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American Journal of Epidemiology Advance Access originally published online on October 13, 2006
American Journal of Epidemiology 2006 164(12):1150-1159; doi:10.1093/aje/kwj341
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American Journal of Epidemiology Copyright © 2006 by the Johns Hopkins Bloomberg School of Public Health All rights reserved; printed in U.S.A.

ORIGINAL CONTRIBUTIONS

Value of the Sagittal Abdominal Diameter in Coronary Heart Disease Risk Assessment: Cohort Study in a Large, Multiethnic Population

Carlos Iribarren1,2, Jeanne A. Darbinian1, Joan C. Lo1,3,4, Bruce H. Fireman1 and Alan S. Go1,2,4

1 Division of Research, Kaiser Permanente of Northern California, Oakland, CA
2 Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA
3 Endocrinology and Metabolism Section, San Francisco General Hospital, San Francisco, CA
4 Department of Medicine, University of California, San Francisco, San Francisco, CA

Correspondence to Dr. Carlos Iribarren, Division of Research, Kaiser Permanente of Northern California, 2000 Broadway, Oakland, CA 94612 (e-mail: cgi{at}dor.kaiser.org).

Received for publication March 13, 2006. Accepted for publication April 28, 2006.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Whether visceral obesity predicts coronary heart disease (CHD) risk above and beyond overall fatness remains unsettled. Moreover, whether the association between visceral obesity and CHD risk differs by sex, age, race, and overall fatness is poorly understood. The authors conducted a cohort study among 101,765 adult members of Kaiser Permanente of Northern California who underwent multiphasic health checkups between 1965 and 1970. After a median of 12 years and adjustment for age, race, body mass index (BMI), educational level, smoking, alcohol consumption, and hormone replacement therapy (in women), the upper quartile of standing sagittal abdominal diameter, relative to the lowest quartile, was associated with a 1.42-fold increased hazard of CHD in men (95% confidence interval: 1.30, 1.55) and a 1.44-fold increased hazard of CHD in women (95% confidence interval: 1.30, 1.59). Further adjustment for metabolic mediators attenuated the association minimally. Standing sagittal abdominal diameter was a consistent predictor of CHD across racial groups but was more strongly associated with CHD in the younger age group. Joint consideration of BMI/standing sagittal abdominal diameter categories better discriminated risk of CHD compared with use of BMI alone. In conclusion, standing sagittal abdominal diameter was a strong predictor of CHD independently of BMI and added incremental CHD risk prediction at each level of BMI.

abdominal fat; body mass index; cohort studies; coronary disease; obesity

Abbreviations: BMI, body mass index; CHD, coronary heart disease; SAD, sagittal abdominal diameter


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Visceral obesity has been associated with metabolic abnormalities (1, 8) that increase the risk of type 2 diabetes and coronary heart disease (CHD) (9–16). However, whether visceral obesity predicts CHD risk above and beyond overall fatness remains unsettled (17). Furthermore, the degree to which the association between visceral obesity and CHD risk differs by sex, age, race, and level of overall fatness remains poorly understood (18).

Several studies suggest that sagittal abdominal diameter (SAD, a simple anthropometric index of visceral obesity) is a better correlate of obesity-related metabolic disturbances, particularly of insulin resistance, than body mass index (BMI), waist circumference, or waist-to-hip ratio (19, 20). However, to our knowledge, only two previous cohort studies have reported on the relation between SAD and CHD (21, 22).

BMI is a commonly used index of relative weight (23). It is easy to measure and allows consistent definitions of overweight and obesity across populations. However, BMI does not accurately reflect regional fat distribution. Hence, the BMI categories recommended by the World Health Organization (23) may include people who might differ greatly, depending on the degree of visceral adiposity, in terms of CHD risk.

In this study, we sought to address the following three research questions in a large, multiethnic, population-based cohort: 1) Is the association between standing SAD and CHD independent of BMI and traditional risk factors? 2) Does the relation between standing SAD and CHD vary by sex, age, race, or BMI level? and 3) Does the joint consideration of BMI and standing SAD provide better risk stratification than use of BMI alone?


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 References
 
Study cohort and procedures
The source population consisted of Kaiser Permanente of Northern California subscribers who attended voluntary multiphasic health checkups at the Kaiser Permanente Oakland and San Francisco Medical Centers between 1965 and 1970. Kaiser Permanente is an integrated health care delivery system providing medical care for about one third of the population in the San Francisco Bay Area. Kaiser Permanente subscribers are representative of the region, although the extremes of income are underrepresented (24).

The multiphasic health checkup was a visit to an automated multitest laboratory to complete questionnaires and clinical and laboratory tests (25, 26). Information on age, sex, race, educational level, height and weight, cigarette smoking, alcohol consumption, systolic and diastolic blood pressures, fasting serum total cholesterol, history of physician-diagnosed hypertension and diabetes mellitus, use of antihypertensive medication and of insulin or oral hypoglycemic agents, and use of hormone replacement therapy was collected by using self-administered questionnaires and standardized laboratory methods (25, 26). Hypertension was defined as systolic blood pressure of ≥140 mmHg and/or diastolic blood pressure of ≥90 mmHg and/or self-reported physician-diagnosed hypertension and/or use of antihypertensive therapy. Diabetes was defined by self-reported physician-diagnosed diabetes and/or use of insulin or oral hypoglycemic agents. No data were available on fasting blood glucose or insulin levels. The SAD, the distance between the back surface and the top of the abdomen midway between the lower rib margin and the superior anterior iliac crest, was measured with an anthropometer after a gentle expiration by the patient in a standing position (26). No concurrent measures of waist or hip circumferences were taken, and no assessments of usual diet or physical activity level were carried out. Renal function was assessed as glomerular filtration rate estimated by the Modification of Diet in Renal Disease Study formula (27). When data from more than one multiphasic health checkup visit were available, only those from the last or most current visit were used.

The study cohort is a subset of a larger sample of 144,749 Kaiser Permanente members who attended the multiphasic health checkup between 1965 and 1970. We sequentially excluded 2,130 persons less than age 18 years; 5,513 persons of "other" or missing race; 31,353 for whom BMI or standing SAD measurements were missing; and 3,988 who self-reported CHD, had been hospitalized for CHD, or died prior to 1971. Thus, the final analytic sample comprised 101,765 subjects.

The incidence of hospitalizations for CHD (International Classification of Diseases, Eighth and Ninth Revision codes 410–414) was determined by using primary hospital discharge diagnoses from January 1, 1971, through December 31, 2003. When a recurrent hospitalization with the same code occurred, only the first event was selected. The validity of ascertaining CHD by using our automated hospital discharge files has been documented elsewhere (28). Deaths from 1971 through the end of 2003 were ascertained by using the California Automated Mortality Linkage System (CAMLIS), which has a sensitivity of 0.97 compared with the National Death Index (29). For the period 1971–1998, the underlying cause of death was categorized according to the International Classification of Diseases, Eighth and Ninth Revision codes noted above. For deaths in 1999–2003, International Statistical Classification of Diseases and Related Health Problems, Tenth Revision codes I20–I25 were used. Person-time was calculated as years elapsed from January 1, 1971, to CHD hospitalization, death, closing date, or termination of health plan membership before the closing date, whichever occurred first. About 12 percent of participants were censored because of an incident CHD event (hospitalization or death), 16 percent because of death from any cause, and 53 percent because of termination of health plan membership; 19 percent were censored at the end of the follow-up period. The median follow-up time was 12 years (range, <1–33 years). The research protocol was approved by the Kaiser Foundation Research Institute Institutional Review Board, and all study participants gave written informed consent for the use of their multiphasic health checkup data for research purposes.

Statistical analysis
All analyses were conducted separately for men and women. We first used descriptive statistics and compared characteristics by quartiles of standing SAD. The significance of bivariate associations was examined by using analysis of variance for continuous variables and the asymptotic Jonckheere-Terpstra test (30) for categorical variables. The association of standing SAD with CHD was determined by using Cox proportional hazards models (31), with three levels of adjustment: for age and race (model 1); for age, race, BMI, educational level, smoking, alcohol consumption, and hormone replacement therapy (in women) (model 2); and for model 2 covariates plus total cholesterol, hypertension, diabetes, and renal function (model 3).

Race included Black, Asian, and White (reference group); educational levels were high school or less (reference group), some college, college graduate or higher, and unknown; cigarette smoking status included former, current, unknown, and never (reference group); and levels of alcohol consumption were less than three drinks a day, three or more drinks a day, unknown, and nondrinkers (reference group). Renal function was categorized as estimated glomerular filtration rate of <30, 30–59, 60–89, ≥90 ml per minute/1.73 m2 (reference level), and missing (3.5 percent of men and women). Total serum cholesterol was entered as four categories: <160, 160–199 (reference group), 200–239, ≥240 mg/dl, and a fourth dummy variable representing missing values (6 percent of men and women). To evaluate possible differential associations between standing SAD and CHD by age, race, and BMI, we performed stratified models (for each gender separately) as well as formal tests for interaction between standing SAD and age (as continuous variables), standing SAD and BMI (as continuous variables), and standing SAD with Black and Asian race, respectively. We also tested for interactions between standing SAD as a continuous variable and indicator variables of underweight, overweight, and obesity separately in men and women. To discern whether the age- and race-adjusted model with 12 joint categories of BMI and standing SAD provided a better fit to the data compared with an age- and race-adjusted model that included only main effects for BMI levels (underweight, overweight, and obesity relative to normal weight), we performed a likelihood ratio test with 9 degrees of freedom.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 References
 
On average, the cohort was in late young adulthood at baseline, and the majority of participants were White (table 1). About half the men and 42 percent of the women had some college education or higher, 66 percent of men ever smoked (vs. 53 percent of women), and more men than women reported consuming three or more alcoholic drinks a day (16 percent vs. 6 percent). BMI, the prevalence of hypertension and diabetes, and systolic blood pressure were higher in men than in women. Whereas standing SAD was larger in men than in women, total cholesterol and diastolic blood pressure were similar between sexes.


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  		TABLE 1 Baseline characteristics* of the 1965–1970 Kaiser Permanente Multiphasic Checkup Cohort, Oakland and San Francisco, California

 
Among men, standing SAD was positively related to age and inversely related to educational level (table 2). Men with a larger standing SAD were less likely to be current smokers and more likely to be abstainers or consumers of three or more alcoholic drinks a day. As expected, standing SAD was positively associated with BMI, total cholesterol, systolic and diastolic blood pressures, hypertension, and diabetes. Estimated glomerular filtration rate decreased with increasing standing SAD. Among women, standing SAD was also positively related to age and inversely related to educational level (table 3). Similar patterns were seen for the associations of standing SAD with smoking, alcohol consumption, and metabolic factors in women compared with men. No association was found between standing SAD and hormone replacement therapy. The Pearson correlation between standing SAD and BMI was 0.64 for men and 0.72 for women. The strength of the correlation between standing SAD and BMI varied by sex, race, and age group, being lowest among Asian men aged 65 years or older (r = 0.46) and highest among Black women aged 65 years or older (r = 0.77).


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  		TABLE 2 Association of sagittal abdominal diameter with baseline characteristics{dagger} of men (n = 45,181) in the 1965–1970 Kaiser Permanente Multiphasic Checkup Cohort, Oakland and San Francisco, California

 

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  		TABLE 3 Association of sagittal abdominal diameter with baseline characteristics{dagger} of women (n = 56,584) in the 1965–1970 Kaiser Permanente Multiphasic Checkup Cohort, Oakland and San Francisco, California

 
Age-adjusted CHD rates increased with increasing quartiles of standing SAD in each of the sex and race groups (figure 1). A consistent pattern of higher CHD rates with increasing standing SAD quartile was present in each age group for both men and women (data not shown). Other than for the subgroup of obese men, the age-adjusted rate of CHD also increased consistently with larger standing SAD in all BMI categories for both sexes (data not shown).


Figure 1
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  		FIGURE 1 Age-adjusted coronary heart disease (CHD) rates per 10,000 person-years according to sex, race, and quartiles of standing sagittal abdominal diameter (SAD), The Kaiser Permanente Multiphasic Cohort, Oakland and San Francisco, California, 1965–1970. Diamonds, Whites; squares, Blacks; triangles, Asians.

 
After adjustment for age and race (model 1) for men, the upper quartile of standing SAD was significantly associated with a 1.70-fold increased hazard of CHD; each standard deviation increment in standing SAD was associated with a 1.22-fold increased hazard of CHD (table 4). Additional adjustment for BMI, educational level, smoking, and alcohol consumption (model 2) attenuated the risk estimates to 1.42 and 1.13, respectively. After we additionally considered metabolic factors that may be related to standing SAD (model 3), the risk estimates were only marginally reduced. Results for women were remarkably similar to the results observed for men.


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  		TABLE 4 Sex-specific association between sagittal abdominal diameter and risk of coronary heart disease in the 1965–1970 Kaiser Permanente Multiphasic Checkup Cohort, Oakland and San Francisco, California

 
Stratification by age groups revealed that the association between standing SAD and CHD was more pronounced in the younger age group (18–44 years), consistently for both sexes (table 5). Accordingly, there were highly statistically significant (negative) interactions between age and standing SAD (as continuous variables) for men and for women (p < 0.0001). Whereas adjustment for covariates in models 2 and 3 preserved this pattern for men, standing SAD became more strongly associated with CHD risk for women aged 45–64 years after multivariate adjustment. When the analysis was stratified by race (table 5), we noted that the association between standing SAD and CHD was of similar magnitude across race groups. In agreement with these results, the interactions between standing SAD as a continuous variable and Black race or Asian race were not statistically significant for either sex (all p > 0.12). On the other hand, the association between standing SAD and CHD according to BMI categories differed by sex (see also table 5). Among men, standing SAD was more predictive among normal-weight subjects, whereas standing SAD tended to be more predictive among overweight women. A significant negative interaction between standing SAD and BMI as continuous variables was present for men (p = 0.009) but not for women (p = 0.10). In addition, significant interactions existed between standing SAD and categorical variables for overweight (p = 0.008) and obesity (p = 0.01) for men but not for women (p = 0.80 and p = 0.30, respectively). Standing SAD was not associated with CHD risk among underweight men and women, but this group experienced a small number of events.


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  		TABLE 5 Sex-specific association between sagittal abdominal diameter and risk of coronary heart disease according to strata of age, race, and body mass index in the 1965–1970 Kaiser Permanente Multiphasic Checkup Cohort, Oakland and San Francisco, California

 
The likelihood ratio test comparing the age- and race-adjusted model including BMI categories only with the model including 11 joint BMI/standing SAD effects was highly statistically significant for men ({chi}2 = 101.6 (9 df); p < 0.0001) and for women ({chi}2 = 83.7 (9 df); p < 0.0001). The estimates of the BMI/standing SAD joint effects on CHD risk, after adjustment for model 2 covariates, are depicted in figure 2. Relative to normal weight and having a standing SAD in quartile I, the hazard of CHD increased monotonically for women according to increasing standing SAD at each level of BMI (except for a J-shaped pattern for overweight women); the hazard ratio of combined obesity and standing SAD in quartile IV was 2.1. For men, the CHD hazard ratio increased monotonically with increasing standing SAD among normal-weight and overweight subjects, but a nonlinear trend was seen among obese subjects; the hazard ratio of combined obesity and standing SAD in quartile IV was also 2.1. Adjustment for metabolic variables in model 3 (data not shown) attenuated the strength of the associations, but most remained strong and statistically significant.


Figure 2
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  		FIGURE 2 Multivariate-adjusted sex-specific hazard ratios of coronary heart disease (CHD) according to joint categories of body mass index and standing sagittal abdominal diameter (SAD), The Kaiser Permanente Multiphasic Cohort, Oakland and San Francisco, California, 1965–1970. Black bars, obese subjects; striped bars, overweight subjects; white bars, normal-weight subjects.

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
References
 
To our knowledge, we report the first longitudinal study of the long-term risk of CHD associated with SAD measured in a standing position among younger and older adult men and women of diverse ethnic backgrounds. Our data confirm that standing SAD correlates with an adverse metabolic risk factor profile and significantly predicts increased risk of CHD independently of other risk factors and BMI for men (21, 22), and they add new prospective information on the SAD-CHD relation among women. We found that standing SAD tended to be more predictive of CHD in younger than in older age groups of men and women. Additionally, we found standing SAD to be equally predictive of CHD risk across racial groups. Information on Hispanic ethnicity was not available (these patients were included in the White race category). We also found that standing SAD tended to lose predictive power for men (but not for women) at higher BMI levels. Finally, we found clear evidence that consideration of standing SAD at each level of BMI provided better risk stratification than use of BMI alone. This finding suggests that standing SAD conveys additional predictive information that BMI misses.

To put our findings in the proper context, it is important to recognize that the measurement protocols for SAD are quite different across studies; therefore, comparability cannot be assumed. In the Baltimore Longitudinal Study on Aging, where a protocol for SAD measurement (in a standing position) similar to ours was used, all-cause and CHD mortality rates (adjusted for age, height, and BMI) increased with increasing standing SAD in the younger group but not in the older group (22). In the Paris Prospective Study among asymptomatic men free of ischemic heart disease, a standing sagittal xyphoid diameter (with adjustment for thoracic diameter and for estimated subcutaneous truncal fat) was used (21). After adjustment for baseline level of cardiovascular disease risk factors, the risk of fatal myocardial infarction and of sudden death increased proportionally with this modality of standing SAD (21).

The remaining prior experience with SAD as a risk factor for CHD involves supine SAD but at various landmarks defined by umbilicus, highest point, or the iliac crest (approximately L4–L5). The rationale for using supine SAD is that the supine posture would accentuate the contribution of visceral fat to SAD because the subcutaneous fat would fall off to the sides of the examination table (32). The methodology is further complicated by use of ratios. For example, one cross-sectional analysis among middle-aged US men found that the ratio of supine SAD to midthigh girth ("abdominal diameter index") was the most powerful anthropometric measure of CHD risk (33). In a case-control study of hospitalized incident ischemic heart disease cases and neighborhood-matched controls, the abdominal diameter index was the simple index that best discriminated cases from controls (34).

Several cross-sectional studies have shown that supine SAD is strongly related to insulin resistance and hyperinsulinemia (35, 36). Furthermore, there is evidence that supine SAD may correlate better than other simple anthropometric measures such as BMI, waist circumference, and waist-to-hip ratio with metabolic variables of insulin sensitivity (19, 20), although other authors found no clear superiority of supine SAD (37). In addition, in the Bogalusa Heart Study, supine SAD contributed more to the prediction of blood pressure than did other measures of central obesity (38). On the other hand, Reed et al. (17) found that the association of supine SAD (and the ratio of supine SAD to the transverse abdominal diameter) with carotid artery intima media thickness was not independent of BMI in a sample of middle-aged utility company employees in Southern California.

The "gold standard" measure of visceral or intraabdominal obesity is obtained by computed tomography (32) or by magnetic resonance imaging (39, 40). However, both are expensive, and computed tomography involves radiation exposure; thus, they are impractical for epidemiologic purposes or in the context of primary care. Supine SAD has been shown to be highly correlated with visceral adipose tissue assessment by computed tomography, although the correlation weakened at very high BMI levels and in very advanced age (41, 42).

Our study has some limitations. First, waist and hip circumferences were not available for the study subjects. Hence, we were unable to determine which simple index of visceral obesity better predicts CHD. Second, SAD was measured in a standing position and not in a supine position; thus, the effect of gravity could have resulted in some systematic differences. Third, we did not have a measure of insulin resistance (fasting glucose and fasting insulin), which is one of the major pathways whereby abdominal obesity contributes to the risk of CHD. Fourth, we lacked data on C-reactive protein or coagulation markers, so we could not determine the extent to which the effect of standing SAD is mediated through enhanced inflammation and/or level of coagulation activation. Fifth, we relied on a single measure of exposure to abdominal obesity and therefore did not model the effects of change in SAD.

Our study supports the utility of using SAD as a simple, noninvasive method to assess CHD risk above and beyond BMI in epidemiologic studies. However, before it can be adopted in clinical practice, further longitudinal studies should determine whether SAD outperforms the widely adopted waist circumference or waist-to-hip ratio measures in a head-to-head comparison. Another issue that warrants further investigation is discerning which protocol of SAD measurement (standing or supine) better discriminates cardiovascular disease risk. A current limitation of any SAD measure (unlike waist circumference) (43) is that no clinical consensus guidelines exist for a threshold at which it becomes clinically significant, although a threshold of ≥25 cm has been proposed (36).

In summary, standing SAD, a marker of visceral obesity, was a strong predictor of CHD independently of BMI in our study, and it added incremental CHD risk prediction at each level of BMI for men and women, for older and younger persons, and across racial groups. These findings suggest that BMI and a measure of visceral obesity such as standing SAD should be considered together for optimal CHD risk assessment.


   ACKNOWLEDGMENTS
 
This study was funded by a grant from the Kaiser Foundation Research Institute Community Benefit Program.

Presented at the 46th Annual Conference on Cardiovascular Disease Epidemiology and Prevention, Phoenix, Arizona, March 2–5, 2006.

Conflict of interest: none declared.


   References
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

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