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Arteriosclerosis, Thrombosis, and Vascular Biology. 1996;16:963-970

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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1996;16:963.)
© 1996 American Heart Association, Inc.

Articles

Risk Factors for Abdominal Aortic Aneurysms in Older Adults Enrolled in the Cardiovascular Health Study

Hope G. Alcorn; Sidney K. Wolfson, Jr; Kim Sutton-Tyrrell; Lewis H. Kuller; Daniel O'Leary;

the Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh (Pa).

Correspondence to Hope Gelfand Alcorn, DrPH, Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, 130 DeSoto St, Pittsburgh, PA 15261.

Abstract

B-mode ultrasound examinations of the abdominal aorta were performed from 1990 to 1992 to evaluate the prevalence of abdominal aortic aneurysm (AAA) in a subgroup of the Pittsburgh cohort (656 participants, aged 65 to 90 years) of the Cardiovascular Health Study (CHS). In this pilot study, we evaluated various definitions of aneurysm and the reproducibility of the measurements. In year 5 (1992 to 1993) of the CHS, the entire cohort (4741 participants) was examined. AAA was defined as an infrarenal aortic diameter of >=3.0 cm, or a ratio of infrarenal to suprarenal diameter of >=1.2, or a history of AAA repair. For the entire CHS cohort, prevalence of aneurysms was 9.5% (451/4741) overall, with a prevalence among men of 14.2% (278/1956) and prevalence among women of 6.2% (173/2785). Variables significantly related to AAA were older age; male sex; history of angina, coronary heart disease, and myocardial infarction; lower ankle-arm blood pressure ratio; higher maximum carotid stenosis; greater intima-media thickness of the internal carotid artery; higher creatinine; lower HDL levels and higher LDL levels; and cigarette smoking. The study has documented the strong association of cardiovascular risk factors and measures of clinical and subclinical atherosclerosis and cardiovascular disease and prevalence of aneurysms. We used a definition that is more sensitive than previously reported (diameter or ratio), which allowed the detection of smaller aneurysms and possibly those at an earlier stage of development. Follow-up of this cohort may lead to new criteria for determining the risk factors for progression of aneurysms.


Key Words: abdominal aortic aneurysms • risk factors

The aorta is easily accessible to noninvasive study with ultrasound techniques that allow the detection and measurement of AAA. The objectives of this report are to assess the prevalence of AAA, methods of measuring AAA, and risk factors associated with AAA in the CHS. This report describes an investigation that uses a protocol developed in a pilot study of 656 participants from the Pittsburgh cohort of the CHS and then applies it to the full CHS cohort of 4741 participants.

The CHS is a population-based, longitudinal study of CHD and stroke in adults aged 65 years and older. The main objective of the study is to identify factors related to the onset and course of CHD and stroke. The CHS is designed to determine the importance of conventional cardiovascular disease risk factors in older adults and to identify new risk factors in this age group.

The development of aneurysms involves changes in elastin and collagen in the arterial wall.1 Destruction of the media and the decrease in elastic tissue is an important histological feature of aneurysms. Since uncoiling of the elastic lamina ultimately limits arterial expansion, its destruction leads to uncontrolled dilatation or aneurysm. There is a decrease in elastin of the aortic wall in AAA compared with normal abdominal aortic tissue. The development of the aneurysm depends on the interaction of factors that increase the expansional forces in the aortic wall or decrease the ability to withstand stresses. Localized higher pressure areas due to wave reflection from the aortic bifurcation may account for the localization of aneurysms in the infrarenal areas.2

Ultrasound techniques provide a noninvasive method for detecting AAA. Measurements of abdominal aorta obtained by B-mode ultrasound have been found to be highly reproducible,3 and satisfactory reproducibility of aortic diameter can be obtained.4 Abdominal aneurysms are easily identified and can be measured accurately.3 4 5 Standard textbooks define AAA simply as a dilation of the aorta. There is as yet no consensus regarding a precise definition of AAA with respect to size. Some authors define AAA on the basis of the absolute diameter of the infrarenal aorta.6 7 8 9 10 11 12 Even within the criterion of absolute diameter, various cut points are used, ranging from 2.57 to 4.013 cm. Other authors have contended that it is not the absolute size that is important but the size of the infrarenal diameter relative to the suprarenal diameter. The I/S ratio has been used to define AAA.6 9 14 15 Different thresholds are used, ranging from 1.2 to 1.5.6 9 14 16 The CHS provides a precise and more sensitive way to define AAA, which may lead to a better understanding of its natural history.

Methods

The CHS enrolled participants aged 65 years or older in each of four US communities: Forsyth County, North Carolina; Sacramento County, California; Washington County, Maryland; and Pittsburgh (Allegheny County), Pennsylvania between June 1989 and May 1990 (year 2). Eligible participants were sampled from Medicare lists. Complete study design and rationale have been reported.17 The first year of the funded study was organizational and did not include examinations (1988 to 1989). There were 5201 adults (2955 women and 2246 men) included in the baseline examination (year 2).17 In year 5 (1992 to 1993) of the study, 687 blacks were recruited at three centers to increase this population in the CHS cohort, bringing the total population to 5888.

The baseline evaluation included a home interview and physical examination in the clinic. The CHS included measures of prevalent cardiovascular disease by self-report that were then verified by review of clinical records and information from physicians. The baseline examination included a resting electrocardiogram,18 echocardiogram,19 carotid artery duplex sonography,20 and ankle-arm blood pressure measurements.21 The measurement of the abdominal aorta by ultrasound was not included at the baseline examination. After completion of a successful pilot study in Pittsburgh during the third and fourth years of the CHS (1990 to 1991 and 1991 to 1992), the abdominal aneurysm examination was added to the fifth annual examination at all centers in 1992 to 1993. By year 5 of the CHS, 259 participants had died, 755 had no clinic visit, 93 had a clinic visit but no abdominal scan, and 47 had nonmeasurable scans, but 7 participants had an aneurysm repair and were included as having an AAA, which brought the denominator to 4741.

The aorta tapers during its course in the abdomen as a consequence of the branching of numerous arteries. The infrarenal aorta normally should be of smaller diameter than the suprarenal aorta, resulting in a ratio <1.0. Measures of aortic diameter in which B-mode ultrasound is used allow easy detection of AAA. Scans were recorded on Super VHS videotape and later scored by a reader.

To design and evaluate a protocol for measuring AAA, a pilot screening program was offered to the 1275 participants in the Pittsburgh cohort in 1990 to 1992. Six hundred fifty-six participants volunteered. Participants underwent B-mode ultrasound of the abdominal aorta at the Peripheral Vascular Diagnostic Laboratory located in Montefiore University Hospital, Pittsburgh, Pa. The scanner was a Toshiba SSA 270A color Doppler duplex imager with a 3.75-MHz convex probe. Based on the success of this pilot study, the entire CHS cohort underwent the abdominal aortic ultrasound examination in 1992 to 1993 (fifth annual CHS examination). The protocol was derived from that used in the pilot study.

B-mode gray scale images of the abdominal aorta were obtained in both transverse and longitudinal projections. The suprarenal measure of aortic diameter was taken 1 cm distal to the origin of the superior mesenteric artery, just above the level of the left renal artery. Either the superior mesenteric artery or the renal artery had to be visualized to accept the image for measurement. The level of the infrarenal measure of aortic diameter was determined by the site of the maximum aortic artery diameter (lumen plus wall) below the renal arteries.

An AAA was defined as (1) an infrarenal aortic diameter >=3.0 cm, or (2) an I/S ratio >=1.2, or (3) a history of AAA repair. While this definition does not necessarily represent disease that would cause clinical concern, it represents what we believe will establish the lowest level of disease that can be reliably detected by B-mode ultrasound. The intent was to identify early disease so that the natural history of AAA could be evaluated. In the pilot group, cases that were borderline by the above measurement criteria were overread by a physician and classified as an AAA if an obvious aneurysmal configuration was confirmed. In the full CHS cohort, all aneurysms as well as age- and sex-matched control subjects (for follow-up) were overread by a physician. Questionable scans were adjudicated by consultation with a second physician.

Data on smoking and alcohol use were obtained by participant report. Alcohol use was reported by frequency and amount and was summarized as average number of alcoholic drinks consumed per week.

History of CHD was defined as myocardial infarction, angina, coronary bypass surgery, or coronary angiography. The electrocardiogram was considered abnormal if any of the following were present: ventricular conduction defect, major Q-wave abnormalities, left ventricular hypertrophy, isolated ST-T wave abnormalities, atrial fibrillation, or first-degree atrioventricular block according to the Minnesota Code. Blood pressure was categorized as hypertensive or normotensive. Blood pressure values represent an average of two systolic and two diastolic readings measured with the Hawksley random-zero sphygmomanometer. Hypertension was defined as seated systolic blood pressure >=140 mm Hg, seated diastolic blood pressure >=90 mm Hg, or participant report of a physician's diagnosis of hypertension for which the participant was taking antihypertensive medication.

Carotid atherosclerosis was evaluated by ultrasound. Maximum intima-media thickness of the internal carotid arteries is the average of maximum measurements from the internal carotid near and far walls of three separate planes (average of 12 maxima: near and far wall, three internal views, right and left sides). Maximum carotid stenosis is the maximum of right and left carotid stenosis detected by Doppler ultrasonography.

The presence of lower extremity arterial disease was identified by the ankle-to-arm systolic blood pressure ratio, commonly called the ankle-arm index.22 23 24 An ankle-arm index <=0.9 was considered indicative of lower extremity arterial disease. The Rose questionnaire was used to determine intermittent claudication.

Reproducibility of the suprarenal and infrarenal aortic diameters and the I/S ratio was evaluated with Pearson and intraclass correlation coefficients. {kappa} analysis was used to assess the reproducibility of presence of aneurysm. The {chi}2 statistic was used to measure associations of AAA with age, sex, race, height, weight, smoking and alcohol use, prevalent clinical and subclinical disease, HDL, LDL, hematocrit, hemoglobin, white blood count, creatinine, glucose, and blood pressure.25 Variables measured on a continuous scale were classified by clinically relevant categories if known and otherwise by quartiles. Logistic regression was used to evaluate the association between the variables and AAA after adjustment for age, sex, height, weight, and smoking status. All calculations were performed with the use of SPSS 6.1 for Windows.

Results

Reproducibility of study measures was evaluated in 76 participants (38 with and 38 without an AAA) whose scans were scored by two separate readers. The individual suprarenal and infrarenal aortic diameter measures as well as the I/S ratio showed high reproducibility. Both Pearson and intraclass correlation coefficients were >=.87. There was also high intraobserver agreement on presence of aneurysm, with a {kappa} value of 0.92 (Table 1Down).


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  		Table 1. Reader Reproducibility of Aortic Diameter

Among the 656 participants in the pilot study, 43 AAAs were identified, for a prevalence of 6.6%. AAA has been defined in a variety of ways in previous literature. Table 2Down provides the prevalence of aneurysms in the pilot study based on several definitions. The prevalence of aneurysm for the entire cohort was 9.5% (451/4741) based on aortic diameter >=3.0 cm, or I/S ratio >=1.2, or history of AAA repair. The prevalence was 4.6% when based on history of repair or diameter >=3 cm only and 8.8% when based on history of repair or I/S ratio >=1.2 (Table 3Down). There were 29 (6.2%) of 468 aneurysms that were >=5 cm in diameter.


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  		Table 2. Prevalence of AAA in Pilot Study With Different Definitions (n=656 Participants From the Pittsburgh Cohort)


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  		Table 3. Prevalence of Aneurysms in Total CHS Cohort Based on Differing Definitions

The following relationships and probability values reported are adjusted for age, sex, smoking, height, and weight. The relationship of participant characteristics measured at years 2 and 5 of the CHS to AAA measured in year 5 of the study is presented in Table 4Down. AAAs were more prevalent in men than women (14.2% versus 6.2%; P=.001) (FigureDown). AAAs were more prevalent among smokers, ranging from 6.8% in those who had never smoked to 14.4% among current smokers (P<.0001). Alcohol use was highly skewed, with most of the participants reporting no consumption at all (n=2548) and a very few (n=301) reporting consumption of >=14 drinks per week. Alcohol consumption was not significantly associated with AAA. The prevalence of aneurysms was directly related to both weight and height (Table 4Down). There were no differences in prevalence of aneurysm by center, varying from 8.7% to 10.6% based on diameter >=3 cm and/or I/S ratio >=1.2 across four centers.


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  		Table 4. Relationship Between Demographic Characteristics and Presence of AAA in Total CHS Cohort (N=4741)



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  		Figure 1. Distribution of prevalent AAA by age and sex (women, darker columns; men, lighter columns) in the CHS (N=4741).

Aneurysm prevalence was higher among individuals with a history of clinical atherosclerotic disease. The prevalence of AAA was correlated with history of angina (P<.0001), history of myocardial infarction (P<.0001), and history of CHD (P<.0001). AAA was also strongly related to subclinical cardiovascular disease measures, including carotid artery stenosis (P<.0001), intima-media thickness of the internal carotid artery (P<.0001), and an ankle-arm index <=0.9 (P<.0001) (Table 5Down). Laboratory values significantly associated with prevalence of AAA were higher creatinine levels (P=.0007), lower HDL cholesterol levels (<40 mg/dL; P=.006), and higher LDL cholesterol levels (P=.006) (Table 6Down). Hematocrit and white blood count were not significantly associated with AAA.


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  		Table 5. Cardiovascular Disease Measures and Cardiac History and Presence of AAA (N=4741)


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  		Table 6. Relationship Between Laboratory Values and Presence of AAA (N=4741)

There was no significant relationship between blood pressure levels and prevalence of AAA, although the prevalence of aneurysm was higher among individuals with treated hypertension (Table 7Down). The risk factor associations were similar regardless of the definition used.


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  		Table 7. Blood Pressure, Hypertension History, Hypertension Medication History, and Presence of AAA (N=4741)

Discussion

Until the last decade, the etiology of AAA was thought to be related to atherosclerosis alone. Common risk factors implicated in the growth and development of AAA included hypertension and smoking. Recent studies have reported familial clustering of AAA, suggesting both genetic and environmental components of the disease process.26 27 28 29 30 31 32 33 34 35 36 37 38 39 40

Four sources of data have previously been used to evaluate the prevalence of AAA: (1) routine mortality statistics,41 42 43 44 (2) autopsy studies,45 46 (3) clinical and epidemiological studies,47 48 and (4) population screening.49 50

The majority of aneurysms are asymptomatic before they rupture or leak. Abdominal palpation of the aorta is inaccurate. In the Oxford Screening Program,49 for example, 843 men were evaluated by abdominal palpation and ultrasound. The sensitivity of abdominal palpation compared with ultrasound varied from 35% to 43%, depending on the criteria for the diagnosis. Abdominal palpation for identification of AAA is biased by size of the aneurysm, location, and degree of abdominal obesity.

There is evidence that the prevalence of AAA is increasing. Melton et al47 reported an apparent sevenfold increase in Rochester, Minn, from 1951 to 1980. The aneurysms were identified from hospital records, clinical ultrasound examinations, and death certificates. The prevalence of aneurysms increased with age and was higher in men than women. The major increase over time was in small aneurysms <5 cm in diameter and primarily diagnosed by ultrasound of the abdomen, suggesting that the increase in aneurysms was due to better ascertainment of aneurysms.

A large ultrasound screening study for aneurysms in general practices was completed in England50 from 1984 to 1992 in 8944 men and women aged 65 to 80 years. Aneurysms were diagnosed if the diameter of the aorta was >=3 cm in diameter. There were 356 (4%) with aneurysms, 294 (7%) of 3958 in men and 62 (1.2%) in women. Twenty-eight (8%) of the 356 aneurysms were >6 cm.

Reed et al51 reported that 151 clinical aortic aneurysms were identified among 8000 men of Japanese ancestry followed for 20 years. The baseline risk factors that predicted aortic aneurysms were higher blood pressure, serum cholesterol levels, and cigarette smoking. The incidence of clinical aortic aneurysms was also directly related to height.

The follow-up of the initial American Cancer Society 1 million volunteers by Hammond and Garfinkel52 reported that cigarette smoking was an important determinant of the risk of death due to aortic aneurysm. The follow-up of the Whitehall Study53 also showed that cigarette smoking and diastolic blood pressure were important determinants of death due to aortic aneurysms.

The prevalence of AAA is much higher among individuals with clinical atherosclerotic vascular disease, CHD, peripheral vascular disease, and stroke26 54 55 56 or atherosclerosis detected at postmortem examination.46 51

The prevalence of AAA is dependent on the definition used and by our definition was 9.5% in this population of adults aged 65 years or older. The prevalence was higher than previously reported in the Oxford Screening Study (6.3%)49 or the British Practitioners Study (4.0%).50 The higher prevalence is probably due to differences in definition of aneurysm and characteristics of the population.

Our goal was to identify the smallest aneurysms that could be reliably detected by ultrasound. A combination of absolute and relative size was used. Using absolute diameter only, one might miss an obvious AAA in a small-statured person. Using a ratio definition alone is not practical because a measurable ultrasound view above the renal arteries is not always available and because even large aneurysms extending both above and below the renal arteries could give a normal ratio. In the pilot study we found that using both size and ratio definitions increased sensitivity. Based on individual review of each case, the ratio cut point of 1.2 appeared to be the best discriminator of whether or not a physician agreed that an aneurysm was present. In the pilot study, even after these two criteria were combined, there were two borderline cases that the physician determined to be aneurysms. In one case the participant had an infrarenal diameter of 2.9 cm, and the other case had an I/S ratio of 1.17. Based on this case-by-case review, the definition of AAA for the full study required either an infrarenal aortic diameter >=3.0 cm, an I/S ratio >=1.2, or a history of AAA repair. It was not practical to use the physician overread of negative measurements in the full cohort.

We intentionally chose a relatively small value (>=1.2) for the I/S ratio. The infrarenal aorta normally should be of smaller diameter than the suprarenal aorta, resulting in a ratio <1.0. Only one study in women reported arteriographic measurements of the abdominal aorta. In women with normal aortas, the diameter above the renal arteries was 23.6±0.4 mm, just below the renal arteries was 17.3±0.4 mm, and just above the iliac bifurcation was 14.4±0.5 mm.57 In another study in men in which the maximum anteroposterior diameter for measurement location was used, the normal aortic diameter was reported to be between 15 and 25 mm.11 Two studies in which CT scanning was used reported mean aortic diameter measures in men and women by decade of life, and the I/S ratios ranged from 0.77 to 0.95.58 59 In the CHS, without regard to presence or absence of aneurysm, the mean I/S ratios ranged from 0.99 to 1.05 in men and women aged 65 years and older (Table 8Down). The nature of our definition is such that, as desired, it resulted in detection of a number of small aneurysms that may not yet be of sufficient size to require medical or surgical intervention. The combination of ratio and absolute size increased the sensitivity of AAA detection and should be used in future epidemiological studies. As the relationship to clinical outcome is documented, it may also prove to have clinical significance. The CHS provides an opportunity to follow these participants and determine the impact of initial aneurysm size.


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  		Table 8. Mean Aortic Diameter by Abdominal Ultrasound in the CHS (N=4734)

This is the first population study that has measured the prevalence of AAA, other measures of clinical and subclinical atherosclerosis, and cardiovascular risk factors in men and women with the use of abdominal ultrasound. The prevalence of subclinical disease in the CHS60 increased with age more in women than in men, and more men were found to have clinical cardiovascular disease. A likely hypothesis is that because of the strong association of clinical cardiovascular disease and AAA, the higher prevalence of clinical cardiovascular disease and mortality in older men results in a greater loss in the population due to death of men with AAA and clinical cardiovascular disease. It may also reflect the fact that men may have already developed AAAs by age 70 years, while women are still developing aneurysms as a result of protection from estrogen before menopause.

Men have a larger aortic diameter than women because of greater body size. The prevalence of aneurysm, defined only as >=3 cm in diameter, would be expected to be higher in men. However, the morbidity due to ruptured aneurysm is also much higher in men and parallels the greater prevalence of aneurysm in men. The higher prevalence in men is therefore unlikely to be due only to their greater body size but is also due to the higher prevalence of vascular disease in men compared with women, as well as the high prevalence of cigarette smoking (a major risk factor for aneurysm). In future analyses, it may be useful to adjust for the size of the aorta and definition of aneurysm for height and/or weight.

Individuals with subclinical or clinical atherosclerotic disease were more likely to have AAA. This result is consistent with previous reports in the literature that have noted a higher prevalence of clinical cardiovascular disease and peripheral vascular disease among patients with abdominal aneurysm. The strong association of atherosclerotic disease with AAA does not prove an etiologic association between them. Similar pathogenic factors, such as the decrease in elastic fibers with increasing age or inflammatory changes in the arterial wall, could contribute to the development of both AAA and atherosclerosis. A study of AAA among populations with lower prevalence of atherosclerosis, such as in Japan, China, and Southern Europe, might be informative.

Other factors associated with higher prevalence of detected AAA include older age, male sex, former and current smoking, greater weight and height, higher creatinine, lower HDL values, and higher LDL levels. These factors for detecting AAA are similar to previous reports of studies of clinical aneurysms. Cigarette smoking is clearly an important risk factor for AAA. The association of cigarette smoking and AAA may even be stronger than that for coronary artery atherosclerosis.51

The relationship between aneurysms and lipoproteins, such as LDL and HDL, is consistent with the association of aneurysms with atherosclerosis. The strong relationship between increasing creatinine levels and aneurysms could be due to a higher prevalence of renal artery disease, possibly secondary to renal atherosclerosis and stenosis. Unfortunately, there are no concurrent measures of renal artery stenosis in the CHS or other measures of renal function.

Height has been shown to be related to aortic aneurysms in other studies.51 The association may be related to the effects of reflection of the pulse wave from the aortic bifurcation or to differences in the size of the aorta. There was also, as noted, a positive association between body weight and aneurysms, suggesting that the effect may be due primarily to the size of the aorta in relation to the chosen diameter cut point (>=3.0 cm for this study).

The absence of a relationship between blood pressure levels and AAA is not consistent with the clinical studies reported. The Oxford Screening Study31 and the Screening Study Among Hypertensives in Norway61 also failed to document a strong relationship between hypertension and the prevalence of AAA, however. It is possible that an increase in blood pressure is primarily related to the enlargement of the AAA in clinical presentation in cases with rupture or risk of rupture and not to the prevalence of AAA as diagnosed by ultrasound. It is also possible that individuals with hypertension are more likely to be evaluated clinically for the identification of aneurysms, ie, palpation of abdomens with increased pulsations secondary to hypertension, which is misdiagnosed as an AAA. The high prevalence of treatment of hypertension in this cohort might reduce the association of blood pressure and aneurysm if reduction of blood pressure reduces the risk of aneurysm or results in regression of prevalent aneurysms. There was no significant relationship between blood pressure levels and risk of aneurysm after the population was stratified into categories of history of hypertension and treatment or no treatment of hypertension.

Over time we will be able to reevaluate the participants in the CHS to determine the relationship between changes in the size of the aneurysm with baseline blood pressure levels and prevalence of hypertension. We will be able to quantify the relationship between size of the aneurysm with risk factors, including hypertension and blood pressure levels.

Our initial analysis, as noted, has shown that the risk factors are similar for participants characterized as having an aneurysm >=3 cm in diameter as well as those with an I/S ratio >=1.2. The degree of progression over time among participants defined as having an aneurysm by these two criteria will be important.

This study indicates that AAA is another component of systemic vascular disease. It is possible that other factors such as genetic attributes are important in determining the growth of AAAs or their risk of rupture. Follow-up of this cohort may lead to new criteria for determining the likelihood for progression at an early stage, when surgery is safer, more effective, and less costly.62 A clinical trial in the United Kingdom is already evaluating surgical therapy for small aneurysms.63

Selected Abbreviations and Acronyms


AAA = abdominal aortic aneurysm
CHD = coronary heart disease
CHS = Cardiovascular Health Study
I/S ratio = ratio of infrarenal to suprarenal diameter


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  		Table 1B. Observer Agreement on Presence of Aneurysm

Acknowledgments

This study was supported by a Grant-in-Aid from the American Heart Association (92015450) and grant N01-HC-85082 from the National Heart, Lung, and Blood Institute, Bethesda, Md.

Appendix

Participating institutions and principal staff were as follows. Forsyth County, North Carolina--Bowman Gray School of Medicine of Wake Forest University: Gregory L. Burke, Alan Elster, Walter H. Ettinger, Curt D. Furberg, Edward Haponik, Gerardo Heiss, Dalane Kitzman, H. Sidney Klopfenstein, Margie Lamb, David S. Lefkowitz, Mary F. Lyles, Maurice B. Mittelmark, Cathy Nunn, Ward Riley, Grethe S. Tell, James F. Toole, Beverly Tucker; Sacramento County, California--University of California, Davis: William Bommer, Charles Bernick, Andrew Duxbury, Mary Haan, Calvin Hirsch, Paul Kellerman, Lawrence Laslett, Marshall Lee, Virginia Poirier, John Robbins, Marc Schenker; Washington County, Maryland--The John Hopkins University: M. Jan Busby-Whitehead, R. Nick Bryan, Trudy L. Bush, Joyce Chabot, George W. Comstock, Linda P. Fried, Pearl S. German, Joel G. Hill, Steven J. Kittner, Shiriki Kumanyika, David Levine, Joao A. Lima, Neil R. Powe, Thomas R. Price, Robert Rock, Moyses Szklo, Melvyn Tockman; Allegheny County, Pennsylvania--University of Pittsburgh: Diane G. Ives, Charles A. Jungreis, Laurie Knepper, Lewis H. Kuller, Robert H. McDonald, Jr, Elaine Meilahn, Peg Meyer, Anne Newman, Trevor Orchard, Richard Schulz, Vivienne E. Smith, Sidney K. Wolfson; Echocardiography Reading Center--University of California, Irvine: Hoda Anton-Culver, Julius M. Gardin, Margaret Knoll, Tom Kurosaki, Nathan Wong; Echo Reading Center--Georgetown University Hospital: John Gottdiener, Eva Hausner, Gabriela Hecht, Steven Kraus, Sue Livengood, Aldo Notargiacomo, Retha Webb; Ultrasound Reading Center--Geisinger Medical Center: Daniel H. O'Leary, Joseph F. Polak, Laurie Funk; Central Blood Analysis Laboratory--University of Vermont: Edward Bovill, Elaine Cornell, Russell P. Tracy; Respiratory Sciences--University of Arizona, Tucson: Paul Enright; Electrocardiography Reading Center--University of Alberta, Edmonton: Kris Calhoun, Harry Calhoun, Farida Rautaharju, Pentti Rautaharju, Loralee Robertson; Coordinating Center--University of Washington, Seattle: Nemat O. Borhani, Annette L. Fitzpatrick, Bonnie K. Lind, Richard A. Kronmal, Bruce M. Psaty, David S. Siscovick, Lynn Shemanski, Lloyd Fisher, Will Longstreth, Trivellore Ragunathan, Patricia W. Wahl, David Yanez, Alice Arnold; National Heart, Lung, and Blood Institute Project Office: Diane E. Bild, Teri A. Manolio, Peter J. Savage, Patricia Smith.

Received August 16, 1995; revision received March 12, 1996; References

  1. MacSweeney STR, Powell JT, Greenhalgh RM. Pathogenesis of abdominal aortic aneurysm. Br J Surg. 1994;81:935-941.[Medline] [Order article via Infotrieve]
  2. Report of a Meeting of Physicians and Scientists, University College London Medical School. Abdominal aortic aneurysm. Lancet. 1993;341:215-220.[Medline] [Order article via Infotrieve]
  3. Bernstein EF, Dilley RB, Randolph HF III. The improving outlook for patients over 70 years of age with abdominal aortic aneurysms. Ann Surg. 1988;207:318-322.[Medline] [Order article via Infotrieve]
  4. Leopold G, Goldberger L, Bernstein E. Ultrasonic detection and evaluation of abdominal aortic aneurysms. Surgery. December 1972;72:939-945.
  5. Yucel E, Fillmore D, Knox T, Waltman A. Sonographic measurement of abdominal aortic diameter: interobserver variability. J Ultrasound Med. 1991;10:681-683.[Abstract]
  6. Webster M, Ferrell RE, St Jean PL, Majumder PP, Fogel SR, Steed DL. Ultrasound screening of first-degree relatives of patients with an abdominal aortic aneurysm. J Vasc Surg. 1991;13:9-14.[Medline] [Order article via Infotrieve]
  7. Karanjia PN, Madden KP, Lobner S. Coexistence of abdominal aortic aneurysm in patients with carotid stenosis. Stroke. 1994;25:627-630.[Abstract]
  8. Canadian Task Force on the Periodic Health Examination. Periodic health examination, 1991 update, 5: screening for abdominal aortic aneurysm. Can Med Assoc J. 1991;145:783-789.[Medline] [Order article via Infotrieve]
  9. Shapira O, Pasik S, Wassermann J, Barzilai N, Mashiah A. Ultrasound screening for abdominal aortic aneurysms in patients with atherosclerotic peripheral vascular disease. J Cardiovascular Surg. 1990;31:170-172.[Medline] [Order article via Infotrieve]
  10. Berridge D, Griffith C, Amar S, Hopkinson B, Makin G. Screening for clinically unsuspected abdominal aortic aneurysms in patients with peripheral vascular disease. Eur J Vasc Surg. 1989;3:421-422.[Medline] [Order article via Infotrieve]
  11. Liddington MI, Heather BP. The relationship between aortic diameter and body habitus. Eur J Vasc Surg. 1992;6:89-92.[Medline] [Order article via Infotrieve]
  12. Bengtsson H, Ekberg O, Aspelin P, Kallero S, Bergqvist D. Ultrasound screening of the abdominal aorta in patients with intermittent claudication. Eur J Vasc Surg. 1989;3:497-502.[Medline] [Order article via Infotrieve]
  13. Collin J. A proposal for a precise definition of abdominal aortic aneurysm: a personal view. Cardiovasc Surg. 1990;31:168-169.
  14. Galland R, Simmons M, Torrie E. Prevalence of abdominal aortic aneurysm in patients with occlusive peripheral vascular disease. Br J Surg. 1991;78:1259-1260.[Medline] [Order article via Infotrieve]
  15. Lederle F, Walker J, Reinke D. Selective screening for abdominal aortic aneurysms with physical examination and ultrasound. Arch Intern Med. 1988;148:1753-1756.[Abstract]
  16. Cronenwett J, Sargent S, Wall M, Hawkes M, Freeman, D, Dain B, Curé J, Walsh D, Zwolak R, McDaniel M, Schneider J. Variables that affect the expansion rate and outcome of small abdominal aortic aneurysms. J Vasc Surg. 1990;11:260-269.[Medline] [Order article via Infotrieve]
  17. Fried LP, Borhani NO, Enright P, Furberg CD, Gardin JM, Kronmal RA, Kuller LH, Manolio TA, Mittelmark MB, Newman A, O'Leary DH, Psaty BM, Rautaharju P, Tracy RP, Weiler PG. The Cardiovascular Health Study: design and rationale. Ann Epidemiol. 1991;1:263-276.[Medline] [Order article via Infotrieve]
  18. Furberg CD, Manolio TA, Psaty BM, Bild DE, Borhani NO, Newman A, Tabatznik B, Rautaharju PM. Major ECG abnormalities in the elderly: the Cardiovascular Health Study. Am J Cardiol.. 1992;69:1329-1335.[Medline] [Order article via Infotrieve]
  19. Gardin JM, Siscovick D, Anton-Culver H, Lynch JC, Smith VE, Klopfenstein HS, Bommer WJ, Fried L, O'Leary D, Manolio TA. Sex, age, and disease affect echocardiographic left ventricular mass and systolic function in the free-living elderly: the Cardiovascular Health Study. Circulation. 1995;91:1739-1748.[Abstract/Free Full Text]
  20. O'Leary DH, Polak JF, Wolfson SK Jr, Bond MG, Bommer W, Sheth S, Psaty BM, Sharrett AR, Manolio TA. The Cardiovascular Health Study: use of sonography to evaluate carotid atherosclerosis in the elderly. Stroke. 1991;22:1155-1163.[Abstract/Free Full Text]
  21. Newman AB, Siscovick DS, Manolio TA, Polak J, Fried LP, Borhani NO, Wolfson SK. Ankle-arm index as a marker of atherosclerosis in the Cardiovascular Health Study. Circulation. 1993;88:837-845.[Abstract/Free Full Text]
  22. Schroll M, Munck O. Estimation of peripheral arteriosclerotic disease by ankle blood pressure measurements in a population study of 60-year-old men and women. J Chronic Dis. 1981;34:261-269.[Medline] [Order article via Infotrieve]
  23. Prineas RJ, Harland WR, Janzon L, Kannel W. Recommendations for use of non-invasive methods to detect atherosclerotic peripheral disease in population studies. Circulation. 1982;65:1561A-1566A.
  24. Criqui MH, Fronek A, Klauber MB, Barrett-Connor E, Gabriel S. The sensitivity, specificity, and predictive value of traditional clinical evaluation of peripheral disease: results from non-invasive testing in a defined population. Circulation. 1985;71:516-522.[Abstract/Free Full Text]
  25. Cushman M, Cornell E, Howard P, Bovill E, Tracy R. Laboratory methods and quality assurance in the Cardiovascular Health Study. Clin Chem.. 1995;41:264-270.[Abstract/Free Full Text]
  26. Cole C, Barber G, Bouchard A, McPhail N, Roberge C, Waddell W, Wellington J. Abdominal aortic aneurysm: consequences of a positive family history. Can J Surg.. 1989;32:117-120.[Medline] [Order article via Infotrieve]
  27. Johansen K, Koepsell T. Familial tendency for abdominal aortic aneurysms. JAMA. 1986;256:1934-1936.[Abstract]
  28. Majumder P, St Jean P, Ferrell R, Webster M, Steed D. On the inheritance of abdominal aortic aneurysm. Am J Hum Genet. 1991;48:164-170.[Medline] [Order article via Infotrieve]
  29. Norrgard O, Rais O, Angquist K. Familial occurrence of abdominal aortic aneurysms. Surgery. 1984;95:650-656.[Medline] [Order article via Infotrieve]
  30. Powell J, Greenhalgh R. Multifactorial inheritance of abdominal aortic aneurysms. Eur J Vasc Surg. 1987;1:29-31.[Medline] [Order article via Infotrieve]
  31. Tilson M, Seashore M. Fifty families with abdominal aortic aneurysms in two or more first-order relatives. Am J Surg.. 1984;147:551-553.[Medline] [Order article via Infotrieve]
  32. Tilson M, Seashore M. Human genetics of the abdominal aortic aneurysm. Surg Gynecol Obstet.. 1984;158:129-132.[Medline] [Order article via Infotrieve]
  33. Clifton M. Familial abdominal aortic aneurysms. Br J Surg.. 1977;64:765-766.[Medline] [Order article via Infotrieve]
  34. Cannon D, Read R. Blood elastolytic activity in patients with aortic aneurysm. Ann Thorac Surg.. 1982;34:10-15.[Abstract]
  35. Martin P. On abdominal aortic aneurysms. J Cardiovasc Surg. 1978;19:597-598.[Medline] [Order article via Infotrieve]
  36. Cohen J, Sarfati I, Wise L. The effect of cigarette smoking on rabbit aortic elastase activity. J Vasc Surg.. 1989;9:580-582.[Medline] [Order article via Infotrieve]
  37. Graham M, Chan A. Ultrasound screening for clinically occult abdominal aortic aneurysm. Can Med Assoc J. 1988;138:627-629.[Abstract]
  38. Mulder D, Winsberg F, Cole C, et al. Ultrasonic BÕ scanning of abdominal aneurysms. Ann Thorac Surg. 1973;16:361-367.[Medline] [Order article via Infotrieve]
  39. Powell J, Bashir A, Dawson S, Vine N, Henney A, Humphries S, Greenhalgh R. Genetic variation on chromosome 16 is associated with abdominal aortic aneurysm. Clin Sci.. 1990;78:13-16.[Medline] [Order article via Infotrieve]
  40. Powell J, Greenhalgh R. Cellular, enzymatic, and genetic factors in the pathogenesis of abdominal aortic aneurysms. J Vasc Surg.. 1989;9:297-304.[Medline] [Order article via Infotrieve]
  41. Stevens K. The incidence of abdominal aortic aneurysms. Br J Clin Pract. 1993;47:208-210.[Medline] [Order article via Infotrieve]
  42. Collin J. The epidemiology of abdominal aortic aneurysm. Br J Hosp Med. 1988;40:64-67.[Medline] [Order article via Infotrieve]
  43. Amy AK, White B, MacBain G. Abdominal aortic aneurysm in Scotland. Br J Surg. 1994;81:1104-1106.[Medline] [Order article via Infotrieve]
  44. Lillienfeld DE, Gunderson PD, Sprafka JM, Vargas C. Epidemiology of aortic aneurysms, I: mortality trends in the United States, 1951 to 1981. Arteriosclerosis. 1987;7:637-643.[Abstract/Free Full Text]
  45. McFarlane MJ. The epidemiologic necropsy for abdominal aortic aneurysm. JAMA. 1991;256:2085-2088.
  46. Bergqvist D, Bengtsson H, Sternby NH. Associated atherosclerotic manifestations. In: Greenhalgh RM, Mannick JA, Powell JT, eds. The Cause and Management of Aneurysms. Philadelphia, Pa: WB Saunders; 1990:47-56.
  47. Melton LJ III, Bickerstaff LK, Hollier LH, VanPeenen HJ, Lie JT, Pairolero PC, Cherry KJ, O'Fallon WM. Changing incidence of abdominal aortic aneurysms: a population-based study. Am J Epidemiol. 1984;120:379-386.[Abstract/Free Full Text]
  48. Eickhoff JH. Incidence of diagnosis, operation and death from abdominal aortic aneurysms in Danish hospitals: results from a nation-wide survey, 1977-1990. Eur J Surg. 1993;159:619-623.[Medline] [Order article via Infotrieve]
  49. Collin J, Walton J, Araujo L, Lindsell D. Oxford screening programme for abdominal aortic aneurysm in men aged 65 to 74 years. Lancet. 1988;2:613-615.[Medline] [Order article via Infotrieve]
  50. Scott RAP, Wilson NM, Ashton HA, Kay DN. Is surgery necessary for abdominal aortic aneurysm less than 6 cm in diameter? Lancet. 1993;342:1395-1396.[Medline] [Order article via Infotrieve]
  51. Reed D, Reed C, Stemmermann G, Hayashi T. Are aortic aneurysms caused by atherosclerosis? Circulation. 1992;85:205-211.[Abstract/Free Full Text]
  52. Hammond EC, Garfinkel L. Coronary heart disease, stroke, and aortic aneurysm. Arch Environ Health. 1969;19:167-182.
  53. Strachan DP. Predictors of death from aortic aneurysm among middle-aged men: the Whitehall Study. Br J Surg. 1991;78:401-404.[Medline] [Order article via Infotrieve]
  54. MacSweeney STR, O'Meara M, Alexander C, O'Malley MK, Powell JT, Greenhalgh RM. High prevalence of unsuspected abdominal aortic aneurysm in patients with confirmed symptomatic peripheral or cerebral arterial disease. Br J Surg. 1993;80:582-584.[Medline] [Order article via Infotrieve]
  55. Hertzer NR, Beven EG, Young JR, O'Hara PJ, Ruschhaupt WF III, Graor RA, Dewolfe VG, Maljovec LC. Coronary artery disease in peripheral vascular patients: a classification of 1000 coronary angiograms and results of surgical management. Ann Surg. 1984;199:223-233.[Medline] [Order article via Infotrieve]
  56. Allardice JT, Allwright GJ, Wafula JMC, Wyatt AP. High prevalence of abdominal aortic aneurysm in men with peripheral vascular disease: screening by ultrasonography. Br J Surg. 1988;75:240-242.[Medline] [Order article via Infotrieve]
  57. Darling R, Messina C, Brewster D, Ottinger L. Autopsy study of unoperated abdominal aortic aneurysms: the case for early resection. Cardiovasc Surg.. 1977;56:3. Circulation. 1977;56(suppl 2):161-164.
  58. Horejs D, Gilbert PM, Burstein S, Vogelzang RL. Normal aortoiliac diameters by CT. J Comput Assist Tomogr.. 1988;12:602-603.[Medline] [Order article via Infotrieve]
  59. Dixon AK, Lawrence JP, Mitchell JRA. Age-related changes in the abdominal aorta shown by computed tomography. 1984;35:33-37.
  60. Kuller L, Borhani N, Furberg C, Gardin J, Manolio T, O'Leary D, Psaty B, Robbins J. Prevalence of subclinical atherosclerosis and cardiovascular disease and association with risk factors in the Cardiovascular Health Study. Am J Epidemiol. 1994;139:1164-1179.[Abstract/Free Full Text]
  61. Lindholm L, Ejlertsson G, Forsberg L, Norgren L. Low prevalence of abdominal aortic aneurysm in hypertensive patients. Acta Med Scand. 1985;218:305-310.[Medline] [Order article via Infotrieve]
  62. Katz DA, Littneberg B, Cronenwett JL. Management of small abdominal aortic aneurysms. JAMA. 1992;268:2678-2686.[Abstract]
  63. Powell JT, Greenhalgh RM, Ruckley CV, Fowkes FGR. Prologue to a surgical trial. Lancet. 1993;342:1473-1474.[Medline] [Order article via Infotrieve]




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