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(Hypertension. 2001;37:1242.)
© 2001 American Heart Association, Inc.
Scientific Contributions |
Alcohol Consumption and the Incidence of Hypertension
The Atherosclerosis Risk in Communities Study
From the Division of Cardiology, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Rio Grande do Sul (F.D.F.), Brazil; the Department of Biostatistics (L.E.C.) and the Department of Epidemiology (G.H.), School of Public Health, University of North Carolina, Chapel Hill; School of Public Health and Tropical Medicine, Tulane University Medical Center (P.K.W.), New Orleans, La; and the Department of Epidemiology, The Johns Hopkins University School of Hygiene and Public Health (F.J.N.), Baltimore, Md. Dr Fuchs was, at the time of preparing this manuscript, a visiting professor at the Welch Center for Prevention, Epidemiology and Clinical Research, The Johns Hopkins University, Baltimore, Md.
Correspondence to Flávio Danni Fuchs, MD, PhD, Serviço de Cardiologia, Hospital de Clínicas de Porto Alegre, Ramiro Barcelos, 2350, 90.035-003, Porto Alegre, RS, Brazil. E-mail ffuchs{at}hcpa.ufrgs.br
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Abstract |
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Abstract—A close relationship between alcohol consumption and hypertension has been established, but it is unclear whether there is a threshold level for this association. In addition, it has infrequently been studied in longitudinal studies and in black people. In a cohort study, 8334 of the Atherosclerosis Risk in Communities (ARIC) Study participants, aged 45 to 64 years at baseline, who were free of hypertension and coronary heart disease had their blood pressures ascertained after 6 years of follow-up. Alcohol consumption was assessed by dietary interview. The type of alcoholic beverage predominantly consumed was defined by the source of the largest amount of ethanol consumed. Incident hypertension was defined as a systolic blood pressure
140 mm Hg or
diastolic blood pressure 90 mm Hg or use of
antihypertensive medication. There was an increased risk of
hypertension in those who consumed large amounts of ethanol (210 g
per week) compared with those who did not consume alcohol over the 6
years of follow-up. The adjusted odds ratios (95% confidence interval)
were 1.2 (0.85 to 1.67) for white men, 2.02 (1.08 to 3.79) for white
women, and 2.31 (1.11 to 4.86) for black men. Only 4 black women
reported drinking >210 g ethanol per week. At low to moderate levels
of alcohol consumption (1 to 209 g per week), the adjusted odds
ratios (95% confidence interval) were 0.88 (0.71 to 1.08) in white
men, 0.89 (0.73 to 1.09) in white women, 1.71 (1.11 to 2.64) in black
men, and 0.88 (0.59 to 1.33) in black women. Systolic and
diastolic blood pressures were higher in black men who
consumed low to moderate amounts of alcohol compared with the
nonconsumers but not in the 3 other race-gender strata. Models with
polynomial terms of alcohol exposure suggested a nonlinear association
in white and black men. Higher levels of consumption of all types of
alcoholic beverages were associated with a higher risk of hypertension
for all race-gender strata. The consumption of alcohol in amounts 210
g per week is an independent risk factor for hypertension in
free-living North American populations. The consumption of low to
moderate amounts of alcohol also appears to be associated with a higher
risk of hypertension in black men.
Key Words: hypertension, alcohol-induced • risk factors • alcohol
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Introduction |
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Epidemiological and experimental investigations have established a close association between alcohol consumption and hypertension.1 Among the >50 epidemiological studies that have addressed this question, some have recorded a linear dose-response relationship, sometimes starting with a consumption threshold of 3 drinks per day (30 g of ethanol).2 3 4 5 6 7 8 9 10 11 12 13 14 In others, the relationship has been nonlinear, especially in women, and some authors have speculated that ingestion of smaller quantities of alcohol may reduce blood pressure.15 16 17 18 19 20 21 22 23 These discrepancies may reflect differences in investigational design, methods, and populations. Only a few studies have been longitudinal15 24 25 26 27 ; in most, alcohol consumption has been assessed on only one occasion; in some, habitual alcohol consumption has been insufficiently assessed; and in others, there has been insufficient control for putative risk factors for hypertension. The association between blood pressure level and type of alcoholic beverage and the influence of time since the consumption of alcohol on the relationship have received only limited attention.14 Although the relationship between alcohol consumption and level of blood pressure has been addressed in studies conducted in populations from a variety of geographic regions, there are limited data from studies conducted in blacks.3 4 5 6
The Atherosclerosis Risk in Communities (ARIC) Study cohort28 provides an excellent opportunity to examine the nature of the association between consumption of ethanol and the subsequent development of hypertension. In addition to a longitudinal design and random selection of free-living individuals, the ARIC Study provides a special opportunity to evaluate the association in different ethnic and gender strata. We present the relationship between alcohol consumption and the subsequent occurrence of hypertension in the ARIC cohort.
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Methods |
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Study Population
The design of the ARIC Study has been described in previous publications.28 The overall ARIC Study cohort consists of 15 792 persons aged 45 to 64 years at their baseline examination (visit 1), approximately one fourth of whom were selected from 4 communities in the United States: Forsyth County, NC; Jackson, Miss; selected suburbs of Minneapolis, Minn; and Washington County, Md. The latter 2 communities are predominantly white. Only blacks were sampled in Jackson, whereas 12% of the study sample from Forsyth County were black. The response rate was 46% of eligible individuals in Jackson and
65% in the other 3 communities.
Baseline data were collected between 1987 and 1989 (visit 1).
Participants underwent reexamination in 1990 to 1992 (visit 2, 93%
return rate) and 1993 to 1995 (visit 3, 86% return rate).
Our analyses were restricted to the participants who
were self-described as black or white. After exclusion of those with
hypertension (blood pressure 140/90 mm Hg and/or treatment with
antihypertensive medication) or coronary heart disease at their
baseline examinations and of those who died during follow-up, a total
of 8334 participants had their blood pressure and hypertension
medication use ascertained at the time of the third follow-up
examination and constitute the sample for the present
analysis.
Measurements
Alcohol Consumption
Alcohol consumption was ascertained at all visits by
means of an interviewer-administered dietary questionnaire. Subjects
were asked whether they currently drank alcoholic beverages and, if
not, whether they had done so in the past. Current drinkers were asked
how often they usually drank wine, beer, or hard liquor. In calculating
the amount of alcohol consumed (in grams per week), it was assumed that
4 oz of wine contains 10.8 g, 12 oz of beer contains 13.2 g,
and 1.5 oz of liquor contains 15.1 g of ethanol.
The type of alcoholic beverage predominantly consumed was defined when the amount of ethanol of one type of beverage (wine, beer, or liquor) corresponded to two thirds or more of the total amount of ethanol consumed.
Blood Pressure and Incidence of
Hypertension
Sitting blood pressures were measured after 5 minutes
of rest by use of a Hawksley random-zero sphygmomanometer. The average
of the second and third of 3 measurements was used in the
analyses. Systolic and diastolic blood
pressures are defined as the first and the fifth Korotkoff sounds.
Participants were asked not to smoke or to consume coffee, tea, or
chocolate for 4 hours before their clinic appointment. Study
technicians were trained in the measurement of blood pressure with the
use of Korotkoff sound tapes and a double stethoscope. They were
retrained and recertified every 6 months. Digit preference and
systematic differences between technicians were monitored. Presumed
problems were discussed with the staff at the field centers, and
additional retraining was provided when needed.
Individuals were classified as having hypertension at the
time of visit 3 if they had a systolic blood pressure
140 mm Hg or a diastolic blood pressure 90
mm Hg or if they reported taking antihypertensive
medication.
Measurement of Other Baseline
Covariates
Home and clinic interviews included assessment of
educational level (highest grade completed), cigarette smoking, the
presence of diagnosed cardiovascular disease or
diabetes, and parental history of hypertension. An index of physical
activity in sports (sport index), ranging from 1 (low) to 5 (high), was
derived by using the physical activity questionnaire of Baecke et
al.29 Anthropometric
measurements were carried out with participants wearing light clothing
and no shoes. Body mass index (BMI) was calculated as weight in
kilograms divided by height in meters
squared.
Statistical Analysis
All of the analyses were conducted within 4
race- and gender-specific strata (white men and women and black men and
women). The magnitude and shape of the associations were
analyzed by considering hypertension (present/absent) and
systolic and diastolic blood pressures as separate
dependent variables. The crude association between incident
hypertension and alcohol consumption was explored first by strata of
alcohol consumption over intervals of 70 g per week, considering
the average of the amount reported at the time of visits 1 and 2. The
amount determined at one of these visits was used for participants with
missing values for the other. The overall agreement between the
classification of individuals based on intervals of 70 g of
ethanol consumption per week, calculated with the data from visit 1 and
the average of both visits, was 89%. The estimates arising from
average exposure were more stable and were used in the
analyses. An additional analysis used only consumption
at visit 2 to avoid the possibility of a deterioration in health
leading to reduced alcohol consumption.
The 70-g intervals were subsequently pooled according to similarity of risk and the availability of a reasonable sample size in each race-gender stratum. The association between the incidence of hypertension and previous exposure to ethanol was analyzed by means of multiple logistic regression modeling, controlling for several risk factors for hypertension, including age, educational achievement, BMI, diabetes, and physical activity. Use of the waist-to-hip ratio instead of BMI and of the baseline serum insulin level instead of diagnosis of diabetes did not change the results substantially. Inclusion of smoking history, baseline blood pressure, parental history of hypertension, a variety of nutritional variables (including dietary sodium, potassium, calcium, magnesium, fibers, carbohydrates, and saturated and unsaturated fatty acids), and serum levels of sodium, potassium, calcium, and magnesium did not change the estimates substantially, and these variables were excluded from the final model. Interaction terms between exposure to ethanol and other variables were included in separate models, but none reached statistical significance. The association between type of beverage predominantly consumed and incidence of hypertension was examined in similar models, controlling for the amount of ethanol consumed and also considering the interaction between the amount of ethanol and type of beverage.
Simple and multiple linear regression models, with tests for nonlinearity, were used for the analysis of the relationships between both systolic and diastolic blood pressures and alcohol consumption.30 Blood pressure means were compared by ANCOVA. The covariates were those previously described. In all analyses with blood pressure as the dependent variable, the individuals taking antihypertensive medication at visit 3 were excluded. All analyses were performed with SPSS, version 7.0.31
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Results |
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Race- and gender-specific distributions for several baseline characteristics are presented in Table 1. The proportion of individuals who were overweight according to World Hypertension League criteria32 (BMI
25
kg/m2) varied from 47.4% (white women) to
77.7% (black women). The prevalence of diabetes and incidence of
hypertension were higher among blacks than whites. For both genders,
the percentage of current drinkers was higher for whites than for
blacks. In most race-gender strata, the 6-year incidence of
hypertension varied by levels of several characteristics, including
age, BMI, education, drinking status, parental history of hypertension,
and diabetes mellitus
(Table 2).
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A crude and multivariate analysis of
the relationship between incidence of hypertension and alcohol
consumption among the 4 race-gender strata is presented in
Table 3. Analysis with 6 intervals of exposure to
ethanol (none and 1 to 69, 70 to 139, 140 to 209, 210 to 279, and 280
g per week) yielded a similar association between the incidence of
hypertension and alcohol consumption at the several levels in the range
of 1 to 209 g per week. A different association was observed for
those in the 210 g per week category. Therefore, the intervals of
alcohol consumption were pooled in the 3 categories presented
in
Table 3. A contrasting association between low to moderate
alcohol consumption and incidence of hypertension was evident for black
men compared with the other 3 race-gender strata. In unadjusted
analysis, consumption of low to moderate amounts of alcohol
appeared to provide protection in white men and women and in black
women, but low to moderate consumption was associated with an increased
risk of hypertension in black men. This pattern of association with low
to moderate alcohol consumption persisted after adjustment for several
risk factors for hypertension but was formally significant only in
black men. In the 3 race-gender strata in which it was possible to
study the effect of a higher consumption of alcohol compared with
nondrinking, there was an increased risk of hypertension in both
univariate and multivariate
analyses (statistically significant in black men). Adjusting
for baseline systolic blood pressure reduced the size of the
estimates slightly in some race-gender strata.
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A systematic underreporting of alcohol consumption by white men who denied drinking could explain the J-shaped association noted in the previously mentioned analyses. To explore the reliability of our measurement of alcohol consumption, we examined mean HDL cholesterol levels across the 3 alcohol intake ranges and the 6 increments of 70 g per week of alcohol intake identified in Table 4, in accordance with the well-known relationship between alcohol consumption and HDL levels. With both analyses, either for the whole sample or for the stratum of white men on its own, a consistent, monotonic, "dose-response" curve was observed, with significantly higher values of HDL cholesterol found in those with a progressively higher consumption of alcohol. For example, white men who reported no intake of alcohol had a mean HDL cholesterol of 40.7±10.6 mg/dL compared with 45.1±12.3 and 51.4±14.9 mg/dL for those who consumed between 1 and 209 g and >210 g per week, respectively (P<0.001 by ANOVA, P<0.001 in all post hoc Scheffé tests).
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Consumption of 210 g ethanol per week (3 drinks per
day) was associated with an increased risk of hypertension in the 4
race-gender strata combined. The odds ratio was 1.47 (95% CI 1.15 to
1.89) after adjustment for race, age, BMI, education, sport index, and
diabetes. The attributable risk (unadjusted) of developing hypertension
among those exposed to >30 g ethanol per day was 17.1%. The
attributable risk for the total ARIC population was 0.9%, because only
385 of the study participants (4.6% of the cohort) consumed at least
210 g ethanol per week.
The contrast between white and black men in their association between ethanol consumption and incidence of hypertension persisted in additional analyses. Among 102 white men who started drinking small amounts of ethanol between visits 1 and 2, the incidence of hypertension was 13.7%. Among 285 who stopped drinking alcohol during this period, the corresponding incidence was 18.2%. Although the number of participants in each category was small, an opposite trend was observed in black men. Specifically, 40.9% of the 22 subjects who started drinking developed hypertension by visit 3 compared with 31.6% of 57 individuals who stopped drinking between visits 1 and 2.
Stratification of the data by age (dichotomized at 50 years) suggested that the alcohol–blood pressure relationship was independent of age for the entire ARIC population and for those in each of the 4 race-gender strata (data not shown).
To exclude the possible influence of a diagnosis of hypertension at the time of visit 2 on the pattern of alcoholic beverage consumption, an analysis was carried out to determine the cumulative incidence of hypertension at the time of visit 3, according to the level of alcohol consumption at visit 2, excluding those already hypertensive at that point. Among white men, the incidence of hypertension in those who abstained from alcohol consumption, those who consumed between 1 and 209 g per week, and those who consumed >210 g per week at visit 2 was 11.0%, 8.1%, and 16.7%, respectively (P<0.001 for the difference between groups). The corresponding figures for black men were 15.4%, 19.5%, and 31.3%, respectively (P for linear trend<0.029). The pattern among women was similar (data not shown).
Given the curvilinearity of the relationship between alcohol consumption and blood pressure in some of the race-gender strata, the risk of hypertension was estimated by using quadratic or cubic terms for exposure to alcohol, excluding those participants taking antihypertensive medication at visit 3. In white men, the cubic term of alcohol exposure was statistically significant for systolic blood pressure (data not shown). For diastolic blood pressure, the inclusion of higher-order terms was not significant, suggesting a linear association. In black men, for both systolic and diastolic blood pressure values, higher-order terms were significant, suggesting nonlinearity. Among women, only the modeling for diastolic blood pressure in whites reached statistical significance, and it also suggested nonlinearity.
The pattern for the association between alcohol consumption and systolic and diastolic blood pressures when the exposure to ethanol consumption was stratified according to 6 levels of alcohol consumption is presented in Tables 4 and 5. In white men, lower systolic blood pressures were noted at modest levels of alcohol consumption, and higher blood pressures were noted at higher levels of alcohol consumption. The pattern observed for diastolic pressure among white men and for both systolic and diastolic blood pressures in white women was similar, with lower blood pressure values being noted at lower levels of ethanol consumption and higher values being noted at higher levels of ethanol consumption. In black men, both systolic and diastolic blood pressures were higher at moderate levels of alcohol consumption. Adjusted differences were 10.6 and 8.7 mm Hg for systolic blood pressure and 3.4 and 2.5 mm Hg for diastolic blood pressure for black men consuming 2 or 3 drinks per day compared with their counterparts who were nondrinkers, respectively. The low frequency and amount of ethanol consumed by black women precluded the ability to draw any meaningful conclusions in this group. The associations in white and black men are represented in the Figure.
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The odds ratios of hypertension according to type of
beverage predominantly consumed by those in the 4 race-gender strata
are presented in
Table 6. At low to moderate levels of alcohol consumption,
the overall tendency for white men and women and for black women was
for a reduced risk of hypertension with most beverages, but in most
cases, the confidence limits included the null hypothesis. In black
men, the tendency was in the opposite direction. Estimates for wine
drinkers were unreliable for black men because of their small number.
At higher levels of alcohol consumption (210 g per week), most types
of beverage preference in all of the race-gender strata were associated
with an increased risk of developing hypertension, but again, in most
instances, the association was not statistically significant. To
explore the possibility that residual confounding could be responsible
for some of the differences within certain race-gender strata, the
levels of alcohol consumption were split into 70 g per week
strata. This did not materially affect the size of the
estimates.
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Discussion |
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The ARIC longitudinal study in 4 US communities provided an opportunity to examine some important questions surrounding the relationship between alcohol consumption and blood pressure. Our overall findings are consistent with the proposition that consumption of large amounts of ethanol is an independent risk factor for hypertension. The association between consumption of
210 g
alcohol per week and the subsequent incidence of hypertension was
statistically significant for the sample as a whole. It was also
significant in the subgroup of black men who were drinking 210 g
alcohol per week. In whites, there was a tendency for an increased risk
of developing hypertension, but it did not achieve statistical
significance. The small number of participants drinking 210 g ethanol
per week precluded a meaningful assessment of such risk among black
women. The attributable risk of 19% among consumers of 210 g alcohol
per week (3 drinks per day) suggests that 1 in 5 cases of
hypertension among heavy users of ethanol may be due to alcohol
consumption. The relatively low attributable risk for the sample as a
whole is explained by the relatively low frequency of current heavy
drinkers of alcohol in the ARIC Study population. Our results indicate that the relationship between alcohol consumption and blood pressure is apparent across several types of alcoholic beverages. The variation in blood pressure associations by predominant type of alcoholic beverage may have been due to the effect of chance, but one cannot rule out a variation in the effect of the beverages in different race-gender strata. Alternatively, the differences in risk may have merely reflected the effect of a more general behavior associated with the kind of preference in alcohol consumption.
Our principal finding was the association between the consumption of low to moderate amounts of ethanol (up to 3 drinks per day) and either the incidence of hypertension or increase in blood pressure levels in blacks. In white men, there was no evidence of an increase in systolic or diastolic blood pressure over time at this level of consumption. Similarly, for most beverages, a low to moderate intake of alcohol was not associated with a higher incidence of hypertension in white men and with an increased incidence in black men.
The validity of self-reported alcohol consumption has been questioned.33 An underestimation of alcohol intake across the entire cohort, or selectively in heavy users, could have resulted in an underestimation of the level of alcohol consumption at which blood pressure starts to increase, but it would not have changed the slope of the association. The possibility that the higher incidence of hypertension in white men who reported no alcohol consumption might have reflected underreporting of intake, as suggested by Klag et al12 for American men, seems unlikely. There is no reason to believe that such behavior would be restricted to white men because this pattern was not observed in black men. The strong association between HDL cholesterol levels (a proxy for alcohol use) by category of alcohol intake and the overall agreement between classification of the participant’s alcohol intake at visit 1 compared with the average of visits 1 and 2 strengthens the interpretation that the questionnaire that was given to the ARIC participants captured alcohol consumption reasonably well.
The possibility that the presence of hypertension or other conditions could have influenced the pattern of alcohol consumption was addressed in several ways. First, participants with prevalent coronary artery disease at baseline were excluded, and diabetes was taken into account in the multivariate analysis. The association between incidence of hypertension at visit 3 and level of exposure at visit 2, excluding those who were already hypertensive at the second visit, was even stronger than the corresponding relationship when the exposure to alcohol was measured in visit 1. This finding strengthens the interpretation that the effect of alcohol on blood pressure is transitory and most closely related to an individual’s current pattern of consumption.14 34
Various nutrients (including sodium, potassium, calcium, magnesium, fibers, carbohydrates, and saturated and unsaturated fatty acids) and serum levels of electrolytes and lipids were not associated with the incidence of hypertension in this cohort, nor did they modify the associations between alcohol exposure and the incidence of hypertension. A specific interaction between the effects of alcohol and calcium intake, suggested in some35 36 but not in all37 previous studies, was not noted in the ARIC cohort.
Few studies have reported an association between alcohol consumption and blood pressure in blacks. In the Kaiser-Permanente Study,5 blacks undergoing multiphasic health examinations had a less pronounced alcohol-blood pressure association than did their white participants. In the Coronary Artery Risk Development in Young Adults (CARDIA) Study, the pattern of association between alcohol intake and blood pressure was similar in blacks and whites3 ; the black-white blood pressure differences were attributed mainly to BMI and not to ethanol consumption, per se.38 In a population-based cross-sectional survey of black men in Pitt County, NC, Strogatz et al4 observed a direct and strong relationship between alcohol intake and both systolic and diastolic blood pressures in men and women. The strength of the association in black men was almost of the same magnitude as that observed in the ARIC population. In the follow-up of the Pitt County cohort, a change in drinking status was significantly associated with concurrent change in blood pressure level, with an increase in blood pressure being noted in those who started drinking and a corresponding reduction in those who stopped drinking.39
The findings in black men in the ARIC population and in black men and women in the Pitt County study may be due to an unknown confounding factor. The influence of changing the pattern of drinking or the occurrence of a binge pattern on the association between alcohol, blood pressure, and hypertension incidence in black men cannot be excluded. We are not aware of any description of a higher alcohol sensitivity in blacks, as has been demonstrated in Asians.40 If our finding is confirmed in other epidemiological surveys or in intervention studies, this mechanism should be added to those already proposed as explanations for the higher incidence of hypertension in blacks.41 To date, there has not been any intervention study clearly demonstrating the effects of alcohol consumption in different race-gender strata.
The mechanism of alcohol-induced hypertension is unclear.1 34 Effects on the renin-angiotensin-aldosterone axis, adrenergic nervous system discharge, heart rate variability, ionic fluxes, cortisol secretion, or insulin sensitivity have been proposed as underlying mechanisms of action. The large number of such hypotheses suggests that none is sufficient to explain the relationship. Furthermore, any such mechanism must reconcile the acute vasodilator effect of ethanol with a longer-term increase in blood pressure. The possibility of a biphasic effect of alcohol on blood pressure, as observed by Kawano at al42 in Japanese patients with essential hypertension and recently described in non-Asians43 and free-living individuals,14 is appealing.
Our findings have potential implications for both public health and medical practice. Based on the evidence of a protective effect against coronary heart disease derived from the consumption of low to moderate amounts of ethanol,44 the observation that low amounts of alcohol intake may not increase blood pressure in most race-gender strata could lead to a more tolerant view of the consumption of alcohol in small amounts on the part of physicians and the media. Although this may be reasonable for whites, it may not be appropriate for blacks, at least with respect to the risk of developing hypertension. The consequences of the competing effects of alcohol on risk factors for coronary heart disease in blacks, favorable for blood lipids and detrimental for blood pressure, deserve greater attention.
Caution is warranted in generalizing these findings beyond the ARIC population. Although our observations in white men and women are consistent with those reported by several other investigators, the pattern seen in the black men examined in the ARIC Study has been reported only once before4 and warrants replication. It should also be noted that the sample of blacks enrolled in the ARIC Study is predominantly urban and was drawn predominantly from 1 city. At this point, generalization to African Americans as a whole may be premature.
In conclusion, we have demonstrated that consumption of
210 g alcohol per week is a risk factor for hypertension in
free-living North American populations, independent of race, gender,
age, and other risk factors for hypertension. The consumption of low to
moderate amounts does not appear to increase substantially the risk of
hypertension in whites, whereas it is associated with an increased risk
of hypertension in black men. Further race-specific studies on the
alcohol and hypertension relationship are warranted. In the interim, we
recommend taking a cautious view regarding the health effects of a low
to moderate intake of ethanol in
blacks.
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Appendix 1 |
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The ARIC Study is carried out as a collaborative study supported by the National Heart, Lung, and Blood Institute. The following is a partial list of participating personnel at the ARIC study centers: University of North Carolina Coordinating Center, Chapel Hill: Jeffery M. Abolafia, MS, Nancy Y. Anderson, MS, and Hope E. Bryan, MS; University of North Carolina at Chapel Hill: Kay Burke, Amy Haire, and Phyllis Johnson; Wake Forest University, Winston-Salem, NC: Kelli Collins, Delilah Cook, and Bob Ellison; University of Mississippi Medical Center, Jackson: Barbara L. Davis, Starlee Hayes, and Mattye L. Watson; University of Minnesota, Minneapolis Center: Collette Cosgiff, Maxine Dammen, and Christine Dwight; The Johns Hopkins University, Baltimore, Md: Joyce Chabot, Carol Christman, and Dorrie Costa; University of Texas Medical School, Houston: Harinder Juneja, MD, Johnna Kincaid, and Susan Mitterling; and Methodist Hospital, Atherosclerosis Clinical Laboratory, Houston, Tex: Manish Dhami, Charlie Rhodes, and Julita Samoro.
Received July 10, 2000; first decision August 9, 2000; accepted November 6, 2000.
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