(Circulation. 1995;91:365-371.)
© 1995 American Heart Association, Inc.
Articles |
The Relation of Parental Cardiovascular Disease to Risk Factors in Children and Young Adults
The Bogalusa Heart Study
From the Tulane Center for Cardiovascular Health, Tulane School of Public Health and Tropical Medicine, New Orleans, La.
Correspondence to Gerald S. Berenson, MD, Tulane Center for Cardiovascular Health, 1501 Canal St, 14th Floor, New Orleans, LA 70112-2824.
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Abstract |
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Background Although cardiovascular risk factors relate to family history of cardiovascular disease, it is not clear how the relation changes from children to young adults.
Methods and Results As part of a community study for cardiovascular health, parental history of diseases was obtained from 8276 offspring 5 to 31 years old, 36% black and 64% white. Between 5- to 10-year-old children and 25- to 31-year-old young adults, prevalence of parental heart attack increased from 5% to 25%. More prevalent in blacks than in whites, parental stroke increased from 2% to 9% in whites versus 3% to 19% in blacks; parental diabetes rose from 7% to 19% in whites versus 9% to 33% in blacks; and parental hypertension increased from 26% to 59% in whites versus 40% to 72% in blacks. Offspring with parental heart attack history were significantly overweight after 10 years of age and showed elevated levels of total cholesterol, VLDL cholesterol, LDL cholesterol, insulin, and glucose after 17 years of age, irrespective of weight. Offspring of diabetic parents were significantly overweight, irrespective of age. They showed significant increases in levels of insulin, glucose, triglycerides, total cholesterol, VLDL cholesterol, and LDL cholesterol after age 24 years, independent of weight. Offspring of hypertensive parents displayed overweight regardless of age, higher levels of blood pressure after age 10 years, and elevations of triglycerides and VLDL cholesterol after age 24 years irrespective of weight. Analyzed by race and sex in young adults, parental heart attack related strongly to LDL cholesterol in the white offspring, especially white males, and to insulin in the black offspring. Parental diabetes showed a stronger association with overweight and glucose in black females. Also noted was the relation between parental hypertension and overweight in black females.
Conclusions Parental history is an important surrogate measure for cardiovascular risk in the offspring. However, parental history information alone is not sufficient to designate younger children for selective screening for high cholesterol, because of the young age of parents.
Key Words: cardiovascular diseases • risk factors
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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The adverse association of cardiovascular risk factors in both children and adults with parental history of disease is well recognized.1 2 Familial aggregation of cardiovascular diseases (myocardial infarction, stroke, diabetes, and hypertension) is well documented.3 4 5 6 7 8 9 10 11 Therefore, cardiovascular screening programs have incorporated parental history of diseases as an important indicator for risk.12 13 14 However, it is not clear whether these associations remain the same during childhood and young adulthood and how they vary with age, race, and sex.15 16 17 Our previous studies on the pediatric population in Bogalusa showed a higher prevalence of parental myocardial infarction in children with dyslipoproteinemia.18 Other studies showed similar findings.19 20 21 However, in both black and white children, no significant differences were found in mean levels of lipids and lipoprotein fractions in children with and without parental myocardial infarction.10 22
The present study examines the prevalence of parental history of heart attack, stroke, hypertension, and diabetes mellitus on an epidemiological scale. Within a biracial population of offspring (black and white), it investigates association between parental disease and adverse levels of risk factor variables at different growth periods ranging from childhood to young adulthood.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Parental History and Study Population
The Bogalusa Heart Study is a cross-sectional and longitudinal epidemiological study to determine the early natural history of atherosclerosis using the semirural, biracial community of Bogalusa, La. Between 1973 and 1991, six cross-sectional surveys have been completed; all included school-aged children, and four included post–high school young adults. More than 10 000 different individuals have participated in the study. Starting from the second cross-sectional survey in the school year 1976-1977, parental history of disease was incorporated into the study. Immediately before the date of screening, parental health history of cardiovascular disease was obtained from the child's parent or guardian, along with parental permission for the examination. The questionnaire asked whether either or both parents had a history of "heart attack," "sugar diabetes," "high blood pressure," or "stroke." During each of the subsequent cross-sectional surveys of school-age children, parental history was obtained from each parent through self-reporting (Table 1
). In the two most recent cross-sectional
surveys, post–high school young adults provided their parental history
through questionnaires. For subjects participating in multiple surveys,
data from the latest survey were presented in the present
study.
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No attempt was made to validate the parental history information. In the 1987-1988 cross-sectional survey for the 5- to 17-year-olds, the participants were also asked whether their father and mother were true (biological) parents. It is estimated from a sample of 2910 offspring in this survey, 97% (98% mother, 95% father) of the parents were blood-related. This rate may apply to the total study population because of the nature of the community study.
Table 2
lists the race, sex, and age distribution of the
subjects (n=8276) with parental history information. The race and sex
distribution is close to that of the Bogalusa population. Between the
subjects with and without parental history information, no significant
difference was found in levels of the risk factor variables studied
(data not shown). Therefore, subjects included in the present study
represented essentially the total population.
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General Screening
All examinations followed essentially the
same protocols, which
have been described previously.23 All observations were
collected by trained personnel, with replicate recording procedures and
randomization schemes. Subjects were instructed to fast 12 hours before
the screening, and compliance was determined by an interview on the
morning of the examination. Blood was drawn by antecubital venipuncture
to obtain serum and plasma. In analyses involving serum/plasma
variables, only fasting subjects (about 85% of the total population)
were included.
Height was measured to ±0.1 cm, and weight was measured to ±0.1 kg. As a measure of overweight, the ponderal index [weight (kg)/height (m)3] rather than Quetelet index [weight (kg)/height (m)2] was used because of its smaller correlation with height.24 Subscapular skinfolds were measured to ±1 mm. Replicate blood pressure levels were measured on the right arm of subjects in a relaxed, sitting position. Blood pressures were recorded as the first, fourth, and fifth Korotkoff phases. The blood pressure level reported was the mean of six replicate readings taken by two randomly assigned nurses. For ease of comparison between children and young adults, only the fourth phase was used as diastolic blood pressure.
Laboratory Analyses
From 1976 through 1986, serum total
cholesterol and
triglycerides were measured by use of chemical procedures on a
Technicon Auto Analyzer II (Technicon Instrument Corp) according to the
protocol developed by the Lipid Research Clinics
Program.25 From 1987 through 1991, these variables were
determined by enzymatic procedures26 27 on an Abbott
VP
instrument (Abbott Laboratories). Both chemical and enzymatic
procedures met the performance requirements of the Lipid
Standardization Program sponsored by the Centers for Disease Control
and Prevention (CDC), Atlanta, Ga. The laboratory has been monitored by
the CDC's surveillance program. Serum VLDL, LDL, and HDL cholesterols
were analyzed by a combination of heparin-calcium precipitation and
agar-agarose gel electrophoresis procedures.28
Plasma immunoreactive insulin levels were measured by a commercial radioimmunoassay kit (Phadebas, Pharmacia Diagnostics). From 1981 through 1986, plasma glucose was measured with a Beckman glucose analyzer by a glucose oxidase method.29 From 1987 through 1991, plasma glucose was determined as part of a multiple chemistry profile.
Statistical Analyses
The Statistical Analysis System was used
for all
analyses.30 Because it was rare to observe both parents to
have the same disease (<1%), except for hypertension (8%), for ease
of comparison, parental history of disease was defined as positive if
one or both parents had the disease. The prevalence of parental history
of diseases was given for each survey year and each race and age group.
The differences between blacks and whites and across survey years were
compared by a 
2 test. Through an ANCOVA adjusting
for age, race, and sex, selected risk factor levels were compared
between offspring with the presence or absence of parental disease.
Some study variables, such as insulin and ponderal index, were
logarithmically transformed to improve their normality. Adjustment for
obesity was also used when associations were determined between
parental history of diseases and triglycerides, total cholesterol,
lipoprotein cholesterol, blood pressure, insulin, and glucose.
Examinations were also given within each race and sex group when
observed findings differed between race and sex subpopulations, ie,
significant interaction existed between race, sex, and parental
history.
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Results |
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Prevalence of Parental History of Disease
For each survey year and each race and age group, the prevalence of parental diseases is given in Figs 1 through 4
.
Hypertension was the most common disease, followed by diabetes and
heart attack. Except for heart attack, parental disease was more common
in blacks than in whites, with 100% more occurrences of parental
stroke, 50% more of diabetes, and 20% more of hypertension. With
offspring aging, prevalence of parental diseases progressively
increased, as would be expected. There was no significant difference
between the survey years except within the 5- to 10-year-old black
children, in whom a trend of increasing (P<.01) prevalence
of parental heart attack, diabetes, or hypertension was observed from
1976 through 1991.
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Parental History and Offspring Risk Factor Variables
In
Tables 3 through
6,
age-stratified means and SEMs of selected risk factor variables were
given for offspring with presence or absence of parental history of
heart attack, stroke, diabetes mellitus, and hypertension,
respectively. Offspring with parental heart attack became significantly
more overweight starting from puberty. The significant increase in
levels of total cholesterol, VLDL cholesterol, and LDL cholesterol was
not observed until 18 years of age. Except for LDL cholesterol at ages
18 to 24 years, these increases remained significant, after adjustment
for ponderal index and skinfolds, in addition to age, race, and sex.
Also in these offspring with parental heart attack, the highest
increase in levels of insulin was observed for the age group 25 to 31
years and remained significant after correction for ponderal index and
skinfolds. Elevated glucose levels were shown for the age group 18 to
24, which were significant with or without adjustment for ponderal
index and skinfolds. Such consistent associations were not found
between risk factor levels and parental history of stroke.
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Offspring
who had a parental history of diabetes were significantly
more obese, irrespective of age, whether measured by ponderal index or
subscapular skinfolds. The magnitude of the increase was greater for
offspring 
18 years old. With respect to triglycerides, total
cholesterol, LDL cholesterol, VLDL cholesterol, and glucose, adverse
levels were significantly associated with parental diabetes after age
24 years, with or without correction for ponderal index and skinfolds.
Also, within the 5- to 10-year-old group, the association between
increased insulin and parental diabetes remained significant after
correction for ponderal index and skinfolds. In contrast, other
associated significant elevations of risk factor variables became
nonsignificant after adjustment for ponderal index and skinfolds.
Irrespective of age, offspring of hypertensive parents were more overweight and had higher blood pressure levels, as expected. They also had significantly higher levels of triglycerides or VLDL cholesterol within the age group 25 to 31 years and higher levels of insulin and glucose within the age group 18 to 24 years. These observations remained significant after correction for ponderal index and skinfolds in addition to age, race, and sex.
Race and Sex Differences
Effects of parental history of
diseases on offspring risk factor
variables may differ between race and sex groups. Within the offspring
18 to 31 years old, for whom parental history has shown more apparent
effect on risk factor variables, race and sex effects were examined by
ANOVA. They were indicated as significant interactions between race,
sex, and parental history of diseases. As shown in Fig 5, with
parental heart attack, increases in LDL
cholesterol levels were marked in the white offspring, especially white
males; increases in insulin levels were more pronounced in the black
offspring, especially black females. Ponderal index and glucose levels
increased most in black females with parental diabetes. Overweight, as
measured by ponderal index and skinfolds (data not shown), was also
pronounced in black females with hypertensive parents. As a comparison,
in the offspring 5 to 17 years old, similar interaction
(P<.05) existed only between race, sex, and parental
diabetes (Fig 6).
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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The present study examined the parental history of cardiovascular disease obtained as children matured into young adults. Parental history was used as a surrogate measure of potential and future cardiovascular disease of the offspring. Data show that with offspring aging, parental disease becomes more common and its prediction of adverse risk factor levels in offspring more apparent.
The prevalence of positive parental history in the offspring as reported will be higher than that in the actual population of parents. This is because each of the two parents may contribute to the positive parental history for a given offspring. Assuming that there were no occasions when both parents had the same disease and that there were no single-parent families, then the prevalence of parental history of disease would be twofold that of the actual prevalence of disease in the population. Despite a downward national trend for observed cardiovascular disease,31 32 33 in the present study, except in the 5- to 10-year-old black offspring, for whom parental diseases of heart attack and diabetes showed an increased trend, no drastic changes were found in the occurrence of parental diseases over the past two decades. As is known, the incidence of hypertension in the adult population is shown to be the most common disease, followed by diabetes and heart attack. With respect to race, whites are more likely to have heart attack and blacks are more likely to have stroke, diabetes, or hypertension. These observations are consistent with general experience with the adult population in the United States. Other epidemiological studies show similar results when offspring ages are matched.2
Offspring with a positive history for parental cardiovascular disease already show adverse risk factor levels starting in childhood. Certain factors become more obvious at a later developmental stage. The present study demonstrated the adverse effect in risk factor variables associated with parental history of disease, especially after the pubertal development stage. As shown previously in the Bogalusa children and adolescents1 10 as well as in other studies,9 11 there is an association between blood pressure levels in children and family history. The importance of this relation is highlighted by the positive association between blood pressure levels in children and changes in left ventricle size and function as detected by echocardiography34 35 36 and a relation between cardiac anatomy and function with familial history of hypertension.37 38
Interestingly, certain risk factor levels in children were found to change adversely and selectively with parental diseases. Examples cited from the present study show adverse levels of blood pressure and lipid/lipoprotein associated with parental myocardial infarction and adverse levels of lipid/lipoprotein, obesity, and insulin associated with parental diabetes mellitus. The present study also shows that these adverse effects become more apparent at older ages when risk increases for offspring along with a greater number of occurrences of parental disease.
These effects, however, are underestimated because of the inaccuracy associated with self-reporting.10 Educational and socioeconomic status of the parents could also have an influence. The reliability of our questionnaire could be estimated by use of answers from multiple cross-sectional surveys; disconcordance was identified if a negative parental history was found to be positive in a previous cross-sectional survey. A 3-year interval is long enough for an individual to answer a questionnaire independently of that from a preceding examination. The disconcordance rate thus estimated should be close to the true reporting error rate. From survey to survey, the error rate (false-positive) varied from 20% to 30% for heart attack, 26% to 54% for stroke, 19% to 36% for diabetes, and 18% to 24% for hypertension. The parental history of stroke was shown to have the lowest reliability from survey to survey, indicating that the public perception of a stroke is relatively less adequate. Coupled with the relatively fewer occurrences, this may explain, in part, the difficulty in relating parental stroke to cardiovascular risk factor levels in offspring. This difficulty may also be due to the different risk factor origins of strokes, such as hypertensive stroke, ischemic large vessel disease stroke, cerebral vascular hemorrhage, and lacunar strokes. Thus, the predictive nature of parental history for the risk factor profile of offspring should be viewed with the above limitations in mind.
An appreciation of the present observation will help understand the expected occurrence of disease, how family history during examination of young individuals needs to be updated, and how cardiovascular risk factors may be influenced. To identify children with elevated cholesterol levels, the present National Cholesterol Education Panel advocates a selective cholesterol testing approach that relies heavily on parental history of disease.12 For young children, this may not be sufficient because parents may be too young to have clinical manifestations of the disease. The prevalence increases as children age, as might be expected. Studies of longitudinal cohorts with clinically verified parental history of disease should allow a clear examination of the progress of associated risk change from childhood into adulthood. A more accurate quantification of parental disease can therefore be obtained as a predictor of cardiovascular risk for offspring relative to other predictors, such as behavior and early risk factor profile. Yet, a positive parental history even as obtained in a large epidemiological study can serve as a marker for increased risk in both children and young adults. Such information, usually obtained at a clinical level, will help identify individuals at higher risk and encourage a more intensive effort for prevention.
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Acknowledgments |
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This research was supported by grant HL-38844 from the National Heart, Lung, and Blood Institute of the US Public Health Service. The Bogalusa Heart Study represents the collaborative efforts of many people, whose cooperation is gratefully acknowledged. We especially thank the Bogalusa staff, Bettye Seal, and the children and young adults of Bogalusa, without whom this study would not have been possible.
Received June 2, 1994; accepted August 19, 1994.
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References |
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|
TopAbstractIntroductionMethods Results Discussion References |
|---|
1. Blonde CV, Webber LS, Foster TA, Berenson GS. Parental history and cardiovascular disease risk factor variables in children. Prev Med. 1981;10:25-37. [Medline] [Order article via Infotrieve]
2.
Burke GL, Savage PJ, Sprafka JM, Selby JV, Jacobs DR, Perkins
LL, Roseman JM, Hughes GH, Fabsitz RR. Relation of risk factor levels
in young adulthood to parental history of disease: the CARDIA Study.
Circulation. 1991;84:1176-1187.
3. Rose G. The radiological patterns in ischaemic heart disease. Br J Prev Soc Med. 1964;18:75-80. [Medline] [Order article via Infotrieve]
4. Rosenman RH, Brand RJ, Jenkins CD, Friedman M, Straus R, Wurm M. Coronary heart disease in the Western Collaborative Study. JAMA. 1974;233:872-877.
5.
Rissanen AM, Nikkila EA. Coronary artery disease and its risk
factors in families of young men with angina pectoris and in controls.
Br Heart J. 1977;39:875-883.
6. Laskarzewski P, Morrison JA, Horvitz R, Khoury P, Kelly K, Mellies M, Glueck CJ. The relationship of parental history of myocardial infarction, hypertension, diabetes and stroke to coronary heart disease risk factors in their adult progeny. J Epidemiol. 1981;113:290-306.
7.
Khaw K, Barrett-Connor E. Family history of heart attack:
modifiable risk factor? Circulation. 1982;74:239-244.
8.
Beaty TH, Neel JV, Fajans SS. Identifying risk factors for
diabetes in first degree relatives of non-insulin dependent diabetic
patients. Am J Epidemiol. 1982;115:380-397.
9. Munger RG, Prineas RJ, Gomez-Marin O. Persistent elevation of blood pressure among children with a family history of hypertension: the Minneapolis Children's Blood Pressure Study. J Hypertens. 1988;6:647-653. [Medline] [Order article via Infotrieve]
10.
Shear CL, Webber LS, Freedman DS, Srinivasan SR, Berenson GS.
The relationship between parental history of vascular disease and
cardiovascular disease risk factors in children: the Bogalusa Heart
Study. Am J Epidemiol. 1985;122:762-771.
11.
Clarke WR, Schrott HG, Burns TL, Sing CF, Lauser RM.
Aggregation of blood pressure in the families of children with labile
high systolic blood pressure: the Muscatine Study. Am J
Epidemiol. 1986;123:67-80.
12. National Cholesterol Education Program. Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Bethesda, Md: US Department of Health and Human Services, Public Health Service, National Institutes of Health, National Heart, Lung, and Blood Institute, January 1989. NIH publication 89-2925.
13. Report of the Expert Panel on Blood Cholesterol Levels in Children and Adolescents. Pediatrics. 1992;89(suppl):529-594.
14.
National High Blood Pressure Education Program Joint National
Committee. The 1984 report of the Joint National Committee on
detection, evaluation, and treatment of high blood pressure. Arch
Intern Med. 1984;144:1045-1057.
15. Slack J, Evans KA. The increased risk of death from ischaemic heart disease in first degree relatives of 121 men and 96 women with ischaemic heart disease. J Med Genet. 1966;3:239-257.
16. Rissanen AM. Familial occurrence of coronary heart disease: effect of age of diagnosis. Am J Cardiol. 1979;44:60-66.[Medline] [Order article via Infotrieve]
17.
Nora JJ, Lortscher RH, Spangler RD, Nora AH, Kimberling WJ.
Genetic-epidemiologic study of early-onset ischemic heart disease.
Circulation. 1980;61:503-508.
18. Dennison BA, Kikuchi DA, Srinivasan SR, Webber LS, Berenson GS. Parental history of cardiovascular disease as an indication of screening for lipoprotein abnormalities in children. J Pediatr. 1989;115:186-194. [Medline] [Order article via Infotrieve]
19.
Glueck CJ, Fallat RW, Tsang R, Bunch CR. Hyperlipidemia in
progeny of parents with myocardial infarction before age 50. Am J
Dis Child. 1974;127:70-75.
20.
Schrott HG, Clarke WR, Wiebe DA, Connor WE, Lauer RM.
Increased coronary mortality in relations of hypercholesterolemic
school children: the Muscatine Study. Circulation. 1979;59:320-326.
21.
Moll PP, Sing CF, Wiedman WH, Gordon H, Ellefson RD, Hodgson
PA, Kottke BA. Total cholesterol and lipoproteins in school children:
predictions of coronary heart disease in adult relatives.
Circulation. 1983;67:127-134.
22. Freedman DS, Srinivasan SR, Shear CL, Franklin FA, Webber LS, Berenson GS. The relation of apolipoproteins A-I and B in children to parental myocardial infarction. N Engl J Med. 1986;315:721-726. [Abstract]
23. Berenson GS, McMahan CA, Voors AW, Webber LS, Srinivasan SR, Frank GC, Foster TA, Blonde CV. Cardiovascular Risk Factors in Children: The Early Natural History of Atherosclerosis and Essential Hypertension. New York, NY: Oxford University Press; 1980:1-450.
24.
Voors AW, Webber LS, Frerichs RR, Berenson GS. Body height and
body mass as determinants of basal blood pressure in children: the
Bogalusa Heart Study. Am J Epidemiol. 1977;106:101-108.
25. Lipid Research Clinics Program. Manual of Laboratory Operations, Vol 1: Lipid and Lipoprotein Analysis. Washington, DC: National Institutes of Health; 1974. DHEW publication No. (NIH) 75-628.
26. Allain CC, Poon LS, Chan CSG, Richmond W, Fu PC. Enzymatic determination of total serum cholesterol. Clin Chem. 1974;20:470-475. [Abstract]
27. Bucolo G, David H. Quantitative determination of serum triglycerides by the use of enzymes. Clin Chem. 1973;19:476-482. [Abstract]
28. Srinivasan SR, Berenson GS. Serum lipoproteins in children and methods for study. In: Lewis LA, ed. CRC Handbook of Electrophoresis, Vol III: Lipoprotein Methodology and Human Studies. Boca Raton, Fla: CRC Press; 1983:185-204.
29. Beckman Instruments Inc. Beckman Glucose Analyzer Operation Manual. Fullerton, Calif: Beckman Instruments Inc; 1976.
30. SAS Institute Inc. SAS/STAT® User's Guide, Version 6. 4th ed. Cary, NC: SAS Institute Inc; 1989.
31.
McGovern PG, Burke GL, Sprafka JM, Xue S, Folsom AR, Blackburn
H. Trends in mortality, morbidity, and risk factor levels for stroke
from 1960 through 1990: the Minnesota Heart Survey. JAMA. 1992;268:753-759.
32.
Cooper R, Sempos C, Hsieh SC, Kovar MG. Slowdown in the
decline of stroke mortality in the United States, 1978-1986.
Stroke. 1990;21:1274-1279.
33. Tracy RE. A modified cohort method for secular trend analysis: heart disease mortality in the USA 1914-1963 and follow-up to 1983. Med Hypotheses. 1991;34:262-271. [Medline] [Order article via Infotrieve]
34.
Burke GL, Culpepper WS, Webber LS, Chiang RA, Arcilla RA,
Berenson GS. Blood pressure and echocardiographic measures in children:
the Bogalusa Heart Study. Circulation. 1987;75:106-114.
35.
Schieken RM, Clarke WR, Lauer RM. Left ventricular hypertrophy
in children with blood pressures in the upper quintile of the
distribution: the Muscatine Study. Hypertension. 1981;3:669-675.
36. Johnson GL, Kotchen JM, McKean HE, Cottril CM, Kotchen TA. Blood pressure related echocardiographic changes in adolescents and young adults. Am Heart J. 1983;105:113-118. [Medline] [Order article via Infotrieve]
37.
Adams TD, Yanowitz FG, Fisher AG, Ridges JD, Nelson AG, Hagan
AD, Williams RR, Hunt SC. Heritability of cardiac size: an
echocardiographic and electrocardiographic study of monozygotic and
dizygotic twins. Circulation. 1985;71:39-44.
38. Nielsen JR, Oxhoj H. Echocardiographic variables in progeny of hypertensive and normotensive parents. Acta Med Scand. 1988;S693:61-64.
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