented coronary heart disease. Further,
this study provides the first empirical estimates in the United
States population of the yield of multiple risk factor screen-
ing in unaffected siblings soon after a premature coronary
heart disease event in a young brother or sister.
guidelines, and 2) to
were eligible if they had a documented coronary disease
event before 60 years of age. The majority (93%) of partici-
pating index patients were identified between January 1983
and June 1986 during a coronary heart disease hospitaliza-
tion. An additional 7% were identified in a cardiac rehabili-
tation program after a recent coronary heart disease event.
All but two had angiographicdily
disease; these two patients had sllstained a documented
myocardial infarction. The mean age of index patients was
49 + 1 I years; 83% were male. Risk factor distributions were
not analyzed in index patients becalrse 6% had experienced
coronary disease events before the hospitalization.
patients were receiving anti-ischemic
tentially confound risk factor prevalences and awareness. Of
90 eligible index patients, g6 (95%) provided
Asymptomatic siblings. The 86 probands
asymptomatic biologic siblings 30 to 59 years ofage (mean 45
2 7.5); 51% were male and 99% were white. The majority
(78%) were high school graduates and 20% were colleie
All siblings c60 years of age without known coronary
heart disease, as determined by telephone interview
verification by the physician of record, were invited for a
cardiovascular history, physical examination and laboratory
evaluation. Of 172 eligible GbIings, I50 (87%) participated in
the screening evaluation, which was performed an average
of 2 months (range 2 weeks to 4 monrhs) after hospital
discharge of the index patient. The majority (19) of the
remaining 22 siblings cited geographic distance from the
screening site as the reason for refusal.
Screening protocol. A self-administered
was mailed to siblings before the screening appointment to
elicit self-reporting of the presence or absence of hyperten-
sion, hyperlipidemia, diabetes, cigaret!e smoking and cur-
ren: and past medications and illnesses. These items were
again elicited in a personal interview by a research nurse just
heart disease patients. Index patients
medications that po
before the screening examination (see Appendix).
ling was considered aware of the presence of a risk factor if
he or she indicated “possibly yes” or “yes” to the elicited
risk factor information either on the questionnaire or during
Physical examination and laboratory evaluation.
lings received a history and physical examination
cardiologist according to a standardized
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RliK FACTORS IN F4MILIES
J oint National
(A, brothers; B. sisters). Numal
Hgand systolic blood pres=ure c I40 mm Hg; high normal = diastolic
blood pressure 85 to 89 mm Hg; mild hypertension
pressure 90 lo I04 mm Hg; moderate hypertension
pressure I05 to I I4 mm Hg; severe hypenension
pressure 2 I I5 mm Hg: borderline
140 to 159 mm Hg; isolated systolic hypertension
on High Blood Pressure recommendation
= diastolic blood pressure < 85 mm
in siblings according to the
= diastolic blood
= diastolic blood
= diastolic blood
isalated systolic hypertension =
= 2160 mm Hg.
screening, with 73% of hyperiipidemic
hyperiipidemic sisters unaware of lipid elevations. (Table 4).
There were no time trends in the prevalence of hyperiipide-
mia or in awareness based on self-reporting by year, Preva-
brothers and 75% of
IACC Vol. 12. No. 5
iences and awareness were aimosi identical across ail years
of the study.
Cigarette smoking (Table 5). The overall prevalence of
current smoking was 38%. The prevalence of smoking in
each age group was similar for brothers and sisters. Al-
though brothers appeared to smoke more cigarettes/day than
did sisters, this difference was not statistically significant.
Again, the prevaiences were approximately
year, with slightly fewer brothers (36%) smoking in 1986.
Diabetes or KG abnormali&.
given by three sisters and two brothers.
brother and one sister had a fasting glucose level ~130 mg/
di. which was verified with abnormal
results. The overall prevalence of diabetes was 4.7%; two
siblings (2%) were unaware. Ail self-reported
No sibling had evidence of a prior myocardiai infarction
or of myocardiai ischemia on rest ECG. Left ventncuiar
hypertrophy by voltage criteria was present in three siblings
who were also hypertensive.
Multiple risk factors (Fig. 3). In analyzing the prevalence
of combinations of risk factors, diabetes was not included
because ail diabetic subjects also had one or more of the
three major risk factors. Of the total, 117 (78%) had one or
more risk factors. The overall prevalence of risk factors was
higher in brothers (83%), than in sisters (73%). Only 17% of
brothers were free of risk factors, whereas 27% of sisters
were without risk factors.
equal by study
A history of diabetes was
BI~IMI pressure. The cut points of 140 mm Hg for systolic
and 90 mm Hg for diastolic blmd pressure were selected to
define hypertension not onty because these levels corre-
spond with the Joint National
Pressure classification but because they represent levels in
the coronary heart disease risk curves where the slope of
risk increases sharply (23). The few prior family studies
(5.25,26) that measured blood pressure in siblings reported a
Committee on High Blood
Table 3. Plasma Lipid Distribution of IS0 Siblings of 86 Premature Coronary Heart Disease Probands
Brothers (age. yr)
Sisters (age, yr)
30 IO 39
(n = 24)
40 IO 49
(n = 32)
50 IO 59
(II = 21)
(n = 77)
30 IO 39
(n = 16)
40 to 49
In = 291
50 to 59
(II = 28)
(II = 73)
Mean lotal cholesterol (mgldl)
Mean LDL choltsterol (mddl!
T’hc Lipid Research Clinics Prevaleitce Study raw-. gender- and age-specific reference population percentiles. LDL = low denshy lipoprotein=, (20).
226 r 58
223 2 38
230 + 4s
209 ? 51
215 k 42 226 k 49 207 c 41 229 f 36
147 i: 56
148 f 40
IQ c 43
130 f 53
124 I 34
139 + 35
131 2 41
JACC Vol. 12, No. 5
CORDNARY RISK FACTORS
Table 4. Awareness
Heart Disease Probands
in 150 Siblings of 86
Hyperfiprdem,.a cm Scre-nmg”
Self-report of hyperiipidemia
triglycerides 2250 mg/dl or receiving lipid-lowering drug treatment.
= low density lipoprotein cholesterol ~I60 mddl. or
lower prevalence of hypertension, approximately
likely because blood pressure cut points were set exces-
sively high, above the 90th percentile or >I60 to 170 mm He
systdlic and >I@0 to 110 m-m Hn diastolic level. When both
the Lipid Research Clinics Prevatence Study reference pop-
ulation percentile distributions
guidelines of the Joint National Committee on High Blood
Pressure are used. it is clear that brotbnrs and sisters of
patients with documented coronary arterv disease before aee
60 have a high prevalence of b&d
and risk-gssociated i984
pressure levels that aYe
Figure 2. The prevalence of lipid abnormalities in siblings accord-
ing to the National Cholesterol Education
Gr::‘zlines and the Triglyceride Consensus
(A, brothers: B, sisters). High risk low density lipoprotein choles-
terol = ~160 mg/dl; low high densiiy lipoprotein cholesterol = 535
mgldl; high triglycerides = 5250 mgMl.
Program Adult Treatment
associated with increased coronary heart &sea% risk and
may require medical evaluation and treatment. Brothers had
a greater prevalence of hypertension
dias!olic blood pressure. Only
and of “high normal”
31% of brothers were classi-
fied as having
were already receiving antihypertensive
only 26% “true normal” subjects among brothers.
The majority of brothers and almost hal of the sisters
were unaware of blood pressure elevations.
problem in analyzing the awareness data in our study is the
proliferation of rewch
studies and national initiatives
targeting blood pressure education for both the general
population and physicians between 1983 and the present.
There is no evidence from our study to sugest that hyper-
tension detection in the sibling group had markedly im-
1983 and 1986. it is unlikely that the
prevalence of hypertension
in siblings was decreasing over
of the study or that it is significantly lower at this
time. However, new initiatives of the National High Blood
Pressure Education Program may result in improved detec-
tion of high blood pressure in the coming years.
Plasma lipids. The LDL cholesterol cut point of 160 mg/
dl was used to define hvpercholesterolemia
the National Cholesterol Education Program’s Adult Treat-
ment Guidelines. Coronary heart disease risk curves dem-
onstrate a sharp increase in the slope of risk at total
cholesterol levels of 240 mg/dl, which correspond approxi-
mately to an LDL cholesterol
!21,23,24). Although triglyceride elevations have not been
independently associated with coronary
studies, levels of 2250 mgldl classified as elevated in this
study represent the approximate
sibling age groups in this study. Airhough only a small
percentage of brothers (6.5%) and sisters (1.4%) were con-
sidered to have abnormal lipids solely on the basis of
triglyceride levels, including those siblings as hyperlipidemic
may be justified because d
trigiyceride elevation in the sibling sample represents famil-
ial combined hyperlipoproteinemia,
a macke~~ly increased coronary heart disease risk (27). “High
risk” L:IL cholesterol was the most frequent abnormality
cb+ KQ * II both men and women. As with hypertension,
abnormai lipids were more common in brothers than in
with 54% and 78%. respectively. exhibiting desirable
lipId patterns on screening.
twareness of elevated lipid levels was low in both
brci5ers and sisters with 73% unaware. The National Che-
lesterol Education Program physician initiatives tPegan in
1987 with publication of the Adult Treatmen!
Improved practice patterns and increased public education
efforts may improve awareness of elevated lipid levels in the
future. Data from this study suggest. however, that sign&
cant awareness changes did not occur between 1983 and
on the average
hours apart. of these. 5%
on the basis of
cut point of 160 mg/dl
disease In most
!Mth percentile for the
which is associated with
BECKER ET At.
JACC Vol. 12. No. 5
RISK FACTORS IN FAMILIES
Table 5. Smoking Prevalence end Number of Cigarettes in 150 Siblings of 86 Premature Coronary Heart Disease Prabands
Brothers (age. yr)
Sisters (age. yr)
30 to 39
(n = 241
40 IO 49
(n = 32)
so to 59
tn = 21)
tn = 77)
30 to 39
In = WI)
40 IO 49
tn = 29)
50 IO 59
(n = 28)
(n = 73)
Current smokers (5%)
cigarettes per day
42 44 29 39 38 41 32 37
17 r 29 18 + 27 21 238 19 + 31 8 f I2 I6 ? 25 12 f 24 13 f 22
1986. This finding is further substantiated by data from the
National Institutes of Health Cholesterol Awareness Sur-
veys of both the gergeral public and physicians in 1983 and
1986, which dernol;c!mred only modest changes in the
number of people who had blood cholesterol levels checked
and no increase between 1983 and 1986 in the number of
people who were told that cholesterol levels were elevated
Cigarette smoking. The prevalence of current smoking in
both brothers and sisters was higher than the 27 to 30% of
the general population who smoked cigarettes during the
sibling screening period, 1983 to I986 (30). Prior studies
(26,311 in high risk families have reported a wide range of
smoking prevalence levels in sisters (I5 to 53%) and consist-
Figure 3. The
prevalence of major risk factors
= low density lipoprotein
250 mg/dl or on a lipid-
= bl ood
pressure 2 140190 or on anti-
= current regular cigarette
in siblings (A,
B 160 mg/dl. or triglycerides
ent levels of approximately 45% in brothers. Most of these
studies have not been done in the American population.
Although in our study the prevalence rates were similar in
brothers and sisters, brothers appeared to be heavier smok-
ers. Given that there is evidence of a multiplicative
ties between cigarette smoking and family history of’ early
coronary disease (32,33), it is likely that smoking prevalence
alone does not reflect the true importance of smoking as a
risk factor in the sibling population. The validity of self-
reporting was not examined, but prior studies (35) suggest
that the bias is in favor of underreporting,
a perception of social undesirability.
The reported diabetes
agrees with prior studies in families with coronary
disease, which have shown a prevalence rate of I to 5%
(26,31). Although this was a low frequency risk factor, a
small number of siblings with probable diabetes were un-
aware of their condition.
MuMpIe risk factors. The majority of brothers and sisters
had at least one of the major risk factors for coronary heart
disease. It is possible that other more recently reported
familial risk factors, such as abnormal piatelet activation (32)
and apolipoprotein abnormalities
those siblings who appear “normal”
generally agreed that premature coronary heart disease is of
multifactorial origin, it is not surprising that such diverse risk
factor patterns exist in high risk families.
clearly have a higher prevalence of all risk factors; 42%
exhibited two or more of the three major risk factors.
Conclusions. This study demonstrates that the age-, gen-
der- and race-adjusted distributions
plasma lipids are considerably higher in clinically unaffected
siblings of peopie Gth premature coronary
than in a general reference population.
siblings have one or more risk factors as assessed by
contemporary nationally established guidelines for determin-
ing risk levels of blood pressure and plasma lipids; further,
mer;y were uMware of the presence of potentially modifiable
risk factors. Because high risk families such as these account
for >50% of coronary heart disease before 55 years of age
i36.37). intensive efforts should be made to identify and alter
modifiable risk factors. This study provides empirical sup-
port for recent recommendation
Education Program (21) that physicians provide comprehen-
possibly related to
prevalence of 4.7%
(35), may be prevalent in
on screening. As it is
of blood pressure and
The majority of
of the National Cholesterol
J ACC Vol. 12. No. 5
sive risk factor screening to people with a family history of
premature coronary disease.
Items Used to Elicit Self-Report of the
Presence of Risk Factors
1. Have you ever had any of the foilowing levels checked:
a. your blood pressure?
b. your blood cholesterol?
c. your blood triglycerides?
d. your btood sugar?
RESPONSES: YES. NO, POSSIBLY YES, NOT SURE
For each item, if “YES”
were asked to give the level if known.
“NORMAL” or “HIGH,”
source of information.
or “POSSIBLY YES,” responiients
indicate if the ievel was
indicate the approximate date and the
you ever, on any occasion in your life. had any of the
a. high blood pressure?
b. high blood cholesterol?
c. high blood triglycerides?
d. diabetes or a high blood sugar?
RESPONSES: YES, NO, POSSlBLY YES, NOT SURE
For each item, if “YES’ or “POSSIBLY
was asked to name the approximate
information, level if known and specific treatment.
YES,” the respondent
source of date, duration,
you ever taken any medicine for any of the foilowing
a. high blood pressure’!
b. high blood cholesterol?
c. high blood triglycerides?
d. diabetes or a high blood sugar?
YES, NO, POSSIBLY YES, NOT SURE
For each item, if “YES”
were asked IO give the name of the drug if known,
drug if hnown, the duration
or “POSSIBLY YES,” respondents
I!K type of
of use and the medical care source.
“NOT SORE” responses were probed and respondents
fered the opportunity to elucidate
the risk factor may have been present, even if transiently.
any potential occasion on which
10 Item I that categorized
item 3 that indicated
treatment for the specific risk factors.
= “YES” or “POSSIBLY YES” TV item 2 or a response
the number as “HIGH
a “YES” or “POSSIBLY
,” or a response on
YES” to drug
I. Rose G. Familial patterns in Ixhemic heart disease. Br J Prev Sue Med
2. Slack J , Evans KA. The increased rirk of death from ischemic hedr!
discabe in first degree relatives of I!1 men acid 96 wmcn \vith irchemic
heart disease. J Med &net 19sh:3:?3%S7
6. Rirsancn AM. FamrhaIoccurrence afc0ron-q
.I! diagnouls. Am J Cardiol lvl%.44:6&6.
8. Nor:? ‘J . !.nflvRcr RH. Spangler RD. Noct AH. Kimberling WI. Generic
~p~denrologic PW+IY of ezy-ooser
~rehemx heart disease. CirculaliL%
9. Snowden CB. McNzmara PM Garrixm RJ. Fei&tb
Epstein Ft!. Predicting sor?nary heart &i:ebxe in shlinp: a mt’lriv~;mte
dxe$$mect. Am J Epidemiol I%2:!15:?IF??.
hi. Kannel WB.
111 ten Kate LP. Boatman H. Da&r 5P. Mocat~ky AG FamdrJ qge@;rrmn
of coronary heart d1sea.z and it\ re;alicr! lo krmwr: genettc rirk factors.
Am J Cardlol IW?$&94>53.
l I. Shea S. Ottman R. Gabrieli C, Srega ?,. Nichoh A. Family hlrrq
mdependent ri?k factor for coronary &III
,%zxe J Am Co11 C+rdiol
12. R~:xmen AM. Nikkill
hmdler of men wrth fatal and non-fatal coronary hean diseaw. Zr Heail
EA. Aggrcp!ilm of coronary risk iactors in
13. Gold~lem J L. Hazzard WR. Schn,.; HG. Bierman EL. Motul&y
Lipid level? in 500 rurvlvors rrf myocardial miarcliun. J Clin inwd
14. Perkms KA Family history of coronary heart disease: ir it dn indepn-
dent risk fx:or? Am J Epidcmiol 19&;!24:182-93.
15. Central Patient Registry and Coordinating Center for the Lipid Rerearch
Climcx Reference Manual for the Lipid Research Clinics Prevalence
Sludy. Vol. I and 2. Chapel Hill: University of North Carolina. 1974.
16. Repon of The J oint National Committee on Detection. Evatuation and
Treatmen of High Blood Pressure. Arch lnlem Med lY84;144:!U45-57.
17. Rose G. Ellackbum H. Cardiovascular Survey Metho&.
Orgmlration Monograpn Series No 56 i%.
18. Manual of Laboratory Opetalioes. Lipid Rerearch Clinic% Progam: ‘J ot.
I: Lipid and Lipoprotein Analysis. Belhetda. Maryland: Natiowal Insti-
tutes of He&h. NIH Publication 75-628. 1974.
19 Friedewald WT. Levy RI. Frcdickwn DS. Estimation of the concentra-
tmn of low-denshy lipoprobzin cholesterol in plasma without use of the
prepanrivc uhrdcemrifuge. Clin Clem 197?;!8:499-502.
20. The Lloid Research Clinics Powlation Sludies Data BoJ k: Vol. I: The
Preval&ce Study. Bethesda, #arylanJ :
NIH Publication No. 80-1527, 1980.
National Indllutes of He&h,
?I. Experl Panel. Nalional Cholesterol Educabon Program. Expert panel MI
detection. evalualion and treatment of high blood cholesterol in adults.
Arch Intern Med 19811;11:3f&9.
22. Conrensus Conference:
1984;?Sl: t 19f+200.
J J . Hulley SE. Browner WS. Kuller ’ H. Wenworth
choleqterol. blood pressure and mortality: rmplic~lions from a cohort of
361.662 mep. Lance1 19&X:933-6.
Trealmenl of hypertriglyceridemia
14. Kannel WB. McGee D.
the Fmmmgham Study.
Gordon T. A general cardiovascular
Am J Cardiol 19%x38:4&51.
25. Gudmund-son S.“hoFgtitsson G. ThorsteinssonT. Sigfusson N. Sigurds-
yen G Ri& factor screr~.ing among51 firs1 degree relatives of paIrems with
myocardial infarclian. Dan Med Bull lY~?~l0:25%62.
1280 Download full-text
BECKER ET AL.
JACC Vol. 12. No. 5
November 198li:12734l RISK FACTORS IN FAMILIES
26. Hamsten A. de Faire U. Risk factors for coronary artery disease in families
of young men with myocardial infarction. Am J Cardiol 1987;59:14-9.
27. Goldstein J L, Schrott HG, Hazzard WR, Bierman EL, Molukcy AG.
Hyperlipidemia in coronary heart disease !i. Genetic analysis of lipid
levels in 176 families and delineation of a new inherited disorder.
combined hyperlipidemia. J Clin Invest 1973;52:1544-68.
2%. Shucker B, Wittes J T. Cutler JA. el al. Change in physician
on cholesterol and heart disease. J AMA 1987:258:3521-6.
29. Shucker B. Bailey K.
cholesterol and heart
Heimbach J T, et al. Change in public perspective on
disease, J AMA 1987;258:3327-35.
the United States 1986. 30. Centers for Disease Control. Cigarette smoking in
31. Rissanen AM. Familial occurrence of coronary
clinical manifestation. Acta Med Stand 1985;218:355-63.
heart disease according to
32. Fuster V. Cheseboro JH, Frye RL. Elveback LR. Platelet survival and
the development of coronary artery disease in the young adult: effects of
cigar&e smoking. strong family history and medical therapy. Circulation
33. Hopkins PN. Williams RR, Hun1 SC. Magnified risks from cigarette
smoking for coronary prone families in Utah. West J Med 1984:141:196-
Behav 34. Brockway BS. Chemical validation of self-reported
35. Freedman DS, Srinivasan SR, Shear CL, Franklin FA, Webber LS,
Berenson GS. The relationship of apolipoproteins A-l and B in children to
parental myocardial infarction. N Engl J Med 1986;315:721-6.
36. Williams RR. Understanding genetic and environmental risk factors in
susceptible persons. West J Med 1984:141:799-6&
37. Williams RR, Hasstedt SJ. Wilson DE, et al. Evidenct :!x: xi:
familial hypercholestcrolemia can avoid early coronary death: an anarysis
of 77 gclle carriers in four Utah pedigrees. J AMA 1986:255:2l%24.