Lipids, lipoproteins and coronary heart disease in minority populations

ATHEROSCLEROSIS Atherosclerosis 108 ( Suppl.) ( 1994) S83-- 104

Lipids, lipoproteins and coronary heart disease in minority populations Sandra Harris-Hooker*“, Gary L. Sanfordb “Departments of Medicine and Pathology, bDepartment of Biochemistry, Morehoase School of Medicine, Atlanta, GA, USA

Despite recent advances iu both prevention and treatment, cardiovascular disease (CVD) remains the leading cause of mortality in the US. The Framingham Study was a landmark in defining CHD-related risk factors; unfortunately, very few minorities were included. A major preventable risk factor for CHD continues to be lipid abnormalities, but its association within minority populations is unclear. The few studies that have examined the association of hyperlipidemia with CHD in minorities have shown that total cholesterol was a predictor of CHD risk (e.g., black men aged 3544). Several researchers have reported higher levels of HDL for black men and women compared to white men and women. Since HDL was shown to be inversely related to CHD, this discrepancy in HDL is hypothesized to account for the lower than expected mortality rate. Lipoproteim a) has been identified as an independent risk factor for CHD; blacks have considerably higher levels than whites. Data also indicate the following: Hispanics have lower CVD mortality rates than the general population despite having known risk factors (e.g., obesity, diabetes, low socioeconomic status); Hisipanic women have lower levels of HDL cholesterol; Native-American populations have lower prevalence of CHIg associated with lower LDL-cholesterol and higher HDL-cholesterol. Understanding epidemiologic and patho@ysiologic data regarding differences between various racial groups should help reduce CVD-related morbidity arid mortality in minority populations. Key+rc;)vds:Coronary terolemia

heal? disease; Lipoproteins;

Minorities;

1. Introduction It is difficult to overst,ate the impact of cardiovascular diseases (CVD), particularly coronary heart disease (CHD), in the United States because over five million Americans have symptomatic CHD, and countless others have asymptomatic CHD. There are more than 600 000 hospital ad-w

* Corresponding author, Department of Medicine, Morehouse School of Medicine, 720 Westview Drive, S.W.. Atlanta, GA 30310-1495, USA. Tel.: (404) 752-1768.

Blacks; Hispanics; Native Americans; Hyperchotes-

missions for myocardial infarction and half a million deaths from CHD each year. Atherosclerosis, the principal cause of myocardial infarction, accounts for the majority of these deaths. Since atherosclerotic lesions remain silent until they provoke morbidity and mortality, epidemiologic data are largely expressed in terms of CHD. In 1980 the annual cost for health care related to CHD amounted to approximately $80 billion [ I]. Moreover, despite recent advances in both prevention and treatment, CVD continues to have the highest morbidity and mortality rates in west-

002 l-91 50/94/$07.00 c 1994 Elsevier Science Ireland Ltd. All rights reserved SSDI 002 1-915u(94)0529 1-P

S. Harris-Hooker, G. L. Sanford 1 Atherosclerosis 108 (Suppl.) (1994) S83-SW

sa4

Table 1 The annual average population and total deaths from the four major CVD by race and sex in metropolitan Atlanta, GA, 1979- 1985

Deaths from CVO

Population Race

Sex

Number

%

Number

%

White

Male Female Male Female

617 508 650 119 229 283 264 984 I761 894

35.1 36.9 13.0 15.0 100.0

17 616 21 103 4543 5915 49 177

35.8 42.9 9.2 12.1 100.0

Black Total

industrialized societies, including the USA [2-41. We recently reviewed the mortality from CVD for the period 1979 to 1985 in the Atlanta metropolitan population for racial differences [ 51. We found that of the 22 585 deaths from hypertension, stroke, ischemic heart disease and atherosclerosis, 78.7% occurred among whites and 21.3% among blacks (Table 1). Overall, ischemic heart disease accounted for 47.7% of these four types of CVD deaths for both races and both sexes. The crude mortality rate for the four types of CVD was 31% lower in blacks than in whites (Table 2). However, the age-adjusted mortality rate of black women from all four CVD groups actually exceeded that of white women by 14%, while the age-adjusted rate among black males was only 8% lower than that of white males. The age-specific mortality rates revealed an excess from ischemic heart disease only between the ages of 30 and 59 years and from atherosclerosis between 40 and 59 years of age for black men (Fig. 1). This age-related crossover in females did not occur until the age of 75 years for deaths attributed to these causes (Fig. 2). These data suggest that blacks were at highest risk for all four cardiovascular related diseases at younger ages. It is generally known that different environmental, social, and genetic factors among diverse populations influence a disease’s catastrophic forces, but comparatively little research has been done on cardiovascular-related health problems in minorities [6]. The limited studies that exist have finally begun to dispel the mythologies about the epidemiology and clinical manifestations of CHD in ern

black populations. A list of the most prevalent myths and the facts that should replace them was presented in 1984 by Gillum and Liu [7]. The most widespread of these myths is the notion that CHD is uncommon in blacks. The fact that replaced this fallacy is that CHD is the leading cause of death in US blacks. The percentage of deaths in 1986 attributed to CHD was lower for blacks than for whites: WM 72.2%, WF 67.3%, BM 52.5% and BF 53.6%. However, the death rates for CHD were higher in blacks than in whites, depending on age [6]. In other minorities, such as Hispanics (the second largest minority group in the USA), the extent and quality of the data on the impact of cardiovascular diseases is even more limited than that available for blacks. Part of this limitation is due to the occasional practice of aggregating the mortality data on minorities into a non-white category. In addition, the available data are limited in quality, exactness, and applicability. There are also very few studies that give adequate attention to such factors as socioeconomic status (SES), migration status and level of cultural adaptation. These factors and others have been identified as important predictors of the overall health status (including CHD risk) and quality of care received by ethnic minorities [ 8- lo]. Hispanics have lower cardiovascular mortality rates than the general population, despite factors (high rates of obesity, diabetes, and low SES) known to promote higher rates [ 11 - 131. Heart disease is a significant contributor to allcause mortality in Native Americans as well, but is proportionately less of a contributor thain in the general population. The heart disease de:aath rate for Native Americans under 35 years old is approximately twice as high as for all othlzr ethnic groups. However, heart disease mort:ality increzses less steeply with age in Native A,mericans over 44 years old compared with the: general population [ 14- 161. The established risk factors for CHD are hypertension, hypercholestero!emia, cigarette smoking, diabetes mellitus, type A personality, hyperlipidemia, age and sex. The more controversial or less well established risk factors include obesiity, physical inactivity, low HDL, alcohol consumption, family history of CHD, psychosocial sitress and

S. Harris-Hooker,

G. L. Sanford

1 Atherosclerosis 108 (Suppl.) (1994) S83-SlO4

Table 2 Average annual crude and age-adjusted mortality rates (per 100 000) and black-to-white diseases by sex and race in the Atlanta metropolitan area. 1979-1985 Cause of Death

Hypertension

Stroke

Ischemic Heart disease Atherosclerosis

All four causes

il Mantel-Haenzel

Male

Crude Adjusted RMH (95% C.I.)” Crude Adjusted R:MH (95% C.I.) Crude Adjusted RMH (95% C.I.) Crude Adjusted RMH (95% C.I.) Crude Adjusted RMH (95% C.I.)

S85

rate ratios (RR) from cardiovascular

Female

Black

White

51.6 82.7

21.8 26.1

85.9 139.9

97.2 127.9

122.8 201.1

235.5 282.4

22.8 41.1

53.0 70.0

283.1 464.8

407.5 506.4

RR 2.54 3.17 3.34 (3.10-3.70) 0.83 I .09 1.27 (1.12-1.34) 0.52 0.71 0.75 (0.71 -0.79) 0.43 0.5Q 0.62 (0.55-0.69) 0.69 0.92 I .oo (0.97 I .04)

Black

White

59.6 68.9

30.2 21.1

100. I 114.0

153.0 103.9

119.9 f36.7

199.3 138.1

RR I .97 3.27 3.27 (2.93. 3.42) 0.65 1.10 1.08 (1.02--1.13) 0.60 0.99 0.96 (0.93 I .02)

44.2

81.1 53.7

319.0 363.8

463.6 316.8

39.4

0.49 0.82 0.82(0.76 0.89) 0.69 I.14 I.14(I.1 I 1.18)

pooled estimate and test-based 95% confidence interval.

20.0

Hypertension

10.0 8.0 0 F h

6.0 4-o

w Z pT 2.0

1.0 0.8 0.6 Disease

I

o-29

I

30-39

I

40-49

I

SO-59

1

I

I

60-69

70-79

60+

AGE Fig. I. Average annual age-specific black-to-white Atlanta from 1979 to 1985.

mortality rate ratios from cardiovascular

disease for males in metropolitan

S86

S. Harris-Hooker, G. L. Sanford 1 Atherosclerosis 108 (Suppl.) (1994) S83-SW

20.0 1 lO.O-

8.02

8-O-

:

4.0-

w $

20.

1.0 0.8-

';‘A

37 O-29

30-39

40-49

SO-59

80-89

70-79

80+

AGE Fig. 2. Average annual age-specific black-to-white mortality rate ratio from cardiovascular disease for females in metropolitan Atlanta from 1979 to 198T. _

low SES [!?I. In view of the lack of sufficient studies of CHD in minorities, even the established risk factors are not well substantiated. Though the established risk factors are all important, the evidence linking elevated serum cholesterol (hypercholesterolemia) to CHD is overwhelming, Epidemiologic, clinical and genetic studies all indicate that high serum levels of cholesterol are causally related to increased risk of CHD. Most of these studies, however, were inappropriately carried out in that they included inadequate numbers of, and in some instances no, minorities. This review will not attempt to cover all the literature available on hyperlipidemia and CHD, but will focus on the association of lipids and lipoproteins with CHD in minorities, particularly blacks and Hispanics. 2. Serum cholesterol and risk of CVD The efforts of the National Cholesterol Education Program and the American Heart Association to inform the public about the role of cholesterol in CHD often come under criticism

[2]. The critics suggest that the relationship between cholesterol and CHD is not well established, that lowering serum cholesterol does not extend life, and that low-saturated fat, low-cholesterol diets do little to reduce risk of CHD. These comments have prompted several questions, the most frequent of which obviously are: ( 1) Is high serum cholesterol a risk factor for coronary heart disease? (2) Will lowering serum cholesterol help prevent CHD? One of the most important epidemiologic studies which started the series of strong scientific data that provides positive answers to these questions is the Framingham Heart Study, initiated in 1948 with more than 5000 men and women aged 30 to 52 in Framingham, MA. Thorough medical histories, physical examinations. and risk assessments (including total serum cholesterol, blood pressure. history of cigarette smoking, weight, height, physical activity, alcohol consumption, and stress) were made at the start of the study and at 2-year intervals [ 181.These data from the Framingham Heart Study show that at increasing levels of total

S. Harris-Hooker,

G. L. Sanford

1 Atheroderosis

serum cholesterol, CHD risk also increases (Fig. 3). The extent of CHD risk is also magnified by the addition of other CHD risk factors. Coronary heart disease risk is increased beyond that associated with cholesterol alone when factors such as glucose intolerance, hypertension, cigarette smoking and left ventricular hypertrophy are added to elevated serum cholesterol levels. Fig. 3 shows that the multiple risk factors have an additive effect on the development of CHD. However, elevated cholesterol is an independent risk factor for the development of CHD in the absence of all other risk factors. This same pattern of positive correlation of elevated cholesterol levels to increased heart disease risk has since been revealed by several other studies. In the Multiple Risk Factor Intervention Trial (MRFIT), a 6-year prospective study of more than 350 000 men aged 35-57 who were initially free of overt CHD, 2000 of the 7000 deaths over the 6-year period were attributable to CHD. Of the CHD deaths, 46% were accredited to serum cholesterol levels of 180 m&d1 or greater. A comparison of the rate of CHD-related deaths with total cholesterol once again revealed that the death rate increased progressively with cholesterol levels [ 191. Additional evidence for the relationship between hypercholesterolemia and increased risk of CHD (via atherosclerosis) has also come from experimental studies using animals. The models most relevant to human disease include nonhuman primate and swine fed diets leading to high serum: cholesterol, and the Watanabe hyperlipidemic rabbit (an endogenous hypercholesterolemic model). Using the nonhuman primate model, Faggioto et al. [20] induced hypercholesterolemia (500-1000 mg/dl) which was in the range for patients with familial hypercholesterolemia. These studies demonstrate the direct correlation between the rate of hypercholesterolemia and the development of proliferative lesions. Similar observations involving the development of atherosclerosis have been seen using the Watanabe rabbit [21]. Evidence that reducing high levels of serum cholesterol will decrease risk of CHD has also been provided by the Lipid Research Clinics Coronary Primary Prevention Trial (CPPT). This

108 (Suppl.) (1994) S83-S104

St37

Cholesterol335 (mg/dl) OIVSO” Intolwm~

0

SW

+

101

+

In

.

(I,

191

CIW.“”

0

D

.

.

ECO-L””

0

0

0

.

Fig. 3. These data from

the Framingham

Heart

that at increased levels of total serum cholesterol CHD

risk also increases. The degree of CHD

heightened Adapted

by

the

addition

from: Am. J. Cardiol..

of

other 52 (1983)

CHD

Study show (335 mg/dl)

risk elevation is risk

factors.

9B.

placebo-controlled study evaluated the effect of diet plus cholestyramine versus placebo in more than 3800 asymptomatic men, 35-59 years of age, with primary hypercholesterolemia [ 22,231. During the 7-year study, cholestyramine was shown to reduce total cholesterol and LDL-C by 8.5% and 42.6%. respectively, below levels in the placebotreated group (Table 3). The difference in CHD event rates of 7% in the cholestyramine group versus 8.6% in the placebo group represents a 49% reduction in CVD-related events at 7 years’ follow-up. Like the CPPT results, the findings reported in the Helsinki Heart Study further showed that drug treatment to lower elevated levels of serum cholesterol reduces risk of CHD [24]. The 2000 Helsinki patients treated with gemfibrozil lowered their total and LDL-C levels by an average of 8% and raised their HDL-C levels by 10%. The men in the gemfibrozil group had 34% fewer coronary events than those in the placebo group. Although cholesterol screening and awareness of cholesterol leveis have increased substantially in the USA since 4985. when the National Choles-

S88

S. Harris-Hooker, G. L. Sanford 1 Atherosclerosis 108 (Suppl.) (1994) S83-S104

Table 3 Definite or suspect primary end points and all-cause mortality Cholestyramine resin (n = 1906)

Placebo (n = 1906)

End point

Definite CHD death and/or definite nonfatal myocardial infarction Definite or suspect CHD or nonfatal myocardial infarction

%I Reduction in risk

90% Confidence interval for reduction in risk

No.

%,

No.

%

187

9.8

155

8.1

19

+3

+ 32

256

13.5

222

11.6

I5

-l-l

+27

Adapted from: J. Am. Med. Assoc., 251 ( 1984) 35.

terol Education Program was initiated by the NHLBI, cholesterol screening awareness still varies. Table 4, taken from a report by the CDC, shows cholesterol screening and awareness to be slightly higher among women than among men,

and that younger persons ( 18-34 years of age), blacks and persons with lower education attainment ( < 12 years’ education) were less likely to have their cholesterol level checked and were less likely to report knowing their cholesterol level.

Table 4 Cholesterol screening and awareness of cholesterols levels by demographic category: Behavioral Risk-Factor (BRFSS), 1989 Category

Sample size

Respondents having had their cholesterol level checked

Surveilance System

Respondents knowing their cholesterol level

Overall (‘l/u)

Standardized” ( ‘%I)

Overall ( ‘XI)

Standardized” (%)

Sex Maleb Female

26 519 37 394

56 59’

52 55*

23 24

19 21

Age (years) 18-34b 35-49 50-64 265

22 091 17 736 II 519 12 567

37 61* 75* 77*

33 55* 73* 78*

12 27+ 35* 31*

9 23* 33* 31*

Race Whiteb Black

57 998 5915

58 50*

54 50*

25 9*

21 8*

Education ( years) c < 12 12 > 12b

10 921 21 736 31 099

53* 53* 62

44* 53* 64

14* 21* 29

12* 21* 29

Adapted from: J. Am. Med. Assoc., 264 (1990) 2985. “Standardized for other demographic variables using 1980 U.S. Census data. For example. age is adjusted for sex, race, and educational attainment. bReferent group. ‘Level unknown for 157 BRF SS respondents. *Differs significantly from the referent group (P =Z0.05, Z-test).

S. Harris-Hooker, G. L. Sanford I Atherosclerosis 108 (Suppl.) (1994) S83-S104

S89

Table 5 Serum total cholesterol levels in adults aged 20-74 ye~rb ‘%Iof ali adults Borderline-high value (200- 239 mg/dl) Population group

Desirable ( < 200 mg/dl)

Without CHD and 2 risk factors

With CHD or 2 risk factors

All persons

43

16

14

+

27

=

41

Race Black White

48 42

13 17

15 !4

+ +

24 27

= =

39 41

High value ( > 240 mg/dl)

Total needing lipoprotein analysis

Adapted from: J. Am. Med. Assoc.. 262 ( 19851)45.

Differences by race declined after standardization for age, sex, and educational attainment [25]. The evidence positively shows that lowering blood levels of total cholesterol retards the rate of progression of coronary lesions and reduces CHD morbidity and mortality. However, an evaluation of total cholesterol may not be adequate to reduce CHD events: a complete lipoprotein analysis and an examination of other risk factors may be necessary. Applying the Adult Treatment Panel (ATP) guidelines to data from the second National Health and Nutrition Examination Survey (NHANES II), Sempos et al. [26] estimated the percentage of adults 20 years and older with serum total cholesterol levels that warrant their having lipoprotem analysis. Serum total cholesterol levels were found to be high in 27% of adults aged 20-74 years (Table 5). In addition, 14OA1 had boderline-high values with CHD or at least two other risk factors, bringing the total percentage needing lipoprotein analysis to 41% Virtually the same values were found for blacks (39%) and whites (41%). Among those who need lipoprotein analysis, approximately 88O/)were candidates for medical advice and intervention for high levels of blood cholesterol, 63% had high-risk LDL cholesterol and 25% had borderline-high risk values. Similar results were found for blacks and whites.

3. Lipids and lipoproteins as predictors of CHD Epidemiologic studies have repeatedly shown that total cholesterol, high density lipoprotein (HDL-C) and low density lipoprotein (LDL-C) cholesterol are strong, consistent and independent predictors of CHD [27-291. While high levels of total and LDL-C were found to increase the risk of CHD, increasing concentrations of HDL-C lowered the risk of CHD. A recent account of data from the Framingham Heart Study suggests that LDL-C level is a better predictor of CHD than total cholesterol for men and women over 50 years old [30]. However, the predictive power of LDL-C is lower in older than in younger persons [ 3 11.The ATP report identifies LDL-C as a major factor for intervention because these lipoproteins are thought to play the most important role in atherogenesis. An LDL-C level exceeding 4.15 mmol/l ( 160 mg/ dl) is defined as high risk according to the ATP report. Approximately 33% of older men and 50% of older women have these levels of LDL-C. A report from the Coronary Artery Risk Development in Young Adults (CARDTA) study disclosed that both white and black men showed an increase in LDL-C and apo B with increasing age. shown in Figs. 4 and 5 [32]. No significant difference in LDL-C levels was noted for black men compared

S. Harris-Hooker, G. L. Sanford 1. Atherosclerosis 108 (Suppl.) (1994) S83-S104

s90

Z i; z S 0 6 Z z c

1?5170. 165160155.

16-20

AGE

27-30

125 1 129 s SI e' -

115

z 5 i

110

1

B

'ii 105 !i 100

t

Fig. 4. Concentration (1989) 656.

95 m

27.30

of (A) total and (B) LDL cholesterol (mg/dl) by age, race and gender. Adapted from: Arteriosclerosis,

with white men. However, total cholesterol levels were higher in the younger black males than in their white counterparts. The NHANES II study also revealed no difference in total and LDL-C between whites and

9

blacks. However, black women were found to have higher total cholesterol, LDL-C, apo B and apo A-I levels (Figs. 4 and 5) but lower triglycerides (Fig. 6B) than white women. Pronounced gender differences were also noted in whites: men

S. Harris-Hooker, G. L. Sanford 1 Atheroselerasis 108 (Suppl.) (1994) S83-S104

150-

= ?

s91

A

145 -

E r

140 -

u c 5 G h z

135 -

130-

= :: c

125 -

120 19-20

27-30 AGE

lOO-

B

18-20

27.30 AGE

Fig. 5. Concentration of (A) apolipoprotein Arteriosclerosis, 9 ( 1989) 656.

A-l and (B) apolipoprotein

had higher LDL-cholesterol and apo B than women. Comparison of the data from the Starr County, TX study [33] with similar data for the general population from the Lipid Research Clinics Program (LRC) shows that the distribution of lipoprotein in the Mexican American population is similar to that for the general population. Both Mexican American men and women showed increased LDL-C with increasing age. Significant

B Umg/dl) by age, race. and gender. Adapted from:

differences between men and women were found for LDL-C and apo B levels. Serum high density lipoprotein cholesterol (HDL-C) has been the subject of clinical and epidemiologic investigations because of its perceived inverse association with CHD risk. As most recent studies have shown, CHD incidence in blacks, especially younger males, is somewhat lower than that for whites, although they have

s92

S. Hurris-Hooker.

G. L. Sanfi,rd

1 Azheroselerosis

IOS (S~ppi.)

(1994)

S83-SiO4

g

White Women

A

la-20

27-30 AGE

Fig. 6. Concentration 656.

of (A) HDL and (B) triglycerides (mg/dl) by age, race and gender. Adapted from: Arteriosclerosis. 9 ( 1989)

S. Harris-Hooker,

G. L. Sanford I Atherosclerosis 108 (SuppI.) (1994) S83-S104

Table 6

HDL cholesterol (mg/dl) for adults ages 20-74 years, by sex. race, and age group, with means and age-adjusted means, USA 1976- 1980 Race/sex group

(years)

White men

20-74

Age group Persons examined

Estimated population in thousands

Mean

4019

55 808

Black men

20-24 25-34 35-44 45-54 55-64 65-74 ‘O-74

424 751 545 506 865 858 462

8052 13 864 9808 9865 8642 5576 6102

65 I12 54 47 92 92 4563

1043 1546

White women

20- 24 25534 35-44 45-54 55-64 65-74 20-74

1112 1044 801 555 60 785

Black women

20-24 25534 35-44 45-54 55-64 65-74 20-74

542 875 626 546 973 1001 581

8408 14 494 IO 584 10 369 9601 7329 7579

20-24 25-34 35544 45-54 55-64 65-74

77 122 84 81 99 118

I304 1953 1415 1215 959 733

44.4 44.5 + 45.9 44.4 43.4 43.3 45.4 44.8 51.8 51.9+ 53.0 49.9 50.8 s3.3 52.9 53.5 53.4 53.4 + 51.8 52.2 52.4 55.1 55.7 52.8 56.2 55.3 + 56.6 55.4 55.1 56.2 58.3 57.1

Adapted from: Am. J. Epidemiol..

129 ( 1989) 181.

greater prevalence of hypertension and other CHD risk factors. Figs. 5A and 6A (taken from the CARDIA study) demonstrate that among adults aged 18-24, black males had higher HDLC and apo A-I levels than white males [32]. The Bogalusa Heart Study also found higher HDL-C in young adult black males compared to whites [34]. Similar findings were reported by the LRC Program Prevalence Study for blacks and whites aged 5-44, black males and females had higher HDL-C in each of the 5 year age groups and for

s93

seven out of eight age groups respectively as compared to their white counterparts [35]. Table 6 gives the mean levels of serum HDL-C according to age, sex, and race [36]. HDL-C levels showed little variation by age within each of the four sex-race groups. In white men, mean HDL-C levels declined to the lowest level of 43.3 mg/dl at ages of 45-54 years, peaked at 45.4 mg/dl at ages of 55-64 years, and decreased thereafter. In contrast, in black men, the intial decline reached its lowest level of 49.9 at ages of 25-34 years, and generally increased thereafter to 53.5 for the aidest age group. In women a somewhat general pattern was seen with age for both whites and blacks: a decline after age 24 and peaking around 55-64 years. The incidence of definite coronary events (DCE) and its relation to total and HDL-C was presented in a 20-year follow-up report by Brunner et al. [37]. The incidence of DCE was inversely correlated with the percentage HDL-C (based on total cholesterol levels). For men, DCE was 28% when HDL-C was less than 14% bu.t only 7% when HDL-C was 21%. For women, DCE was 14% with HDL-C of 17% and only 2% with HDL-C of 23”/0(Fig. 7). This study indicates that the predictability of HDL-C for the risk of CHD is improved when total cholesterol is taken into account, i.e. expressing HDL-C as a percentage of total cholesterol. Overall. young black females and males and adult males have higher HDL-C levels than do whites, differences that would potentially protect them against CHD, given the excess among blacks of certain CHD risk factors, particularly hypertension. The loss of this protective HDL-C difference in adult black females appears most likely to be due to their obesity. Additionally, diabetes and hypertension tend to decrease, whereas alcohol intake and leisure physical activity do not alter, HDL-C levels. The San Antonio Heart Study. involving ages 25-64, white and Mexican Americans, indicated that while total cholesterol and LDL-C were similar, HDL-C was lower for Mexican American females [38]. Data from the Starr County, TX study [33] are given in Table 7, which displays the age-adjusted mean levels of lipids and lipoproteins for Mexican Americans and whites separate1y for

s94

S. Harris-Hooker, G. L. Sanford 1 Atherosclerosis 108 (Suppl.) (1994) S83-S104

40

65

w

HDL-C% .z 14% MEN

q

HDL-C% > 21% MEN

q

HDLC% < 17% W&EN

0

HDL-C% > 26% WOMEN

36

2.5

20

15

10

6

0

35-44

45-54

55.64

Fig. 7. Incidence of DCE during 20 years of HDL cholesterol: percentage and age in men and women. Adapted from: Am. J. Cardiol.. 59 ( 1989) 1271.

each sex. This study also found that HDL-C was equivalent for white and Mexican American males, but Mexican American females demonstrate a uniformly reduced pattern compared with the LRC data for the general female population. Both studies found an increased frequency of obesity for the Mexican American population, suggesting that part of the differences in lipoprotein levels is explainable by behavioral factors. The New York City Lipid Screening Study [39] found similar results for 217 Hispanic mothers of young children (representing a wide range of Hispanic subgroups). Age-specific total and HDL-C levels were lower than those found for the general population reported for the LRC Prevalence Study; LDL-C levels were 20% lower. Further studies are needed to adequately characterize the

association between lipoproteins levels and incidence of CHD in the general Hispanic population. Another lipoprotein that may be associated with increased risk of CHD is lipoprotein(a) (Lp( a)). Lp( a) have overall characteristics similar to LDL, but the apo BlOO is linked to ape(a), which has sequence homology to plasminogen. Due to its structure, Lp(a) has both prothrombotic and proatherogenic potential and may be an important determinant in the pathogenesis of CHD. Early studies, using a less reliable assay method, found that in case-control examinations Lp( a) levels higher than 30 mg/dl were associated with increased risk of myocardial or cerebral infarction [40]. More recent studies have indicated that individuals with a serum Lp(a) level greater than 25 mg/dl have a two-fold increase in risk of

S. Harris-Hoo$wr, G. L. Sanford j’ Atherosclerosis 108 (Suppi.) (1994) S83-S104

Table 7 Lipid and lipoprotein levels by sex and age among hdexicanAmericans in Starr County, TX Sex/age group (years) Females 15-24 25-34 35-44 45-54 55-64 65-74

n

Chol

HDL

LDL

1lE 156 146 108 IO1 47

167 (2.7) 185 (2.9) 189 (3.0) 213 (4.5) 222 (4.0) 231 (6.7)

48 (1.0) 48 (0.9) 48 (0.9) 48 (1.2) 47 (1.1) 49 (1.6)

103 (2.4) II3 (2.6) 118 (2.7) 132 (4.3) 143 (4.1) 151 (6.1)

45 82 61 38 30 29

155 (5.1) 201 (4.6) 211 (6.4) 214 (6.6) 209 (6.5) 208 (8.5)

46 (1.6) 43 (1.3) 42 (1.1) 41 (2.1) 44 (2.5) 43 (1.7)

90 (4.1) 126 (3.9) 134 (6.1) 145 (5.9) 128 (6.2) 136 (6.6)

Males

IS-24 25-34 35-44 45-54 55-64 65-74

Chol, cholesterol; HDL, high density lipoprotein; LDL, low density lipoprotein. Values (mg/dl) are mean ( + S.E.M.). Adapted from: Arteriosclerosis Thromb., 1I ( 1991) 123.

myocardial infarction over controls [41]. For white males the presence of increased levels of Lp(a) is strongly associated with CHD [42]. Serum Lp(a) levels were found to be twice as high in blacks as in whites 143,441, although blacks in this study did not have increased morbidity and mortality from CHD. Both black and white patients with CHD had higher levels of Lp(: 1 (9.23 and 4.37 mg/dl, respectively) than patients without CHD (6.87 and 1.99 mg/dl, respectively) [45]. These studies suggest a weak but significantly positive correlation between Lp(a) and CHD, although the pathogenicity of Lp( a) in blacks may differ from that in whites. Little has been done to examine Lp(a) levels in the Hispanic and Native American populations. Therefore, more extensive studies are needed before definitive conclusions can be made about the racial differences in the relation of this lipoprotein to CHD. There are only a few studies that have examined the cholesterol and lipoprotein levels in Native American populations. The Southwestern American Indians have lower prevalence of CHD and lower total cholesterol than whites; the level rises

s95

little with advancing age. The overall prevalence of myocardial infarction and CHD is 25% lower than that of whites reported in the Framingham Study 1461. The study of Garnick et al. reported on the lipoprotein levels of ten American Indians and five whites [47]. The mean LDL-C level was 88.5 mg/dl for the American Indian group and 111.7 mg/dl for the control group. The apo B levels were also lower in the American Indian group than in whites (53 and 77 mg/dl, respectively). The HDL-C levels were higher for the American Indian group than for whites (56 and 37 mg/dl, respectively). These investigators measured the rates of LDL-C formation and half-life for each group and found that the American Indian group had lower rates of LDL-C formation but no difference in half-life compared with whites. Howard et al. (481 reported that total and LDL-C for nondiabetic Prima Indian men over 35 years of age and women under 25 were lower than for the white population reported in the LRC Prevalence Study; these levels did not increase with age. All Prima Indians, males and females (all ages), had lower HDL-C levels but higher triglyceride levels than those found for their white counterparts. The lower HDL-C levels are in contrast to the higher levels reported by Garnick et al. [47]. There was a strong negative correlation between obesity and HDL-C levels in the Primas, and this may account for the lower HDL-C levels in the Prima males compared with white males. These studies indicate that there are differences in the lipoprotein profiles between Native Americans and whites. However, more detailed studies are required to establish a relationship between lipoprotein levels and the prevalence of CHD for this minority population. 4. Analysis of lipid profiles in mitlority children precursors for CHD are thought to begin in childhood, there has been a great deal of interest in studying the evolution of serum lipoprotein profiles in children. As indicated above, studies in the USA have shown that CHD incidence in blacks, especially men and boys, is somewhat lower than for whites, although blacks have a greater prevalence of hypertension and other CHD risk factors than whites [49,50]. It has Since the pathologic

S. Harris-Hooker,

S96

G. L. Sonford

1 Atherosclerosis

108 (Suppl.) (1994) S83-St04

Table 8 Serum levels (mean + SD.) of HDL>-C in children by race, sex, and age group: the Bogalusa Heart Study Age

Girls

Boys

(years)

HDL?-C (mg/dl)

7-- 10

Black

White

Black

White

18 + 9 = 32) I6 + 9 (a = 67)

14 + 8 60) II + 7 (n = 132)

I5 + 8 (II = 26) I6 + 8 (n = 61)

II (n I3 (n

49 (ra 47 (II

47 & 6 (n = 60) 42 f 7 (11 = 132)

51 f 7 (II = 26) 45 f 6 (n = 61)

47 + 7 (n = 55) 43 + 6 (n = 128)

(a

II-17

HDL,-C

(mg/dl)

7-- IO II -17

+ = + =

9 32) 7 67)

(n =

& = + =

9 55) 8 128)

Race difference”

Sex difference”

P < 0.001

P <

P

<

0.001

NS

P

<

0.05

NS

P < 0.0001

0.05

NS

Source: Circulation, 76 ( 1987) 272. ;‘All Children

been suggested that increased levels of HDL-C in blacks may account for their reduced CHD risk. The variability of HDL-C levels with such factors as sex, diet, and exercise has been related mainly to modifications in a subclass of HDL-C, namely HDL2 151,521.However, very little is known about the racial differences in HDL-C sub!ractions in children. The Bogalusa Heart Study provides lipoprotein profiles of a biracial, pediatric population. It found that black-white differences in HDL-C levels appear similar in the two groups at birth [34]. The change in HDL-C arises as the children reach the preschool age: black children begin to have slightly higher levels than white children. In a related study from the Bogalusa Heart Study, cholesterol levels of serum HDL2 and HDL3 in 5to 17-year-old black and white children were examined [53]. Overall, black children had significantly higher levels of HDLZC and HDL3-C than their white counterparts (Table 8). A significant malefemale difference, with boys showing higher levels than girls, was noted among those in the younger age group for HDL2-C. This study suggests that the black-white difference in HDL-C is due to differences in HDL-C subclasses (HDL2-C and HDL3-C). A male-female crossover in HDL2-C levels occurred among white children, with girls showing lower values before age 11 and boys showing lower values after that age. This may be a constant pattern, since white women do have

higher HDLZC levels than men. A similar crossover trend was not seen for HDLZC in black children. It is also of interest to elucidate cardiovascular risk in the children of other ethnic groups. In this effort, the Bogalusa Heart Study joined investigators in the Brooks County Heart Study to examine CVD risk factors in Hispanic children in Brooks County, TX and black and white children in Bogalusa, LA [54]. Again, findings from the study indicated a higher total cholesterol level for black than for white children. The drop in levels noted earlier by the Bogalusa group for white boys during puberty seemed to occur 2 years earlier in Hispanics. These findings were basically the same for LDL-C, with the drop occurring 2 years earlier for Hispanic boys than in white or black boys. Very low density lipoprotein cholesterol (VLDLC) levels were highest in white children, starting at age 1 I - 12 for boys and 9- 10 for girls. Few differences were noted in levels for Hispanic and black children. Correlations of lipoprotein cholesterol fractions with various measures of obesity (Table 9) were also observed, including ponderal index (weight/height) j and centrality index (subscapular-triceps skinfold ratio). Significant positive associations between these various measures of obesity and LDL-C were noted, except for Hispanic girls. Similar trends were noted for VLDL-C among all the race-sex groups. Correlation co-

S. Harris-Hooker.

G. L. Satgod

1 Atherosckrosis

Table 9 Correlations between serum lipoproteins and various anthropometric Heart Study and Bogalusa Heart Study, 1984 1985 Hispanic Girls (n = 171)

0 48**“*

-0.17*

Girls (tt = 898)

Boys

Girls

(n = 484)

(n = 476)

0.28****

o-23****

0.14**

0.13**** 0.28****

0 ._70**** 0.29****

-0.07 0.23****

0.26*** - 0 ._77***

0.22**** -0.21****

0.22**** _0.21****

0.00 _0.20****

0.12** - 0.05

-0.30****

-0.19****

-0.19****

- 0.00

-0.03

0.08 0,79****

0.29**** -0.31****

Black

Boys (n = 903)

-0.00

0.32**** 0.3s****

s97

measures in children. by ethnic group and sex, Brooks County

White

Boys (n = 176) LDL cholesterol Pondera) index” Centrality index” VLDL cholesterol Ponderal index Centrality index HDL cholesterol Ponderal index Centrality index

108 (Suppl.) (19941 S83-S104

* P < 0.05; l * P < 0.001: **** P < 0.0001. LDL. low density lipoprotein; VLDL. very low density lipoprotein: a Weight (kg)/height (cm)3. b Subscapular:triceps skinfold ratio. Adapted from: Am. J. of Epidemiology. 133 ( 1991) 704.

0.19**** 0.06 0.13**

HDL. high density lipoprotein.

efficients between HDL-C and these obesity measures were all negative and significant, except those for black girls. The pattern of these risk factors in children may be predictive of CVD progression as children become adults. A survey was conducted during 1972- 1975 in Houston, TX to determine the population distribution of cholesterol, triglyceride, blood pressure,

weight, and height among high school students [55] from three major ethnic groups (black, Mexican American and white). The parents of the students were also invited to participate. The overall mean cholesterol values were highest forblacks (Table 10). Mean values for females were generally higher than those for males in all three ethnic groups. For parents, the highest overall

Table IO Plasma cholesterol: mean values and their standard deviations in mg/dl for students and for parents by age. sex and ethnicity: Houston, Texas; I972 - I975

Age

Non-Hispanic

Female

Male X f

SD.

Black

Mexican-American -

White

Female

Male II

X + S.D.

tt

X f

262 23 612

I52 f 31 149 + 31 149 f 26

24 28 I65

155 + 24 163 + 32 I55 It: 24

189+33

I75

214 + 33

6

I81 & 26

198 + 35 214 f 34 I98 f 35

398 85 658

220 + 42 213 &- 36 218 k 39

28 10 44

198 f 30 202 f 35 192+30

II

X f

S.D.

206 39 604

155 + 25 150+20 I55 + 26

SD.

Female

Male )I

X + S.D.

11

X + S.D.

II

37 9 169

I54 + 27 159+23 1.56 4 25

67 44 367

166+27 IlO+ l64+27

98 20 387

32

205 + 45

36 I2 80

212 + 38 209 _+ 38 209439

II I5 9 35

Slafients

I5 118 Overall

148 + 24 I44 _+ 25 148 k 25

Parenrs I 39

204 + 42

69

40-49 2 50 Overall

211 f 35 212 + 36 210 f 36

300 139 508

5

Adapted from: J. Chron. Dis.. 34 (1981) 105.

192 201 223 200

+ f + +

41 42 28 41

58 41 19 I18

S. Harris-Hooker,

S98

G. L. Sanford

/ Atherosclerosis

108 (Suppl.) (1994) SiU-SlO4

Table 11 plasma trigylccride: mean values and their standard deviations, in mg/dl for students and for parents by age, sex, and ethnicity: Houston, Texas; 1972- 1975 Age

Non-Hispanic

X f

S.D.

X f. S.D.

n

Students 5 15

72 f

34

206

7lf32

1 18

80 +

32

39

79 f

Overall

74 + 34

604

Parents < 39

40-49 2 50 Overall

152 153 150 152

f f f f

157 105 85 108

69 300 139 508

X

n

Male

Female

Male

Female

Male

Black

Mexican-American

White

+_

S.D.

X + S.D.

n

262

74 f

35

24

62 f

24

30

23

74 +

30

28

55 f

9

72 & 37

612

71 f

34

165

65 f

24

51 67 99 75

6 28 IO 44

97 108 127 107

+ + & &

54 74 59 68

175 398 85 658

139 140 191 151

f + f f

)i

X + S.D.

37

X

n

f

SD.

n

52 _+ 20

67

58 +

23

98

58 i

21

44

62 +

37

20

169

56 + 23

367

61 + 28

387

32 36 12 80

129f97 124 f 57 95 k 32 118 + 67

11 15 9 35

8R f 39 Y6 * 44 lOF, &- 72 94+47

58 41 19 118

9

114f60 153 f 143 179 * 153 141 + 120

Female

Adapted from: J. Chron Dis., 34 (1981) 105.

mean cholesterol value (218 mg/dl) was for Mexican American males and the lowest ( 192 mg/dl) was for Mexican American females. Among the six student groups, the triglyceride values were highest for whites and lowest for blacks (Table 11). For the parents, the triglyceride values were lower for females than for males in each ethnic group. Among the ethnic groups, the lowest sex-specific values for both students and parents were observed

for black males and for black females, and the highest sex-specific values were observed for white males and for Mexican American females. 5. Other manifestations of lipid-CHD connection The distribution of HDL-C levels varies not only with age, sex, and race but with other possible manifestations of CHD such as income, edu-

Table 12 Age-adjusteda mean HDL cholesterol (mg/dl) for adults aged 20-74 years by race, sex, and (A) income, (B) education level and (C) physical activity, United States 1976-1980 White men

Black men

White women

Black women

44.5 43.8 45.4

52.0 51.4 49.9

53.1 52.9 54.5

56.8 55.7 59.9

O-8

44.0

55.0

51.3

56.7

9-11 12 > high school

43.4 43.8 45.4

52.8 51.7 48.3

50.3 53.0 56.2

53.8 60.3 57.2

(C) Physical activity Inactive Moderately active Very active

43.1 44.4 44.7

48.4 50.6 53.5

51.7 53.3 54.1

50.2 56.6 58.3

(A) Income level < $10 000

$10 ooo-$19 999 2 $20 000 (B) Educational level (highest grade attended)

Adapted from: Am. J. Epidemiol., 129 (1989) 281. a Age-adjusted by the direct method of the 1980 US Census population.

S. Harris-Hooker, G. L. Sanford 1 Atherosclerosis 108 (Suppl.) (1994) S83-S104

0

Whl!e

s99

Men

Bladr Men a

While Women

H

Bteok Woman

60-6s

Fig. 8. Prevalence of obesity by race, age, and sex. Adapted from: Am. J. Clin. Nutr., 53 ( 1991) 1604%

cation, and physical activity. With the exception of black men, the lowest HDL-C levels were for those earning $10 000-$20 OOO/year and the highest levels were for those earning more than $20 OOO/year[36]. Black men who earned less had higher HDL-C levels, with a gradual decline with increased earnings (Table 12). Education is often used as an indicator of SES. In this study four categories of education were examined showing m5an values of HDL-C for persons who had more than a high school education, with a clear overall positive relation that was more prominent in white women than in white men. In terms of physical activity, within each sex-race group, persons who reported being very physically active had the highest age-adjusted mean HDL-C idvels. Stratifying for income, educational achievement or physical activity did not change the basic characteristics of the data, with higher mean HDL-C levels for women relative to whites; except for lower HDL-C levels among black women who were inactive compared with white women.

The question, ‘What are the ramifications of obesity in minority populations, particularly black women? needs to be examined, since obesity is thought to be one of the major determinants of HDL-C levels. The relative lack of protective higher HDL-C levels in adult black females probably is closely related to obesity. Epidemiologic evidence, however, on the relation of obesity and CVD is inconsistent. In many populations, CVD occurrences increase linearly with body size. In other populations, the relationship is U-shaped, with greatest risk of CVD in both the least obese and the most obese individuals. In yet other populations, obesity is associated with no risk or even decreased risk of CVD. While few studies exist on obesity and CVD incidence in blacks, there is strong evidence that obesity increases several CVD risk factors in blacks including plasma lipids. This association is particularly important in black women, who have almost twice the prevalence of obesity found in white women. The CARDIA and ARIC studies which do include blacks

S. Harris-Hooker, G. L. Sanford 1 Atherosclerosis 108 (Suppi.) (1994) S83-S104

SlOO Table 13 Cardiovascular

risk-factor levels by obesity categories in black men and women, CARDIA (ages 18-30) and ARK

(ages 45-65

years) Characteristic

Total cholesterol (mmol/l) Men Women LDL cholesterol (mmol/l) Men Women Triglycerides (mmol/l) Men Women HDL cholesterol (mmol/l) Men Women Apolipoprotein A-I (g/l) Men Women Apolipoprotein B (g/l) Men Women

18-30-year-old

45-64-year-old

blacks

blacks

Thin (n = 642; 564)

Intermediate (n = 304; 436)

Obese (n = 147; 423)

Thin (n = 142; 91)

Intermediate (n = 357; 347)

Obese (n = 746;1495)

4.40 + 0.85 4.47 & 0.85

4.68 + 0.93 4.68 f 0.88

4.84 & 0.93 4.73 & 0.85

5.22 + 1.14 5.35 f 1.16

5.46 + 1.09 5.66 + 1.19

5.48 f 1.14 5.69 &- 1.24

2.61 f 0.78 2.66 If: 0.80

2.95 f 0.83 2.92 + 0.83

3.18 + 0.88 3.05 + 0.80

3.00 + 1.14 2.92 f 1.14

3.49 + 1.03 3.49 f I.14

3.62 + 1.03 3.59 + 1.16

7.0 + 3.8 6.4 + 2.9

8.5 + 4.7 7.1 + 3.6

10.7 * 7.0 8.1 + 4.2

9.4 k 6.4 11.2 + 9.3

12.4 + 7.5 11.9 + 9.0

14.3 f 12.3 f

1.45 + 0.34 1.53 f 0.31

1.34 + 0.34 1.45 & 0.34

1.16 + 0.26 1.29 + 0.31

1.84 f 0.67 1.91 + 0.67

1.42 + 0.44 1.68 If: 0.52

1.24 + 0.34 1.53 + 0.41

1.44 f 1.44 f

0.22 0.23

1.40 + 0.23 1.43 + 0.22

1.29 + 0.22 1.37 * 0.21

1.52 + 0.36 1.63 & 0.47

1.34 + 0.33 1.47 f 0.34

1.26 + 0.27 1.42 f 0.32

0.84 f 0.23 0.85 + 0.22

0.94 f 0.24 0.93 _+ 0.25

1.02 + 0.26 0.96 _+ 0.26

0.80 f 0.31 0.77 -i_ 0.24

0.90 * 0.30 0.89 t_ 0.31

0.95 * 0.30 0.92 f 0.32

12.6 6.4

Number of men; number of women. Numbers vary somewhat by characteristics. Data were missing for 10% or less of all individuals. Adapted from: Am. J. Clin. Nutr.. 53 (1991) 1604s.

examined prevalence of obesity by race, age and sex. They found that 13% of black men and 30% of black women aged 18-30 years were obese, compared with 14% for white men and women. For the age group 45-65, 60% of black men and 77% of black women were obese, compared with 56% and 46% for white men and women, respectively (Fig. 8). The CARDIA and ARIC groups also examined the adverse relation of obesity to cardiovascular risk factors in blacks [56]. Their results indicate that levels of every risk factor variable were successively more severe across the three obesity categories (thin, intermediate, obese). Total cholesterol, LDL-C, triglycerides and apo B all increased across the sum of skinfold categories, whereas HDL-C and apo A-I decreased (Table

13). An analysis of the relation of anthropometric measures to lipoproteins in children again found significant positive associations between various measures of obesity and LDL-C (Table 9). The quest for factors that pertain to hyperlipidemia has been expanded to include psychosocial and bevavioral factors. Several studies have shown that certain behavioral patterns (i.e. Type A personality) and serum cholesterol are significantly related [57,58]. The association of several measures of anger and its relation to lipid and lipoprotein concentrations has also been examined. The results demonstrated a moderate association between HDL-C and the outward expression of anger, and a negative association (decreased levels) between not expressing anger and HDL concentration. As with other measur-

S. Harris-Hooker,

G. L. Smford

1 Atherosclermis 108 (Suppl.) (19941 S83-SlO4

able risks for CHD, investigations on the relation of psychosocial factors and lipid/lipoproteins levels are limited. Recently, Johnson et al. [59] examined psychological predictors of lipids in healthy blacks and found that HDL-C, LDL-C and triglycerides were significantly associated with certain measures, namely, state and trait curiosity and trait anger. State curiosity is a subscale for measuring the intensity of curiosity, and trait curiosity and anger are subscales which require respondents to report the frequency of expericncing feelings of anger, curiosity, etc. Hispanics may also differ from other populations at high risk for CHD in a range of psychosocial factors, such as motivational orientation toward work and life in general, available social support mechanisms, and stress levels; behavioral variables including smoking, alcohol consumption and exercise; and family history of CHD and chronic diseases [60-621. In terms of behavioral characteristics, more non-Hispanics than Hispanics were smokers, and more non-Hispanic women than Hispanic women consumed alcohol frequently. Non-Hispanics were more likely than Hispanics to exercise recreationally; however, there was little diffbrence between the two groups in physical activity at work. The mean scores on CHD risk factors indicate no difference between the two groups on psychosocial stress index. Hispanic men had the highest triglyceride and serum cholesterol levels. As expected from the men and mortality studies, the non-Hispanic women reported a positive family history of CHD more frequently than the Hispanic men and women. 6. Summary and conclusions Even with the dramatic decrease in CHD mortality that has occurred since 1968, there is reason for concern about the level of CHD in the USA. CHD is still the leading cause of death in the USA; mortality rates from CHD are still higher than those in many other countries and recent evidence points to a leveling off in the rate of decline in CHD mortality for all blacks, especially black women. It has been estimated that more than ha.lf of the decline in CHD mortality be-

SIOl

tween 1968 and 1976 was related to changes in lifestyle, particularly serum cholesterol levels. Numerous epidemiologic and laboratory studies have confir.med the continuous, positive correlation of elevated serum levels to increased CHD risk. Clinical studies have shown that modification of serum cholesterol by diet or drugs can lower risk. The benefit of lowering serum cholesterol levels extends to men and women, young and old, those with high-risk LDL-C levels and those with borderline high-risk levels. The data available on minorities appear to indicate that this extension would include them as well, but there is a need for further studies on minority populations in order to make such powerful conclusions about the lipid/lipoprotein connection in this group of individuals. A broad variety of sociocultural, demographic, and habitat variables may play a role in CHD protection in minorities, but the most convincing and consistent biologic data for blacks suggest that higher HDL-C and lower triglyceride levels in blacks than in whites may be major factors. Some investigators even suggest that when advising patients about steps they might take to reduce their risk for CHD, a summary of the factors that appear to increase and decrease HDL-C level would be useful. Factors that increase HDL-C are behavio;.al or hygienic factors, such as leanness, alcohol intake and exercise, as well as estrogen replacement therapy. Factors that decrease HDL level include obesity, cigarette smoking, androgens, inactivity and use of thiazide diuretics. In addition, cardiovascular medications such as alpha and beta blockers are now being evaluated with regard to their effects on HDL-C and, more recently, apo Al. Hispanics have been reported to have low CHD mortality rates. There is a need for additional research into CHD mortality among Hispanics to confirm the low rates observed in previous investigations and to explore the reasons for the low rates. Cardiovascular risk factor observations of children are important in understanding the development of heart disease in adulthood. The lack of thorough prospective studies of risk factors for CHD in minorities, comparative studies of lipoprotein metabolism in healthy men.

S. Harris-Hooker,

s102

G. L. Sanford

/ Atherosclerosis

women and children, and prospective studies relating plasma lipoprotein concentrations, other physiological and behavioral risk factors to the development of CHID all remain serious omissions in our understanding of the pathogenesis of the major cause of death in r?rc USA.

[ISI

[I61

1171

References [I81

III PI

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t41

[51

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PI

PI

1101 [III

[I21 [I31

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S. Harris-Hooker, G. L. Sanford 1 Atherosclerosis IO8 (Suppl.) (1994) S83-S104

I301 Anderson, K.M., Castelli, W.P., Levy, D.L., Cholesterol

1311

1321

[331

I341

[351

1361

I371

[381

[391

1401

[411

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