This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Burke, G. L. Articles by Heiss, G. Search for Related Content PubMed PubMed Citation Articles by Burke, G. L. Articles by Heiss, G.

(Stroke. 1995;26:386-391.)
© 1995 American Heart Association, Inc.

Articles

Arterial Wall Thickness Is Associated With Prevalent Cardiovascular Disease in Middle-Aged Adults

The Atherosclerosis Risk in Communities (ARIC) Study

Gregory L. Burke, MD, MS; Gregory W. Evans, MS; Ward A. Riley, PhD; A. Richey Sharrett, MD; George Howard, DrPH; Ralph W. Barnes, PhD; Wayne Rosamond, PhD; Richard S. Crow, MD; Pentti M. Rautaharju, MD; Gerardo Heiss, MD, PhD for the ARIC Study Group

From the Departments of Public Health Sciences (G.L.B., G.W.E., G.H.) and Neurology (G.L.B., W.A.R., G.H., R.W.B.), Bowman Gray School of Medicine, and Department of Epidemiology, School of Public Health, University of North Carolina (W.R., G.H.), Chapel Hill; ARIC Ultrasound Reading Center, Winston-Salem, NC (W.A.R., R.W.B.); National Heart, Lung, and Blood Institute, Bethesda, Md (A.R.S.); Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis (R.S.C.); and the ECG Reading Center University of Alberta, Edmonton, Canada (P.M.R.).

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Background and Purpose This study was done to assess the relationship between prevalent cardiovascular disease and arterial wall thickness in middle-aged US adults.

Methods The association of preexisting coronary heart disease, cerebrovascular disease, and peripheral vascular disease with carotid and popliteal intimal-medial thickness (IMT) (measured by B-mode ultrasound) was assessed in 13 870 black and white men and women, aged 45 to 64, during the Atherosclerosis Risk in Communities (ARIC) Study baseline examination (1987 through 1989). Prevalent disease was determined according to both participant self-report and measurements at the baseline examination (including electrocardiogram, fasting blood glucose, and medication use).

Results Across four race and gender strata, mean carotid far wall IMT was consistently greater in participants with prevalent clinical cardiovascular disease than in disease-free subjects. Similarly, the prevalence of cardiovascular disease was consistently greater in participants with progressively thicker IMT. The greatest differences in carotid IMT associated with prevalent disease were observed for reported symptomatic peripheral vascular disease (0.09 to 0.22 mm greater IMT in the four race-gender groups).

Conclusions These data document the substantially greater arterial wall thickness observed in middle-aged adults with prevalent cardiovascular disease. Both carotid and popliteal arterial IMT were related to clinically manifest cardiovascular disease affecting distant vascular beds, such as the cerebral, peripheral, and coronary artery vascular beds.

Key Words: atherosclerosis • cardiovascular diseases • epidemiology • ultrasonics

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Advances in noninvasive B-mode ultrasound techniques for the measurement of arterial intimal-medial thickness (IMT) allow for the assessment of atherosclerosis in free-living population-based settings.¹ These ultrasound techniques involve the assessment of IMT in the carotid artery and other relatively superficial vascular beds. Measures of wall thickness are currently used as surrogates for and intermediate end points of atherosclerosis in observational studies and are also used to document regression or progression of atherosclerosis in clinical trials.^{2 3 4 5 6 7} However, the relationship between arterial wall thickness (measured by ultrasound) and cardiovascular disease has not been well documented. Although it has been observed that individuals with clinically manifest coronary heart disease, cerebrovascular disease, and peripheral vascular disease have more atherosclerosis than disease-free individuals,^{8 9 10 11 12} most such observations have been made in select populations such as hospitalized patients or as part of autopsy series. An association between increased carotid artery IMT and a more adverse cardiovascular disease (CVD) risk factor profile has also been documented.^{6 13 14 15 16} However, only one study has examined the relationship between IMT and cardiovascular disease in population-based samples.¹⁷ This article examines the relationship in middle-aged adults of prevalent coronary heart disease, cerebrovascular disease, and peripheral vascular disease to carotid and popliteal arterial wall thickness (thus including arterial measurements) in more central (carotid) and more peripheral (popliteal) locations.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
The Atherosclerosis Risk in Communities (ARIC) Study is a prospective study investigating the etiology and natural history of atherosclerosis and its clinical sequelae. The ARIC Study has measured CVD risk factors and outcomes in a population-based sample of 15 800 adults aged 45 to 64 at the baseline examination (1987 through 1989). The cohort consists of a probability sample selected from four US communities.⁴ Approximately 4000 adults were enrolled in the study from each of the following areas: the northwest suburbs of Minneapolis, Minn; Washington County, Md, which includes the city of Hagerstown; Forsyth County, NC, which includes the city of Winston-Salem; and Jackson, Miss. The Jackson center enrolled only black participants to allow more statistical power to conduct racial comparisons. The number of participants in each race and gender group ranged from 1400 (black men) to more than 5400 (white women). The mean age of the cohort was similar across race and gender groups and ranged from 53 to 55 years. More detailed description of the recruitment technique has been previously reported.⁴

B-mode real-time ultrasound (Biosound 2000 II SA) was used to evaluate the arterial wall thickness in the carotid and popliteal arterial beds. The carotid arteries were examined bilaterally in the areas of the common carotid artery (1 cm proximal to the dilatation of the carotid bulb), the carotid bifurcation (1 cm proximal to the flow divider), and the internal carotid artery (1 cm distal to the flow divider) on the left and right sides (Fig 1). To enhance the reproducibility of carotid measures in this population-based sample, standardized interrogation angles were used. The popliteal artery was assessed at a single site using similar techniques. Data are presented from this vascular bed to assess the relationship between prevalent disease and wall thickness in a more peripheral artery. Wall thickness measures presented here are from participants examined after May 15, 1987, and thus ultrasound data were available for 13 870 participants.

View larger version (18K): [in this window] [in a new window]   Figure 1. Schematic diagram for sites for measuring carotid arterial wall thickness in the Atherosclerosis Risk in Communities study.

The ARIC ultrasound reading protocol was designed to precisely measure IMT. Measurements were performed centrally at the ARIC Ultrasound Reading Center. To ensure reliability and validity of these measurements, programs of centralized training, certification, and quality control were implemented for both the sonographers and the readers. More detailed descriptions of the ultrasound scanning and reading techniques have been previously published.^{13 18 19 20 21} In cases of missing data at any of the six carotid sites, maximum likelihood techniques were used to estimate the mean wall thickness.²²

Prevalent disease was defined using both participant self-report and physical measurements, when available. Angina was assessed using the Rose Questionnaire²³ and was defined by the presence of chest pain upon walking that was relieved within 10 minutes after stopping or slowing down. Myocardial infarction (MI) was defined by (1) a participant-reported episode involving hospitalization for 1 week or more; (2) physician diagnosis of MI; or (3) a diagnostic Q wave detected on the baseline resting electrocardiogram. Silent MI was defined as a diagnostic Q wave detected on the baseline resting electrocardiogram in the absence of self-report or hospitalization. Peripheral vascular disease was defined by a self-reported history of angioplasty or bypass surgery of the lower extremity or by the self-reported presence of pain in the lower extremities while walking that was relieved within 10 minutes after standing still. Cerebrovascular disease was defined as a self-reported stroke or transient ischemic attack that was verified by a study physician's review of reported symptoms. CVD was defined as the presence of any of the following diseases: angina, MI, cerebrovascular disease, or peripheral vascular disease. Diabetes was defined by either self-reported medication use (insulin or oral agents) or a fasting (8 hours or more) serum glucose level of at least 140 mg/dL.

The overall mean far wall IMT thicknesses for the carotid and popliteal arteries were used in these analyses. The association between prevalent disease and wall thickness was evaluated based on (1) differences in age-adjusted mean IMT in relation to the presence or absence of disease and (2) age-adjusted disease prevalence as a function of increasing wall thickness. Analyses are presented both stratified by and adjusted for race and gender. ANCOVA was used to assess differences in mean IMT across prevalent disease groups to adjust for age, race, and gender, and also to determine whether the relationship between wall thickness and prevalent CVD was independent of known CVD risk factor levels (blood pressure, blood lipids, cigarette smoking, and diabetes).

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Prevalence rates for CVD and diabetes are shown by race, gender, and age group in Table 1. The prevalence of all types of CVD and diabetes increased with age in all race and gender groups. The prevalence of MI was higher in men than in women, and angina prevalence assessed by the Rose Questionnaire was greater in women than in men. MI rates were higher in white than in black men, and higher in black than in white women. The number of silent MIs was relatively small, and the rate of silent MI was similar across race and gender groups. The rate of cerebrovascular disease was low, and it was less frequent in white than in black participants. Clinically manifest peripheral vascular disease was rare in these middle-aged adults, but it was more frequent in men than in women. Diabetes prevalence was greatest in black participants in both women (18% versus 7%) and men (16% versus 8%).

View this table: [in this window] [in a new window]   Table 1. Disease Prevalence in Middle-Aged Adults: The ARIC Study

Age-adjusted mean carotid artery far wall IMT is presented in Table 2 for participants with and without prevalent disease. Participants classified as having a history of MI had a mean IMT greater than disease-free participants in all race and gender groups, with an overall difference of 0.07 mm. However, this difference was not statistically significant in black men. Similar IMT differences were observed for angina (0.04 mm), cerebrovascular disease (0.05 mm), peripheral vascular disease (0.15 mm), diabetes (0.06 mm), and all CVD (0.06 mm).

View this table: [in this window] [in a new window]   Table 2. Mean Carotid Far Wall Intimal-Medial Thickness (in Millimeters) by Disease Prevalence in Middle-Aged Adults: The ARIC Study

Fig 2 presents the age-, race-, and gender-adjusted disease prevalence by quartile of carotid wall thickness. The prevalence of MI, angina, peripheral vascular disease, and cerebrovascular disease increased across the IMT quartiles, with the lowest disease prevalence in participants with the smallest IMT and the highest disease prevalence in participants with the largest IMT. Of interest, the association between the overall mean carotid IMT and prevalent disease was also observed at the six sites (left and right common, bifurcation, and internal carotid segments). Participants with two or more prevalent diseases had a greater IMT than those with only one reported prevalent disease (data not shown).

View larger version (12K): [in this window] [in a new window]   Figure 2. Graph showing disease prevalence by carotid wall thickness quartile (age, race, and gender adjusted) in middle-aged adults. CVD indicates cardiovascular disease; MI, myocardial infarction.

To determine the extent to which the relationship observed between prevalent disease and wall thickness was associated with current levels of CVD risk factors, similar analyses were conducted adjusting for hypertension, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, smoking, and diabetes. Although the risk factor–adjusted differences in wall thickness between disease and disease-free groups were reduced in all race and gender groups (Table 3), in general, similar patterns between carotid IMT and prevalent disease were observed for CVD and peripheral vascular disease.

View this table: [in this window] [in a new window]   Table 3. Mean Carotid Far Wall Intimal-Medial Thickness (in Millimeters) by Disease Prevalence Adjusted for Cardiovascular Disease Risk Factors: The ARIC Study

Age-adjusted mean popliteal artery far wall thickness in participants with and without prevalent disease is presented in Table 4. As was the case for carotid wall thickness, popliteal artery wall thickness was greater in participants with prevalent disease than in those free of disease. Of interest, black men had the greatest popliteal wall thickness differences across prevalent disease categories. In general, a relationship between mean popliteal IMT, adjusted for age, race, and gender, and prevalent disease was observed for each vascular disease. Adjustment for the major CVD risk factors reduced the magnitude of the observed race- and gender-stratified associations (Table 5). Again, black men showed the greatest differences, but the overall difference (age-, race-, gender-, and risk factor–adjusted) remained statistically significant for all prevalent diseases.

View this table: [in this window] [in a new window]   Table 4. Mean Popliteal Far Wall Intimal-Medial Thickness (in Millimeters) by Disease Prevalence in Middle-Aged Adults: The ARIC Study

View this table: [in this window] [in a new window]   Table 5. Mean Popliteal Far Wall Intimal-Medial Thickness (in Millimeters) by Disease Prevalence Adjusted for Cardiovascular Disease Risk Factors: The ARIC Study

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
These data demonstrate increased arterial wall thickness, as measured by B-mode ultrasound, in participants with prevalent coronary heart disease, cerebrovascular disease, peripheral vascular disease, and total CVD. The carotid IMT in participants with CVD was 10% greater in those with MI, 6% greater in those with angina, 6% greater in those with cerebrovascular disease, 19% greater in those with peripheral vascular disease, and 8% greater in those with any form of CVD. The observed differences in wall thickness across disease groups are consistent with the associations between prevalent CVD and carotid atherosclerosis observed in previous clinical autopsy and ultrasound studies.^{1 2 3 5 24 25}

In the present study, CVD was associated with increased wall thickness at both the common carotid and popliteal arteries. Although the magnitude and the significance of the observed wall thickness differences between participants with and without disease differed across race and gender groups, the trend of greater IMT with disease was virtually universally observed. It should be noted that although this study involved an extremely large cohort, the numbers of affected participants in certain prevalent disease categories (silent MI, cerebrovascular disease, and peripheral vascular disease) were relatively modest. Other researchers have seen similar associations between ultrasound-measured carotid wall thickness and coronary heart disease,^{17 24 25} although to our knowledge the associations between CVD and popliteal wall thickness have not been previously addressed. A similar pattern was observed in these data between symptomatic CVD and wall thickness at both the popliteal and carotid arteries.

We were interested in determining whether the observed relationships between CVD and wall thickness could be explained in part by differences in CVD risk factors between the groups. After adjustment for known CVD risk factors (blood lipids, blood pressure, smoking, and diabetes), the magnitude of the IMT differences decreased. However, age-, race-, and gender-adjusted relationships of carotid wall thickness with MI, angina, cerebrovascular disease, peripheral vascular disease, and total CVD remained statistically significant after adjustment for risk factor levels. It is important to note that because these analyses were adjusted for current risk factor levels, it is possible that even more of the relationship between wall thickness and prevalent disease could have been explained if we had had access to past levels of risk factors in these participants.

Age, race, and gender differences in prevalent disease confirm what has been observed in other studies. The observed increased prevalence of CVD with increased age is certainly well known. An increased prevalence of diabetes and cerebrovascular disease in US black versus US white participants has been observed in other studies of adults.²⁶ The greater prevalence of MI in men than in women (and in black versus white women) is similar to that seen in previously reported results and corroborated by race and gender differences in US coronary heart disease mortality rates.²⁶ The increased prevalence of angina determined by the Rose Questionnaire in women has been observed in other studies.²⁷

There are a number of potential limitations to our study. Whenever possible, physical measurements were used to define disease. However, in general we relied almost entirely on participant self-report of symptoms or doctor-diagnosed prevalent disease. This could result in a misclassification of some participants as either having disease or being disease free. The impact of this on our estimate of the association between wall thickness and disease would likely be to bias our results toward the apparent lack of a significant association. In addition, individuals with the greatest atherosclerotic burden are less likely to survive a vascular event; our cross-sectional estimates are based only on survivors of these events. Thus, we likely underestimated the true relationship. The fact that the observed effects were consistent across race, gender, and vascular bed adds further credibility to the results.

These data support the existence of a relationship between prevalent CVD and arterial wall thickness in a population-based sample of US adults. Both popliteal and carotid wall thickness were related to CVD manifest in other vascular beds, suggesting that the measurements reflect systemic atherosclerosis. They verify that use of B-mode ultrasound to assess atherosclerosis as an intermediate measurement or end point in prospective observational studies and clinical trials appears to be warranted.

	Acknowledgments

 
This study was supported by contracts N01-HC-55015, N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55021, and N01-HC-55022 from the National Heart, Lung, and Blood Institute, National Institutes of Health. We would like to acknowledge the help of the following people who played an important role in the collection of these data: Catherine Paton (University of North Carolina–Chapel Hill), Jeannette Bensen, Delilah Posey, Amy Haire (Forsyth County Field Center, Winston-Salem, NC); Connie Myers, Virginia Overman, Stephanie Parker, Liz Sullivan (Jackson Field Center, Jackson, Miss); Dot Buckingham, Marilyn Bowers, Ellie Justiniano, Irene Keske (Minneapolis Field Center, Golden Valley, Minn); Carol Christman, Sonny Harrell, Joel Hill, Joan Nelling (Washington County Field Center, Hagerstown, Md); Valerie Stinson, Pam Pfile, Hoang Pham, Teri Trevino (Central Hemostasis Laboratory, Houston, Tex); Sandra Sanders, Charles E. Rhodes, Doris Epps, Selma Soyal (Central Lipid Laboratory, Houston, Tex); Regina DeLacy, Delilah Cook, Carolyn Bell, Teresa Crotts, Suzanne Pillsbury (Ultrasound Reading Center, Winston-Salem, NC); Mal Foley, Tom Goodwin, Richard Hayes, Ann Howard (Coordinating Center, Chapel Hill, NC).

	Footnotes

 
Reprint requests to Gregory L. Burke, MD, MS, Bowman Gray School of Medicine, Medical Center Blvd, Winston-Salem, NC 27157.

Received August 19, 1994; revision received December 14, 1994; accepted December 14, 1994.

	References

Top Abstract Introduction Subjects and Methods Results Discussion References

 

1. Pignoli P, Tremoli E, Poli A. Intimal plus medial thickness of arterial wall: a direct measurement with ultrasound imaging. Circulation. 1986;74:1399-1401. [Abstract/Free Full Text]
2. Furberg CD, Byington RP, Borhani NA, for the MIDAS Research Group. Multicenter Isradipine Diuretic Atherosclerosis Study (MIDAS). Am J Med. 1989;86:37-39. [Medline] [Order article via Infotrieve]
3. Margiti SE, Bond MG, Crouse JR, Furberg CD, Probstfield JL. Progression and regression of carotid atherosclerosis in clinical trials. Arteriosclerosis. 1991;11:443-451. [Free Full Text]
4. The ARIC Investigators. The Atherosclerosis Risk in Communities (ARIC) Study: design and objectives. Am J Epidemiol. 1989;129: 687-702.
5. Fried LP, Borhani NO, Enright P, Furberg CD, Gardin JM, Kronmal RA, Kuller LH, Manolio TA, Mittelmark MB, Newman A, O'Leary DH, Psaty B, Rautaharju P, Tracy RP, Weiler PG. The Cardiovascular Health Study: design and rationale. Ann Epidemiol. 1991;1:263-279. [Medline] [Order article via Infotrieve]
6. Salonen R, Seppanen K, Rauramaa R, Salonen JT. Prevalence of carotid atherosclerosis and serum cholesterol levels in Eastern Finland. Arteriosclerosis. 1988;8:788-792. [Abstract/Free Full Text]
7. The ACAPS Group. Rationale and design for the Asymptomatic Carotid Artery Plaque Study. Control Clin Trials. 1992;13:293-314. [Medline] [Order article via Infotrieve]
8. Strong JP, Solberg LA, Restrepo C. Atherosclerosis in persons with coronary heart disease. Lab Invest. 1968;18:527-537. [Medline] [Order article via Infotrieve]
9. Robertson WB, Strong JP. Atherosclerosis in persons with hypertension and diabetes mellitus. Lab Invest. 1968;18:538-551. [Medline] [Order article via Infotrieve]
10. Solberg LA, McGarry PA. Cerebral atherosclerosis in persons dying with selected diseases. Lab Invest. 1968;18:613-619. [Medline] [Order article via Infotrieve]
11. Tell GS, Crouse JR, Furberg CD. Relation between blood lipids, lipoproteins and cerebrovascular atherosclerosis: a review. Stroke. 1988;19:423-430. [Abstract/Free Full Text]
12. Pearson TA. Coronary arteriography in the study of the epidemiology of coronary artery disease. Epidemiol Rev. 1984;6:140-166. [Free Full Text]
13. Heiss G, Sharrett AR, Barnes R, Chambless LE, Szklo M, Alzola C, and the ARIC Investigators. Carotid atherosclerosis measured by B-mode ultrasound in populations: associations with cardiovascular risk factors in the ARIC study. Am J Epidemiol. 1991;134:250-256. [Abstract/Free Full Text]
14. Howard G, Ryu JE, Evans GW, McKinney WM, Toole JF, Murros KE, Crouse JE. Extracranial carotid atherosclerosis in patients with and without transient ischemic attacks and coronary heart disease. Arteriosclerosis. 1990;10:714-719. [Abstract/Free Full Text]
15. Crouse JR, Toole JF, McKinney WM, Dignan MB, Howard G, Kahl FR, McMahon MR, Harpold GH. Risk factors for extracranial carotid artery atherosclerosis. Stroke. 1987;18:990-996. [Abstract/Free Full Text]
16. Salonen JT, Seppanen K, Rauramaa R. Risk factors for carotid atherosclerosis: the Kuopio Ischaemic Heart Disease Risk Factor Study. Ann Med. 1989;21:227-229. [Medline] [Order article via Infotrieve]
17. O'Leary DH, Polak JF, Kronmal RA, Kittner SJ, Bond MG, Wolfson SK Jr, Bommer W, Price TR, Gardin JM, Savage PJ. Distribution and correlates of sonographically detected carotid artery disease in the Cardiovascular Health Study: the CHS Collaborative Research Group. Stroke. 1992;23:1752-1760. [Abstract/Free Full Text]
18. National Heart, Lung, and Blood Institute (Atherosclerosis Risk in Communities [ARIC] Study). Operations Manual, Number 6A: Ultrasound Scanning Methods, Version 1.0. Chapel Hill, NC: ARIC Coordinating Center, School of Public Health, University of North Carolina; 1987.
19. National Heart, Lung, and Blood Institute (Atherosclerosis Risk in Communities [ARIC] Study). Operations Manual, Number 6B: Ultrasound Reading Methods, Version 1.0. Chapel Hill, NC: ARIC Coordinating Center, School of Public Health, University of North Carolina; 1987.
20. Bond MG, Barnes RW, Riley WA, Wilmoth SK, Chambless LE, Howard G, Owens SB. High resolution B-mode ultrasound scanning methods in the Atherosclerosis Risk in Communities (ARIC) Study. J Neuroimaging. 1991;1:68-73. [Medline] [Order article via Infotrieve]
21. Riley WA, Barnes RW, Bond MG, Evans G, Chambless LE, Heiss G. High resolution B-mode ultrasound reading methods in the Atherosclerosis Risk in Communities cohort. J Neuroimaging. 1991;1:168-172. [Medline] [Order article via Infotrieve]
22. Espeland MA, Byington RP, Hire D, Davis VG, Hartwell T, Probstfield J. Analysis strategies for serial multivariate ultrasonographic data that are incomplete. Stat Med. 1992;11:1041-1056. [Medline] [Order article via Infotrieve]
23. Rose GA, Blackburn H, Gillum RF, Prineas RJ. Cardiovascular Survey Methods. Geneva, Switzerland: World Health Organization; 1982.
24. Salonen R, Salonen JT. Determinants of carotid intima-media thickness in a population-based ultrasound study in Eastern Finnish men. J Intern Med. 1991;229:225-231. [Medline] [Order article via Infotrieve]
25. Craven TE, Ryu JE, Espeland MA, Kahl FR, McKinney WM, Toole JF, McMahan MR, Thompson CJ, Heiss G, Crouse JR. Evaluation of the association between carotid artery atherosclerosis and coronary artery stenosis. Circulation. 1990;82:1230-1242. [Abstract/Free Full Text]
26. Gillum RF. Cardiovascular disease in the United States: an epidemiologic overview. Cardiovasc Clin. 1991;21:3-16.
27. Kannel WB, Abbott RD. Incidence and prognosis of myocardial infarction in women: the Framingham Study. In: Eaker ED, Packard B, Wenger NW, Clarkson T, Tyroler HA, eds. Coronary Artery Disease in Women. New York, NY: Haymarket-Doyma; 1987:208-214.

This article has been cited by other articles:

				N. J. Samani, O. T. Raitakari, K. Sipila, M. D. Tobin, H. Schunkert, M. Juonala, P. S. Braund, J. Erdmann, J. Viikari, L. Moilanen, et al. Coronary Artery Disease-Associated Locus on Chromosome 9p21 and Early Markers of Atherosclerosis Arterioscler. Thromb. Vasc. Biol., September 1, 2008; 28(9): 1679 - 1683. [Abstract] [Full Text] [PDF]

				M. Chonchol, H. Gnahn, and D. Sander Impact of subclinical carotid atherosclerosis on incident chronic kidney disease in the elderly Nephrol. Dial. Transplant., August 1, 2008; 23(8): 2593 - 2598. [Abstract] [Full Text] [PDF]

				E. A. Lasater, W. K. Bessler, L. E. Mead, W. E. Horn, D. W. Clapp, S. J. Conway, D. A. Ingram, and F. Li Nf1+/- mice have increased neointima formation via hyperactivation of a Gleevec sensitive molecular pathway Hum. Mol. Genet., August 1, 2008; 17(15): 2336 - 2344. [Abstract] [Full Text] [PDF]

				M. Juonala, J. S.A. Viikari, M. Kahonen, T. Solakivi, H. Helenius, A. Jula, J. Marniemi, L. Taittonen, T. Laitinen, T. Nikkari, et al. Childhood Levels of Serum Apolipoproteins B and A-I Predict Carotid Intima-Media Thickness and Brachial Endothelial Function in Adulthood: The Cardiovascular Risk in Young Finns Study J. Am. Coll. Cardiol., July 22, 2008; 52(4): 293 - 299. [Abstract] [Full Text] [PDF]

				P. Wenzel, S. Schuhmacher, J. Kienhofer, J. Muller, M. Hortmann, M. Oelze, E. Schulz, N. Treiber, T. Kawamoto, K. Scharffetter-Kochanek, et al. Manganese superoxide dismutase and aldehyde dehydrogenase deficiency increase mitochondrial oxidative stress and aggravate age-dependent vascular dysfunction Cardiovasc Res, July 22, 2008; (2008) cvn182v2. [Abstract] [Full Text] [PDF]

				M. Juonala, M. Kahonen, T. Laitinen, N. Hutri-Kahonen, E. Jokinen, L. Taittonen, M. Pietikainen, H. Helenius, J. S.A. Viikari, and O. T. Raitakari Effect of age and sex on carotid intima-media thickness, elasticity and brachial endothelial function in healthy adults: The Cardiovascular Risk in Young Finns Study Eur. Heart J., May 1, 2008; 29(9): 1198 - 1206. [Abstract] [Full Text] [PDF]

				B. Dursun, E. Dursun, G. Suleymanlar, B. Ozben, I. Capraz, A. Apaydin, and T. Ozben Carotid artery intima-media thickness correlates with oxidative stress in chronic haemodialysis patients with accelerated atherosclerosis Nephrol. Dial. Transplant., May 1, 2008; 23(5): 1697 - 1703. [Abstract] [Full Text] [PDF]

				K. Esposito, M. Ciotola, D. Carleo, B. Schisano, L. Sardelli, D. Di Tommaso, L. Misso, F. Saccomanno, A. Ceriello, and D. Giugliano Post-Meal Glucose Peaks at Home Associate with Carotid Intima-Media Thickness in Type 2 Diabetes J. Clin. Endocrinol. Metab., April 1, 2008; 93(4): 1345 - 1350. [Abstract] [Full Text] [PDF]

				N. Mattsson, T. Ronnemaa, M. Juonala, J. S.A. Viikari, E. Jokinen, N. Hutri-Kahonen, M. Kahonen, T. Laitinen, and O. T. Raitakari Arterial structure and function in young adults with the metabolic syndrome: the Cardiovascular Risk in Young Finns Study Eur. Heart J., March 2, 2008; 29(6): 784 - 791. [Abstract] [Full Text] [PDF]

				P. S. Douglas, R. F. Redberg, R. S. Blumenthal, and M. Ambrose Imaging for Coronary Risk Assessment: Ready for Prime Time? J. Am. Coll. Cardiol. Img., March 1, 2008; 1(2): 263 - 265. [Full Text] [PDF]

				O. T Raitakari, M. Juonala, T. Ronnemaa, L. Keltikangas-Jarvinen, L. Rasanen, M. Pietikainen, N. Hutri-Kahonen, L. Taittonen, E. Jokinen, J. Marniemi, et al. Cohort Profile: The Cardiovascular Risk in Young Finns Study Int. J. Epidemiol., February 8, 2008; (2008) dym225v1. [Full Text] [PDF]

				S. Demircan, A. T. Sezgin, M. Baltali, O. Gulcan, S. Topcu, F. Yigit, T. Erol, R. Turkoz, H. Muderrisoglu, and B. Ozin Intima-Media Thickness in Patients With Rheumatic Mitral Stenosis Angiology, November 1, 2007; 58(5): 614 - 619. [Abstract] [PDF]

				K. Sander, C. Schulze Horn, C. Briesenick, and D. Sander High-Sensitivity C-Reactive Protein Is Independently Associated With Early Carotid Artery Progression in Women But Not in Men: The INVADE Study Stroke, November 1, 2007; 38(11): 2881 - 2886. [Abstract] [Full Text] [PDF]

				O. W Nielsen and A. Sajadieh Diagnosing left ventricular hypertrophy in arterial hypertension BMJ, October 6, 2007; 335(7622): 681 - 682. [Full Text] [PDF]

				S. Sen, A. Hinderliter, P. K. Sen, J. Simmons, J. Beck, S. Offenbacher, E. M. Ohman, and S. M. Oppenheimer Aortic Arch Atheroma Progression and Recurrent Vascular Events in Patients With Stroke or Transient Ischemic Attack Circulation, August 21, 2007; 116(8): 928 - 935. [Abstract] [Full Text] [PDF]

				J. E. Williams, D. J. Couper, R. Din-Dzietham, F. J. Nieto, and A. R. Folsom Race-Gender Differences in the Association of Trait Anger with Subclinical Carotid Artery Atherosclerosis: The Atherosclerosis Risk in Communities Study Am. J. Epidemiol., June 1, 2007; 165(11): 1296 - 1304. [Abstract] [Full Text] [PDF]

				I. J. Kullo and A. R. Malik Arterial Ultrasonography and Tonometry as Adjuncts to Cardiovascular Risk Stratification J. Am. Coll. Cardiol., April 3, 2007; 49(13): 1413 - 1426. [Abstract] [Full Text] [PDF]

				W. Osika, F. Dangardt, J. Gronros, U. Lundstam, A. Myredal, M. Johansson, R. Volkmann, T. Gustavsson, L. Ming Gan, and P. Friberg Increasing Peripheral Artery Intima Thickness From Childhood to Seniority Arterioscler. Thromb. Vasc. Biol., March 1, 2007; 27(3): 671 - 676. [Abstract] [Full Text] [PDF]

				J. C. Stewart, D. L. Janicki, M. F. Muldoon, K. Sutton-Tyrrell, and T. W. Kamarck Negative Emotions and 3-Year Progression of Subclinical Atherosclerosis Arch Gen Psychiatry, February 1, 2007; 64(2): 225 - 233. [Abstract] [Full Text] [PDF]

				C. Napoli, L. O. Lerman, F. de Nigris, M. Gossl, M. L. Balestrieri, and A. Lerman Rethinking Primary Prevention of Atherosclerosis-Related Diseases Circulation, December 5, 2006; 114(23): 2517 - 2527. [Full Text] [PDF]

				M Allocca, A Crosignani, A Gritti, G Ghilardi, D Gobatti, D Caruso, M Zuin, M Podda, and P M Battezzati Hypercholesterolaemia is not associated with early atherosclerotic lesions in primary biliary cirrhosis Gut, December 1, 2006; 55(12): 1795 - 1800. [Abstract] [Full Text] [PDF]

				V. O. Palmieri, I. Grattagliano, P. Portincasa, and G. Palasciano Systemic Oxidative Alterations Are Associated with Visceral Adiposity and Liver Steatosis in Patients with Metabolic Syndrome J. Nutr., December 1, 2006; 136(12): 3022 - 3026. [Abstract] [Full Text] [PDF]

				B. A. Parker, S. J. Ridout, and D. N. Proctor Age and flow-mediated dilation: a comparison of dilatory responsiveness in the brachial and popliteal arteries Am J Physiol Heart Circ Physiol, December 1, 2006; 291(6): H3043 - H3049. [Abstract] [Full Text] [PDF]

				S. G. Tsouli, D. N. Kiortsis, V. Xydis, M. I. Argyropoulou, M. Elisaf, and A. D. Tselepis Antibodies Against Various Forms of Mildly Oxidized Low-Density Lipoprotein Are Not Associated With Carotid Intima-Media Thickness in Patients With Primary Hyperlipidemia Angiology, October 1, 2006; 57(5): 615 - 622. [Abstract] [PDF]

				S. Makita, A. Ohira, Y. Naganuma, Y. Moriai, H. Niinuma, A. Abiko, and K. Hiramori Increased Carotid Artery Stiffness Without Atherosclerotic Change in Patients With Aortic Dissection Angiology, August 1, 2006; 57(4): 478 - 486. [Abstract] [PDF]

				M. J Roman, T. Z Naqvi, J. M Gardin, M. Gerhard-Herman, M. Jaff, and E. Mohler American Society of Echocardiography Report: Clinical application of noninvasive vascular ultrasound in cardiovascular risk stratification: a report from the American Society of Echocardiography and the Society for Vascular Medicine and Biology Vascular Medicine, August 1, 2006; 11(3): 201 - 211. [PDF]

				J. R. Crouse III Thematic review series: Patient-Oriented Research. Imaging atherosclerosis: state of the art J. Lipid Res., August 1, 2006; 47(8): 1677 - 1699. [Abstract] [Full Text] [PDF]

				L. Keltikangas-Jarvinen, L. Pulkki-Raback, S. Puttonen, J. Viikari, and O. T. Raitakari Childhood Hyperactivity as a Predictor of Carotid Artery Intima Media Thickness Over a Period of 21 Years: The Cardiovascular Risk in Young Finns Study Psychosom Med, July 1, 2006; 68(4): 509 - 516. [Abstract] [Full Text] [PDF]

				R. Elosua, J. M. Ordovas, L. A. Cupples, C.-Q. Lai, S. Demissie, C. S. Fox, J. F. Polak, P. A. Wolf, R. B. D'Agostino Sr., and C. J. O'Donnell Variants at the APOA5 locus, association with carotid atherosclerosis, and modification by obesity: the Framingham Study J. Lipid Res., May 1, 2006; 47(5): 990 - 996. [Abstract] [Full Text] [PDF]

				M Kivimaki, G Davey Smith, M Juonala, J E Ferrie, L Keltikangas-Jarvinen, M Elovainio, L Pulkki-Raback, J Vahtera, M Leino, J S A Viikari, et al. Socioeconomic position in childhood and adult cardiovascular risk factors, vascular structure, and function: cardiovascular risk in young Finns study Heart, April 1, 2006; 92(4): 474 - 480. [Abstract] [Full Text] [PDF]

A. T. Hirsch, Z. J. Haskal, N. R. Hertzer, C. W. Bakal, M. A. Creager, J. L. Halperin, L. F. Hiratzka, W. R.C. Murphy, J. W. Olin, J. B. Puschett, et al. ACC/AHA 2005 Guidelines for the Management of Patients With Peripheral Arterial Disease (Lower Extremity, Renal, Mesenteric, and Abdominal Aortic): Executive Summary A Collaborative Report From the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vas