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EARLY PREVENTION OF CORONARY HEART DISEASE

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EARLY PREVENTION OF CORONARY HEART DISEASE BY Jameel A. Al-ata, MD Consultant & Assistant Professor of Pediatrics & Pediatric Cardiology K.A.A.U.H & KFSH-RC JED. – PowerPoint PPT presentation

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Title: EARLY PREVENTION OF CORONARY HEART DISEASE


1
EARLY PREVENTION OF CORONARY HEART DISEASE
  • BY
  • Jameel A. Al-ata, MD
  • Consultant Assistant Professor of Pediatrics
    Pediatric Cardiology
  • K.A.A.U.H KFSH-RC JED.

2
INTRODUCTION
  • Atherosclerosis leading to coronary heart disease
    is complex in origin. Involved in the
    pathogenesis of atherosclerosis are hemodynamic,
    thrombotic, and carbohydratelipid metabolic
    variables, along with intrinsic characteristics
    of the arterial wall.
  • Ross R. The pathogenesis of
    atherosclerosis a perspective for the 1990s.
    Nature 1993362801-809.

3
  • Morbidity due to coronary artery disease is
    generally related to the extent of vascular
    lesions. In this regard, clinical risk factors
    are considered to be useful in predicting the
    severity of atherosclerosis.
  • Roberts WC. Am J Cardiol 198964324-328.
  • Solberg LA, Strong JP. Arteriosclerosis
    19833187-198.

4
  • Environmental factors such as smoking or a
    sedentary lifestyle also contribute to this
    process. The progression of atherosclerotic
    disease and the increasing severity of
    atherosclerosis relate not only to the presence
    and extent of cardiovascular risk factors but
    also to the persistence of risk factors over
    time.
  • Dawber TR. The Framingham Study the
    epidemiology of atherosclerotic disease.
    Cambridge, Mass. Harvard University Press, 1980.
  • Stamler J. Cardiology 199382191-222.

5
INTRDUCTION
  • Hypercholsterolemia is a proven risk for
    premature atherosclerosis M.I.
  • Each 1 reduction in cholesterol reduces MI.
    incidence 2 in adult males.
  • Hypertriglyceridemia is a less significant risk,
    But also known to be associated with premature
    atherosclerosis.

6
INTRODUCTION
  • ONE THIRD of ist MI. patients ( men under 50
    women under 60 years ) have hyperlipoprotienemia,
    HALF have an inherited lipoprotien disorder.
  • In Philadelphia childrens hosp. 75 of children
    have hyperlipidemia strongly ve Fmhx. Of
    premature CHD.
  • 21 ( FH ), 67 ( FCHL ), 11 (
    hyperapobetalipoprotienemia ) 1 (FHTG )

7
INTRODUCTION
  • The understanding of the molecular basis of
    inborn errors of LDL metabolism - such as
    familial hypercholesterolemia due to a defect of
    the LDL receptor - provided us new insights in
    physiology and pathophysiology of LDL metabolism.
  • Most recently we have learned much about the
    vasoprotective HDL cholesterol. HDL is the major
    player in reverse cholesterol transport and some
    of its receptors such as ABCA1 and SR-BI were
    identified. This knowledge gives us a deeper
    understanding of the complex system which
    performs reverse cholesterol transport from
    peripheral tissue and the vessel wall back to the
    liver.

8
INTRODUCTION
  • Fetal programming of coronary heart disease
  • People who develop coronary heart disease grow
    differently from other people both in utero and
    during childhood. Slow growth during fetal life
    and infancy is followed by accelerated weight
    gain in childhood.
  • Two disorders that predispose to coronary heart
    disease, type 2 diabetes and hypertension, are
    preceded by similar paths of growth.

9
INTRODUCTION
  • Mechanisms underlying this are thought to include
    the development of insulin resistance in utero,
    reduced numbers of nephrons associated with small
    body size at birth and altered programming of the
    micro-architecture and function of the liver.
  • Slow fetal growth might also heighten the body's
    stress responses and increase vulnerability to
    poor living conditions in later life.

10
INTRODUCTION
  • Coronary heart disease appears to be a
    developmental disorder that originates through
    two widespread biological phenomena,
    developmental plasticity and compensatory growth.

11
INTRODUCTION
  • Clustering of coronary heart disease risk factors
    among obese children
  • Recent secular trends have resulted in large
    numbers of very overweight children who are at
    increased risk for type 2 diabetes mellitus and
    for various coronary heart disease risk factors,
    including adverse levels of lipids, insulin, and
    blood pressure. All are associated with the
    initial stages of atherosclerosis.
  • The difficulties in preventing and reversing
    obesity, along with the frequent non-adherence of
    adolescents to lifestyle changes and medical
    treatment, will complicate treatment and
    prevention efforts.

12
  • Epidemiologic studies have established that
    multiple risk factors increase the probability of
    cardiovascular events, since risk factors tend
    to reinforce each other in their influence on
    morbidity and mortality.
  • Kannel WB, National Heart, Lung, and Blood
    Institute, 1987. (NIH publication no. 87-2703.)

13
Atherosclerosis of the aorta and coronary
arteries and cardiovascular risk factors in
persons aged 6 to 30 years and studied at
necropsy (The Bogalusa Heart Study).
14
Atherosclerosis of the aorta and coronary
arteries and cardiovascular risk factors in
persons aged 6 to 30 years and studied at
necropsy (The Bogalusa Heart Study).
  • Race and sex differences in aorta and coronary
    atherosclerotic lesions were studied in 150
    persons aged 6 to 30 years.
  • The intimal surface involvement with aorta fatty
    streaks was extensive, 0 to 71, and greater in
    blacks than in whites (32 vs 20, p less than
    0.001).
  • Coronary artery fatty streaks were more
    extensive in male than in female subjects (range
    0 to 22).

15
BHS
  • Fibrous plaque lesions were present but not
    extensive in either the aorta (0 to 12) or the
    coronary artery (0 to 24) specimens. Lesions
    were more prevalent in male than in female
    persons, particularly white male subjects.
  • The relation of fatty streaks to fibrous plaques
    was greater in the coronary vessels than in the
    aorta. In male subjects, aorta fatty streaks were
    strongly related to antemortem levels of total
    cholesterol, low-density lipoprotein cholesterol
    and ponderal index in white male subjects.

16
BHS
  • Coronary artery fatty streaks in white male
    persons were significantly associated with serum
    triglycerides, very low density lipoprotein
    cholesterol, systolic and diastolic blood
    pressure and ponderal index.
  • These results link antemortem risk factors to
    the development of atherosclerotic lesions and
    emphasize the need for preventive cardiology in
    early life. Am J Cardiol
    1992 Oct170(9)8518

17
  • Furthermore, since clustering of risk factors is
    evident in childhood and persists into young
    adulthood, the presence of multiple risk factors
    could indicate the acceleration of
    atherosclerosis in young people.
  • The Bogalusa Heart Study. Prev Med
    19798407-418.
  • Khoury P, Am J Epidemiol
    1980112524-538.
  • Smoak CG, Am J Epidemiol
    1987125364-372.
  • Bao W, Arch Intern Med 19941541842-1847

18
Association between Multiple Cardiovascular Risk
Factors and Atherosclerosis in Children and Young
Adults
  • Autopsy data from epidemiologic studies have
    shown a relation between coronary artery disease
    and cardiovascular risk factors for example,
    high serum total cholesterol concentrations and
    cigarette smoking are important contributors to
    the development of coronary atherosclerosis.

19
  • Autopsy studies from the Bogalusa Heart Study
    have demonstrated a strong association of
    specific antemortem risk factors with vascular
    lesions in children and young adults.
  • These observations have been extended by the
    findings in a larger, multicenter postmortem
    study, Pathobiological Determinants of
    Atherosclerosis in Youth.

20
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21

22
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23
  • The extent of fatty streaks and fibrous plaques
    in the aorta and coronary arteries increased with
    age. The association between fatty streaks and
    fibrous plaques was much stronger in the coronary
    arteries (r0.60, Plt0.001) than in the aorta
    (r0.23, P0.03

24
  • Among the cardiovascular risk factors, body-mass
    index, systolic and diastolic blood pressure, and
    serum concentrations of total cholesterol,
    triglycerides, low-density lipoprotein
    cholesterol, and high-density lipoprotein
    cholesterol,
  • as a group, were strongly associated with the
    extent of lesions in the aorta and coronary
    arteries (canonical correlation a measure of the
    association between groups of variables r0.70
    Plt0.001).

25
  • cigarette smoking increased the percentage of the
    intimal surface involved with fibrous plaques in
    the aorta (1.22 percent in smokers vs. 0.12
    percent in nonsmokers, P0.02) and fatty streaks
    in the coronary vessels (8.27 percent vs. 2.89
    percent, P0.04).

26
  • Subjects with 0, 1, 2, and 3 or 4 risk factors
    had, respectively, 19.1 percent, 30.3 percent,
    37.9 percent, and 35.0 percent of the intimal
    surface covered with fatty streaks in the aorta
    (P for trend0.01).
  • The comparable figures for the coronary arteries
    were 1.3 percent, 2.5 percent, 7.9 percent, and
    11.0 percent, respectively, for fatty streaks (P
    for trend0.01) and 0.6 percent, 0.7 percent, 2.4
    percent, and 7.2 percent for collagenous fibrous
    plaques (P for trend0.003).

27
  • Conclusions These findings indicate that as the
    number of cardiovascular risk factors increases,
    so does the severity of asymptomatic coronary and
    aortic atherosclerosis in young people.

28
Pathobiological Determinants of Atherosclerosis
in Youth (PDAY),
29
Relation of a Postmortem Renal Index of
Hypertension to Atherosclerosis in Youth
  • In a cooperative multicenter study,
    Pathobiological Determinants of Atherosclerosis
    in Youth, of 1164 young men 15 through 34 years
    of age who died of external causes and were
    autopsied in forensic laboratories.
  • They measured atherosclerosis of the aorta and
    the right coronary artery.

30
CONT, ( PDAY )
  • Using the ratio of intimal thickness to outer
    diameter of the small renal arteries to predict
    mean arterial pressure (MAP) during life. Cases
    were classified as either normotensive (MAP lt110
    mm Hg) or hypertensive (MAP 110 mm Hg).

31
CONT, ( PDAY )
  • By this criterion, the prevalence of hypertension
    in blacks was 16 in whites, 12. Hypertension
    was associated directly with blood level of
    glycohemoglobin (an indicator of blood glucose
    concentration) and with body mass index (BMI) but
    inversely with thickness of the panniculus
    adiposus.

32
CONT, ( PDAY)
  • Among hypertensive compared with normotensive
    cases, the extent of raised lesions (mainly
    fibrous plaques) was greater in the aortas of 30-
    to 34-year-old men and in the right coronary
    arteries of 25- to 34-year-old men.
  • The prevalence of raised lesions involving 5 or
    more of the intimal surface was twofold greater
    in the aortas and right coronary arteries of
    hypertensive men throughout the 15-to-34year age
    span of the study cases.

33
  • The prevalence of raised lesions involving 5 or
    more of the intimal surface was twofold greater
    in the aortas and right coronary arteries of
    hypertensive men throughout the 15-to-34year age
    span of the study cases.

34
  • Although hypertension is associated with elevated
    blood glycohemoglobin and adiposity, the effect
    of hypertension on atherosclerosis is not
    accounted for by those variables.

35
Relation of Glycohemoglobin and Adiposity to
Atherosclerosis in Youth ( PDAY )
  • In a cooperative multicenter study
    (Pathobiological Determinants of Atherosclerosis
    in Youth, PDAY) of 1532 young persons 15 through
    34 years of age who died of external causes and
    were autopsied in medical examiners' laboratories

36
  • They quantified atherosclerosis of the aorta and
    the right coronary artery and analyzed postmortem
    blood cells for glycohemoglobin and postmortem
    serum for lipoprotein cholesterol and thiocyanate
    (as an indicator for smoking).
  • They measured the thickness of the panniculus
    adiposus and the body mass index (weight per
    height squared) as indicators of adiposity

37
  • Glycohemoglobin levels exceeding 8 were
    associated with substantially more extensive
    fatty streaks and raised lesions in the right
    coronary artery in persons more than 25 years of
    age and with more extensive raised lesions in the
    aorta in persons more than 30 years of age.
  • Both thickness of the panniculus adiposus and
    body mass index were associated with more
    extensive fatty streaks and raised lesions in the
    right coronary artery.

38
  • The associations of atherosclerotic lesions with
    glycohemoglobin and adiposity were not explained
    by a less favorable lipoprotein profile or
    smoking.
  • The results show that atherosclerosis in young
    adults is associated with the prediabetic or
    early diabetic state, as indicated by elevated
    glycohemoglobin levels, and with obesity.

39
  • Several recent articles reviewed the potential
    mechanisms by which diabetes, hyperinsulinemia,
    and hyperglycemia augment atherogenesis.
  • Of the many mechanisms suggested, two seem most
    likely to be involved in the association of
    glycohemoglobin concentration in these young
    adults
  • 1 ) the effects of dyslipoproteinemia and
    hyperinsulinemia in the prediabetic state, as
    suggested by Haffner et al, and ,
  • 2 ) a direct effect of glycosylation of proteins
    on atherogenesis.

40
  • The glycohemoglobin effect is not accounted for
    by serum lipoprotein cholesterol levels
    (VLDLLDL-C and HDL-C), and there is little
    correlation between glycohemoglobin levels and
    serum lipoprotein levels.
  • However, the possibility remains that individuals
    with elevated glycohemoglobin levels may have had
    abnormal lipoprotein profiles and
    hyperinsulinemia.

41
  • A process similar to the glycosylation of
    hemoglobin occurs in other proteins.
    Subsequently, the carbohydrate-protein complex
    undergoes chemical rearrangement to form
    irreversible advanced glycosylation end products,
    which have a variety of deleterious effects on
    cells and tissues.

42
  • ConclusionsThe observations reported here
    suggest that both elevated glycohemoglobin
    levels, possibly associated with the prediabetic
    state, and obesity are associated with
    accelerated atherogenesis in the third and fourth
    decades of life.
  • The results provide hope that early detection and
    control of obesity and hyperglycemia in young
    persons will reduce the risk of atherosclerotic
    disease in later life.

43
  • Obesity and AtherosclerosisThe health effects
    of obesity have been difficult to study because
    (1) body weight and composition are influenced by
    many different conditions (eg, caloric intake,
    physical activity, smoking, and genetic factors),
    (2) its definition is not precise, (3) fat
    distribution may be as important as total fat,
    (4) duration of exposure and age of the subject
    influence its effects, and (5) obesity is
    associated with a variety of health risks
    (hypertension, coronary heart disease, stroke,
    noninsulin-dependent diabetes, cholelithiasis,
    and some forms of cancer).

44
  • Obesity enhances three other established risk
    factors for coronary heart disease
  • hypertension, dyslipoproteinemia, and diabetes
    mellitus.
  • and is inversely related to another major risk
    factor, smoking.
  • In many instances, when obesity is associated
    with coronary heart disease in univariate
    analyses, multivariate analyses including the
    other risk factors do not show an independent
    effect.
  • but several long-term longitudinal studies have
    found an independent effect after controlling for
    other risk factors.

45
Effects of Serum Lipoproteins and Smoking on
Atherosclerosis in Young Men and Women ( PDAY )
  • Atherosclerosis begins in childhood and
    progresses from fatty streaks to raised lesions
    in adolescence and young adulthood.
  • A cooperative multicenter study (Pathobiological
    Determinants of Atherosclerosis in Youth PDAY)
    examined the relation of risk factors for adult
    coronary heart disease to atherosclerosis in 1079
    men and 364 women 15 through 34 years of age,
    both black and white, who died of external causes
    and were autopsied in forensic laboratories.

46
  • They quantitated atherosclerosis of the aorta and
    right coronary artery as the extent of intimal
    surface involved by fatty streaks and raised
    lesions and analyzed postmortem serum for
    lipoprotein cholesterol and thiocyanate (as an
    indicator of smoking).

47
  • The extent of intimal surface involved with both
    fatty streaks and raised lesions increased with
    age in all arterial segments of all sex and race
    groups.
  • Women had a greater extent of fatty streaks in
    the abdominal aorta than men, but women and men
    had about an equal extent of raised lesions.

48
  • Women and men had a comparable extent of fatty
    streaks in the right coronary artery, but women
    had about half the extent of raised lesions.
    Blacks had a greater extent of fatty streaks than
    whites, but blacks and whites had a similar
    extent of raised lesions.
  • VLDL plus LDL cholesterol concentration was
    associated positively and HDL cholesterol was
    associated negatively with the extent of fatty
    streaks and raised lesions in the aorta and right
    coronary artery.

49
  • Smoking was associated with more extensive fatty
    streaks and raised lesions in the abdominal
    aorta. All three risk factors affected
    atherosclerosis to about the same degree in both
    sexes and both races.
  • Primary prevention of atherosclerosis by
    controlling these adult coronary heart disease
    risk factors is applicable to young men and women
    and to young blacks and whites.

50
  • The effects of VLDLLDL-C and HDL-C
    concentrations and smoking are similar in men and
    women and are similar in blacks and whites. Race
    and sex differences in atherosclerotic lesions
    are not explained by differences in lipoprotein
    cholesterol levels or smoking.
  • These results are similar to those reported
    previously results are including those reported
    from the Bogalusa Heart Study.

51
  • These findings from the PDAY study strongly
    support modification of the risk factors in young
    people to retard the development of early
    atherosclerotic lesions, particularly raised
    lesions.
  • They anticipate that risk factor modification
    would delay the development of lesions, an effect
    that in turn would delay correspondingly the
    onset of clinical coronary heart disease later in
    life.

52
Persistent Elevation of Plasma Insulin Levels Is
Associated With Increased Cardiovascular Risk in
Children and Young Adults The Bogalusa Heart
Study
  • Hyperinsulinemia has been considered to be a
    potent cardiovascular risk factor.
  • community-based population over an 8-year period
    1606 individuals (39 were black) aged 5 to 23
    years participated in the first survey.

53
  • Compared with subjects with levels of insulin
    consistently in the lowest quartile, those with
    levels always in the highest quartile showed
    higher (Plt.001) levels of body mass index (9
    kg/m2),
  • triglycerides (58 mg/dL), LDL cholesterol
    (11 mg/dL), VLDL cholesterol (8 mg/dL), glucose
    (9 mg/dL),
  • systolic blood pressure (7 mm Hg), and
    diastolic blood pressure (3 mm Hg) lower
    (Plt.001) levels of HDL cholesterol (-4 mg/dL)
    and higher (Plt.05) prevalence of parental history
    of diabetes (3.3-fold) and hypertension
    (1.2-fold).

54
  • There were 739 young adults aged 20 to 31 years
    at follow-up.
  • As adults, individuals with consistently
    elevated insulin versus those with consistently
    decreased insulin had increased (Plt.05)
    prevalence of obesity (36-fold), hypertension
    (2.5-fold), and dyslipidemia (3-fold), which was
    attributed to both baseline insulin and change of
    insulin from baseline to follow-up

55
  • . In addition, clustering of these risk factors
    was stronger (Plt.05) in adults with persistent
    insulin elevation.
  • Conclusions Elevated insulin levels persist from
    childhood through young adulthood, resulting in a
    clinically relevant adverse cardiovascular risk
    profile in young adults.

56
HOW TO PRVENT ATHEROSCLEROSIS
  • Begin with children
  • Screening
  • Comperhensive Treatment Program

57
SCREENING
  • Selective, children above 2y.
  • Crieteria
  • 1) Parent OR grandparents with premature IHD.
  • 2) Parent with hypercholest.( 6 mmol/L )
  • 3) Unavailable family history.
  • 4) Associated risk factors ( DM, OBESITY, High
    BP. ).
  • 5) ALL adults 20 y or above, check CHOLESTEROL

58
TREATMENT
  1. A diet aimed at reducing fat intake to 30 of
    total calories, saturated fat to less than 7 and
    cholesterol to less than 200 mg/day. The
    expertise of a dietitian is highly recommended in
    counseling families.
  2. The national Cholesterol Education Program
    Consensus Panel recommended drug therapy after
    the age of 10 years if diet therapy has n0ot
    lowered the lipid levels sufficiently. The only
    drugs currently approved for children are the
    bile acid binding resins, cholestyramine and
    colestipol.

59
TREATMENT
  1. Lifestyle habits modification of the children and
    adolescents such as weight control, not smoking
    and daily exercise.

60
Treatment Recommendations Repeat within 5 years
general dietary recommendations. Repeat and
average with previous measurement if average is
lt 170 mg/dL, then repeat within 5 years if lt
170 mg/DL, then do fasting lipoprotein
profile. Do fasting lipoprotein profile.
61
If fasting lipoprotein profile obtained Measure
twice and average calculated LDL cholesterol with
previous measurement.
62
Repeat profile within 5 years general
recommendations. Risk factor counseling and
dietary recommendations re-evaluate in 1
year. Clinical assessment to evaluate for primary
and secondary causes of hyperlipidemia greater
restriction of dietary saturated fatty acids and
cholesterol if primary or familial
hyperlipidemia suspected, screen other family
members after at least a 6-month trial of
dietary intervention, evaluate for drug
treatment.
63
CONCLUSION
  1. Although selective screening criteria will not
    identify all the children with hypercholesterolemi
    a it will identify many. Hopefully focusing on
    prevention of cardiovascular disease in children
    and adolescents will make a difference in the
    future of health care.

64
THANK YOU
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