This Article Abstract Full Text (PDF) 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 Mast, H. Articles by Sacco, R. L. Search for Related Content PubMed PubMed Citation Articles by Mast, H. Articles by Sacco, R. L.

(Stroke. 1998;29:908-912.)
© 1998 American Heart Association, Inc.

Original Contributions

Cigarette Smoking as a Determinant of High-Grade Carotid Artery Stenosis in Hispanic, Black, and White Patients With Stroke or Transient Ischemic Attack

Henning Mast, MD; John L.P. Thompson, PhD; I-Feng Lin, MS; Christoph Hofmeister; Andreas Hartmann, MD; Peter Marx, MD; Jay P. Mohr, MD; Ralph L. Sacco, MD

From the Stoke Unit, The Neurological Institute, Columbia–Presbyterian Medical Center, New York, NY (H.M., J.L.P.T., A.H., J.P.M., R.L.S.); the Stroke Unit, Neurologische Klinik, Universitätsklinikum Benjamin Franklin, Freie Universität Berlin, Berlin, Germany (H.M., C.H., P.M.); and the Department of Public Health (Epidemiology) in the Sergievsky Center, Columbia University, College of Physicians and Surgeons, New York, NY (R.L.S.).

Correspondence to H. Mast, MD, Stroke Unit, The Neurological Institute, 710 W 168th St, New York, NY, 10032. E-mail ah267{at}columbia.edu

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Background and Purpose—We sought to investigate the association of cigarette smoking with high-grade carotid artery stenosis in Hispanic, black, and white patients with cerebral ischemia in two independent samples.

Methods—Prospectively collected data from the Northern Manhattan Stroke Study (NOMASS) (n=431) and the Berlin Cerebral Ischemia Databank (BCID) (n=483) were used separately for a cross-sectional study estimating the association between cigarette smoking and high-grade carotid stenosis (defined as a luminal narrowing of 60%, diagnosed by duplex and/or Doppler ultrasound). In both studies, cerebral ischemia patients with normal sonographic findings or nonstenosing plaques of their carotid arteries served as a comparison group. Multivariate logistic regression models were used for statistical tests to determine the association between smoking and the dependent variable for high-grade carotid stenosis. Age, sex, hypertension, diabetes, hypercholesterolemia, and race/ethnicity were considered potential confounders. Further analyses of the NOMASS data estimated the effect of the amount of cigarette use and the impact of race/ethnicity.

Results—High-grade carotid stenoses were found in 14% of the NOMASS and in 21% of the Berlin patients. In Berlin the entire sample was white, whereas in New York only 19% of the cohort were white. In both samples, smoking was independently associated with severe carotid stenosis (NOMASS: odds ratio [OR], 1.5; 95% confidence interval [CI], 1.1 to 2.0; BCID: OR, 3.9; 95% CI, 2.4 to 6.4). Patients smoking 20 pack-years or more showed a significant association (OR, 2.0; 95% CI, 1.1 to 3.9), whereas no significant effect was found for lower amounts of cigarette use. In NOMASS, white smokers displayed a significant (OR, 3.2; 95% CI, 1.1 to 8.9) association with high-grade carotid stenosis, the association for black smokers was less strong, and no association was found among Hispanics.

Conclusions—Smoking is an independent determinant of severe carotid artery stenosis in patients with focal cerebral ischemia. The association differs by race/ethnicity, with the greatest effect observed among whites.

Key Words: carotid stenosis • cigarette smoking • stroke

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Recent carotid endarterectomy trials have demonstrated the clinical importance of high-grade carotid artery stenosis. Cigarette smoking is an established risk factor for arteriosclerosis and ischemic stroke.^{1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16} However, prior stroke epidemiological studies evaluating the relationship between cigarette smoking and carotid stenosis have enrolled predominantly white subjects or had insufficient sample sizes of black or Hispanic patients. We investigated the effect of cigarette smoking on carotid stenosis of 60% luminal narrowing or more in two separate prospective samples of patients from Berlin and northern Manhattan with ischemic stroke and TIA. The combination of the two data sets, in addition, allowed for an adequate sample size to address the relationship of cigarette smoking in three different racial/ethnic groups.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
The Northern Manhattan Stroke Study (NOMASS) is a prospective study of stroke patients aged over 39 years who are residents of the northern Manhattan community.¹⁷ For the present investigation 431 consecutive cases of ischemic infarction with completed duplex Doppler ultrasound studies enrolled between January 1, 1990, and April 21, 1994, and treated in the Milstein Hospital wing of the Columbia-Presbyterian Medical Center were analyzed: 62 (14%) with common/internal carotid artery stenosis of 60% or more (including occlusion) and, serving as a reference group, 369 (86%) with bilaterally normal findings (n=78) or only low-grade (<60%) stenosing carotid plaques (n=291) diagnosed by duplex Doppler ultrasound investigations (Siemens Quantum 2000 machine). Classification of degree of stenosis was based on generally accepted definitions¹⁸ and quality control criteria established by the Asymptomatic Carotid Atherosclerosis Study.¹⁹

Smoking was defined as history of current or past regular cigarette use (nonsmoking was defined as never having smoked regularly), and the amount of cigarette consumption was measured by the average number of packs per day and the duration of smoking in years. For this analysis hypertension was assumed to be present under the following conditions: (1) the patient or the patient's family reported that they had been informed of the diagnosis by a physician before the classifying stroke event or antihypertensive medication had been recommended, or (2) the patient's medical documents showed that hypertension requiring treatment had been diagnosed by a physician before the classifying event. Diabetes was defined as chronic hyperglycemia requiring diet, oral medication, or insulin treatment, diagnosed before stroke onset. Hypercholesterolemia was diagnosed when patients had a history of increased blood cholesterol levels requiring diet or medication or increased blood cholesterol levels of 240 mg/dL or more measured after admission. Race/ethnicity was defined by self-identification as Hispanic, white non-Hispanic, black non-Hispanic, or "other" non-Hispanic.

The Berlin Cerebral Ischemia Data Bank (BCID) is a prospective, hospital-based registry for consecutive TIA and ischemic stroke patients.²⁰ For the present study the 483 consecutive cases with complete Doppler ultrasound studies were analyzed: 101 (21%) showing unilateral or bilateral carotid stenosis of 60% or more (including occlusion) and, serving as a reference group, 382 (79%) revealing no pathological findings (n=303) or flow changes indicating only a lesser degree of stenosis (n=79). The degree of carotid stenosis was assessed by conventional Doppler ultrasound investigations (4- and 8-MHz probe studies, EME TC 2000 machine) of the extracranial neck vessels, following generally accepted definitions,^{18 21 22} validated against gold-standard conventional angiography.²³ Unlike duplex Doppler ultrasound, conventional Doppler ultrasound does not detect nonstenosing plaque. Therefore, the number of BCID patients with no pathological Doppler results is larger than in NOMASS.

In the BCID, smoking was classified into two categories: (1) nonsmokers/former smokers (never smoked regularly or stopped regular smoking 5 years ago) and (2) smokers (regular smoking within the last 5 years). The BCID definitions of other risk factors (hypertension, diabetes, hypercholesterolemia) were similar to the ones used in NOMASS. All BCID subjects were white.

In NOMASS, two multivariate logistic regression models controlling for age, sex, race/ethnicity (white versus nonwhite), hypertension, diabetes mellitus, and hypercholesterolemia were used to determine whether (1) history and (2) amount of cigarette consumption measured in pack-years (dichotomized into 1 to 19 pack-years and 20 pack-years) were independent predictors of high-grade carotid artery stenosis. Three further univariate regression models estimated the effect of history of current or past cigarette smoking in three different racial/ethnic groups: Hispanics, blacks, and whites. To test for the significance of a difference in the effect of smoking on carotid stenosis among whites and nonwhites, an interaction term was introduced into the first regression model.

In BCID, one multivariate logistic regression model controlling for age, sex, hypertension, diabetes, hypercholesterolemia, and coronary heart disease was applied to determine whether regular cigarette smoking within the last 5 years was an independent predictor of high-grade carotid artery stenosis.

Additional regression models were set up to test the effect of smoking in strata of different degrees of carotid stenosis/occlusion. Finally, a regression analysis of a merged data set from both samples was done. To test for the significance of a difference in the effect of smoking on carotid stenosis among whites and nonwhites, an interaction term was introduced into the regression model of the merged data set.

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
In NOMASS, 43% of the patients had a history of current or reformed cigarette smoking. Of all NOMASS cases, 28% had smoked for 20 or more pack-years. In BCID, 41% of the patients were cigarette smokers (Table 1). The two samples differed significantly with regard to sex, risk factors, and frequency of carotid stenosis (Table 1). The frequencies of independent variables (cigarette smoking, hypertension, diabetes, hypercholesterolemia, age, sex, and race/ethnicity) in study groups with carotid stenosis (60% or occlusion) and reference cases are shown in Table 2. Despite similar frequencies of cigarette smoking across Hispanic, black, and white race subgroups, the frequency of severe carotid artery stenosis was greater among whites (25% NOMASS, 21% BCID) than in Hispanics (12%) or blacks (11%).

View this table: [in this window] [in a new window]   Table 1. Age, Sex, Risk Factors, and Race/Ethnicity in 431 NOMASS and in 483 BCID Patients

View this table: [in this window] [in a new window]   Table 2. Age, Sex, Risk Factors, and Race/Ethnicity in Patients With High-Grade Carotid Artery Stenosis and Reference Cases With Normal Findings or Low-Grade Stenosis

Both NOMASS and BCID studies revealed that smoking was significantly associated with high-grade carotid artery stenosis, and this effect was independent of other risk factors (Table 3). In contrast, hypertension, diabetes, and hypercholesterolemia had no significant relationship with high-grade carotid stenosis. NOMASS data also showed that smoking of 20 or more pack-years (Table 4) and white race (Tables 3 to 5) determined severe carotid artery stenosis. The association for black smokers was less strong, and no association was found among Hispanic cigarette smokers (Table 5). In NOMASS the difference of the effect of smoking on carotid stenosis between whites and nonwhites was not significant (OR, 2.5; 95% CI, 0.8 to 7.5; P=0.1).

View this table: [in this window] [in a new window]   Table 3. Multivariate Logistic Regression Model Estimating the Effect of Cigarette Smoking on High-Grade Carotid Artery Stenosis

View this table: [in this window] [in a new window]   Table 4. Multivariate Logistic Regression Model Estimating the Effect of Pack-Year Cigarette Consumption on High-Grade Carotid Artery Stenosis (Data From NOMASS)

View this table: [in this window] [in a new window]   Table 5. Univariate Logistic Regression Models Estimating the Effect of History of Cigarette Smoking on Carotid Artery Stenosis in Different Racial/Ethnic Groups (Data From NOMASS)

The impact of smoking was further analyzed in subgroups of different degrees of arterial luminal narrowing. In BCID, the point estimates for subgroups of 60% to 79% stenosis (38 patients), 80% or more stenosis (27 patients), and carotid occlusion (36 patients) showed increasing ORs of 2.8 (95% CI, 1.4 to 5.6), 3.7 (95% CI, 1.6 to 8.5), and 4.8 (95% CI, 2.2 to 10.3), respectively (ORs and CIs are from univariate regression models). In NOMASS, the number of patients in corresponding subgroups was too small (only 9 cases in the group of patients with 60% to 79% stenosis, and only 21 whites with carotid stenosis) for a meaningful statistical analysis.

The final meta-analysis of a merged data set from both samples repeated the previous results of a significant association of high-grade carotid stenosis with cigarette smoking (OR, 2.2; 95% CI, 1.6 to 3.1; adjusted for race/ethnicity). The effect of smoking was again stronger when the analysis was restricted to white smokers (OR, 3.5; 95% CI, 2.3 to 5.4). Reclassifying the stenosis group to include patients with low-grade stenosing plaques (NOMASS) and flow accelerations indicating low-grade (<60%) stenosis (BCID) from the reference group such that the comparison sample now comprised only patients with normal ultrasound findings of their carotid arteries reduced the OR but did not alter the significance of the association between carotid stenosis and cigarette smoking (OR, 1.5; 95% CI, 1.1 to 2.0; adjusted for race/ethnicity). Finally, in the merged data set analysis the difference of the effect of smoking on carotid stenosis between whites and nonwhites became significant (OR, 2.7; 95% CI, 1.6 to 4.5; P=0.0002).

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
In our analysis an independent association of smoking with high-grade carotid artery stenosis was demonstrated. This finding, showing consistency over two studies, may strengthen the notion of a causal role of cigarette smoking in stenosing arteriosclerotic carotid disease. Comparisons between two studies with the use of nonuniform definitions for their main variables (smoking and degree of carotid stenosis) can lead to difficulty with generalizing the results. However, the stability of the findings across our two independent samples supports the assumption of a robust effect.

In principle, data from patient histories on cigarette consumption may be questioned for their validity. The reported rate and amount of smoking are likely to be biased by underestimation. The effect of such misclassification error would most likely be nondifferential because the patients were unaware of the study hypothesis. Therefore, an attenuation of the OR toward the null value could be expected, which implies that the true association may be stronger than shown (we assume that underestimation affects patients with and without carotid stenosis evenly and a systematic error of underreported cigarette smoking in patients without severe carotid stenosis is not a plausible option). Categorizing former smokers and nonsmokers together, as has been done in the BCID, may also raise concerns. Prior studies have suggested a similar and lower stroke risk for nonsmokers and reformed smokers compared with current smokers.^{1 10 11 12 24 25 26} Therefore, the BCID classification may be reasonable, and any error introduced would result in an underestimation of the effect of cigarette smoking on carotid stenosis.

In BCID, the association between smoking and high-grade carotid stenosis was stronger than in NOMASS. Most likely, this can be explained by the racial composition of the purely white Berlin sample and possibly also by the more restricted definition of smoking in the Berlin study. The effect of smoking was similar in the BCID sample and the white subgroup of NOMASS (ORs of 3.9 and 3.2, respectively). In NOMASS (and in the merged analysis), white smokers showed a stronger association with carotid stenosis than blacks, and no effect was found for Hispanic smokers. This may indicate an important, yet unexplained, racial/ethnic difference in the effect of cigarette smoking. In support of these findings, other analyses from NOMASS²⁷ have found significantly less carotid plaques in stroke-free Hispanics than in other racial/ethnic groups.

Studies analyzing the effect of smoking on carotid artery plaques in mixed samples of symptomatic and asymptomatic patients have already suggested an independent link of this particular risk factor with carotid arteriosclerosis.^{13 14 15 16} Our results further establish this association for ischemic stroke and TIA patients with high-grade carotid stenosis of potential surgical relevance. However, the analysis was not restricted to cases of clinically defined symptomatic stenosis and did include stroke (or TIA) patients with carotid stenosis unrelated to the actual clinical pathology. An analysis of strictly symptomatic stenoses would imply sample sizes beyond the scope of any database presently available.

Our results are also restricted to a sample of patients with TIA or stroke and do not include a stroke-free comparison group. Therefore, the cross-sectional association between cigarette smoking and carotid stenosis implies that smoking may be more strongly related to atherogenic strokes rather than nonatherogenic causes such as cardioembolism and small-vessel disease.

Our results not only showed a similar effect of cigarette smoking on high-grade carotid stenosis but furthermore indicated against a significant relevance of other major risk factors of arteriosclerosis. In a selected sample of 240 patients undergoing cerebral angiography, Homer et al¹⁵ found a strong association of smoking with luminal narrowing of the carotid arteries. Unlike the results of our studies, however, hypertension and LDL cholesterol were also shown to have an impact. On the basis of 752 cases with cerebral angiography, Whisnant et al¹⁴ confirmed the importance of cigarette smoking and also a less strong effect of other risk factors. Both investigations did not represent prospective studies in unselected stroke samples and therefore may not lend themselves to direct comparisons. Nevertheless, in conjunction with our findings they support the growing evidence of the major role of cigarette smoking in the etiology of carotid stenosis.

Clearly, not all carotid stenoses can be attributed to smoking. Given the prevalence of cigarette exposure in our two samples and the size of the effect of cigarette smoking on carotid stenosis, we found that the attributable risk for our white stroke patients can be estimated at 45% (NOMASS) and 53% (BCID) or 50% when NOMASS and BCID whites are combined. In contrast, the attributable risk for our black stroke patients was only 15%, and that for Hispanics was even less (13%).

Stroke databanks have estimated that approximately 9% of all ischemic strokes are of carotid origin.^{17 28} This suggests that a substantial proportion of the costs of both stroke treatment and prevention can be allocated to stenosing carotid disease. Unlike other risk factors, cigarette smoking is modifiable in a radical fashion. There is ample evidence that this could positively influence the risk of stroke^{1 11} and reduce the burden on healthcare resources.

We conclude that cigarette smoking is an independent determinant of high-grade carotid artery stenosis in patients with cerebral ischemia. The association differs by race/ethnicity, with the greatest effect observed among whites.

	Selected Abbreviations and Acronyms

 

BCID = Berlin Cerebral Ischemia Databank CI = confidence interval NOMASS = Northern Manhattan Stroke Study OR = odds ratio TIA = transient ischemic attack

	Acknowledgments

 
The NOMASS is supported by the National Institute of Neurological Disorders and Stroke (RO1 NS27517 and RO1 NS29993). The authors thank Q. Gu, MS, for expert statistical advice.

Received October 27, 1997; revision received February 6, 1998; accepted February 9, 1998.

	References

Top Abstract Introduction Subjects and Methods Results Discussion References

 
1. Wolf PA, D'Agostino RB, Kannel WB, Bonita R, Belanger AJ. Cigarette smoking as a risk factor for stroke: the Framingham Study. JAMA. 1988;259:1025–1029.[Abstract/Free Full Text]

2. Wolf PA, D'Agostino RB, Belanger AJ, Kannel WB. Probability of stroke: a risk profile from the Framingham Study. Stroke. 1991;22:312–318.[Abstract/Free Full Text]

3. Wolf PA, Cobb JL, D'Agostino RB. Epidemiology of stroke. In: Barnett HJM, Mohr JP, Stein BM, Yatsu FM, eds. Stroke: Pathophysiology, Diagnosis, and Management. New York, NY: Churchill Livingstone; 1992:3–27.

4. Higa M, Davanipour Z. Smoking and stroke. Neuroepidemiology. 1991;10:211–222.[Medline] [Order article via Infotrieve]

5. Davis PH, Dambrosia JM, Schoenberg BS, Schoenberg DG, Pritchard A, Lilienfeld AM, Whisnant JP. Risk factors for ischemic stroke: a prospective study in Rochester, Minnesota. Ann Neurol. 1987;22:319–327.[Medline] [Order article via Infotrieve]

6. Sacco RL. Ischemic stroke. In: Gorelick PB, Alter M. Handbook of Neuroepidemiology. New York, NY: Marcel Dekker, Inc; 1994:77–119.

7. Dyken ML. Stroke risk factors. In: Norris JW, Hachinski VC, eds. Prevention of Stroke. New York, NY: Springer-Verlag; 1991:83–101.

8. Gorelick PB, Rodin MB, Langenberg P, Hier DB, Costigan J. Weekly alcohol consumption, cigarette smoking, and the risk of ischemic stroke: results of a case-control study at three urban medical centers in Chicago, Illinois. Neurology. 1989;39:339–343.[Abstract/Free Full Text]

9. Bonita R, Scragg R, Stewart A, Jackson R, Beaglehole R. Cigarette smoking and risk of premature stroke in men and women. BMJ. 1986;293:6–8.

10. Abbott RD, Yin Y, Reed DM, Yano K. Risk of stroke in male cigarette smokers. N Engl J Med. 1986;315:717–720.[Abstract]

11. Colditz GA, Bonita R, Stampfer MJ, Willett WC, Rosner B, Speizer FE. Cigarette smoking and risk of stroke in middle-aged women. N Engl J Med. 1988;318:937–941.[Abstract]

12. Shinton R, Beevers G. Meta-analysis of relation between cigarette smoking and stroke. BMJ. 1989;298:789–794.

13. Haapanen A, Koskenvuo M, Kaprio J, Kesäniemi A, Heikkilä K. Carotid arteriosclerosis in identical twins discordant for cigarette smoking. Circulation. 1989;80:10–16.[Abstract/Free Full Text]

14. Whisnant JP, Homer D, Ingall TJ, Baker HL, O'Fallon WM, Wiebers DO. Duration of cigarette smoking is the strongest predictor of severe extracranial carotid artery atherosclerosis. Stroke. 1990;21:707–714.[Abstract/Free Full Text]

15. Homer D, Ingall TJ, Baker HL, O'Fallon WM, Kottke BA, Whisnant JP. Serum lipids and lipoproteins are less powerful predictors of extracranial carotid artery atherosclerosis than are cigarette smoking and hypertension. Mayo Clin Proc. 1991;66:259–267.[Medline] [Order article via Infotrieve]

16. Howard G, Burke GL, Szklo M, Tell GS, Eckfeldt J, Evans G, Heiss G. Active and passive smoking are associated with increased carotid wall thickness. Arch Intern Med. 1994;154:1277–1282.[Abstract/Free Full Text]

17. Sacco RL, Kargman DE, Gu Q, Zamanillo MC. Race-ethnicity and determinants of intracranial atherosclerotic cerebral infarction: the Northern Manhattan Stroke Study. Stroke. 1995;26:14–20.[Abstract/Free Full Text]

18. Zwiebel WJ. Analysis of carotid Doppler signals. In: Zwiebel WJ, ed. Vascular Ultrasonography. 2nd ed. Philadelphia, Pa: WB Saunders; 1986:171–216.

19. Howard G, Chambless LE, Baker WH, Ricotta JJ, Jones AM, O'Leary D, Howard VJ, Elliott TJ, Lefkowitz DS, Toole JF. A multicenter validation study of Doppler ultrasound versus angiography. J Stroke Cerebrovasc Dis. 1991;1:166–173.

20. Mast H, Thompson JLP, Völler H, Mohr JP, Marx P. Cardiac sources of embolism in patients with pial artery infarcts and lacunar lesions. Stroke. 1994;25:776–781.[Abstract]

21. Büdingen HJ, von Reutern GM, Freund HJ. Doppler-Sonographie der extrakraniellen Hirnarterien: Grundlagen, Methodik, Fehlermöglichkeiten, Ergebnisse. Stuttgart, Germany: Georg Thieme Verlag; 1982.

22. Kriessmann A, Bollinger A, Keller HM. Praxis der Doppler-Sonographie: Periphere Arterien und Venen, hirnversorgende Arterien. Stuttgart, Germany: Georg Thieme Verlag; 1990.

23. Stapf C, Hartmann A, Seyfert S, Hupp T, Koch HC, Marx P, Mast H. Carotid stenosis estimation agreement between pre-operative angiography and plaque cylinder from eversion endarterectomy. Cerebrovasc Dis. 1996;6(suppl 2):32. Abstract.

24. Menotti A, Mariotti S, Seccareccia S, Giampoali S. The 25 year estimated probability of death from some specific causes as a function of twelve risk factors in middle aged men. Eur J Epidemiol. 1988;4:60–67.[Medline] [Order article via Infotrieve]

25. Boysen G, Nyboe J, Appleyard M, Sorensen PS, Boas J, Somnier F, Jensen G. Stroke incidence and risk factors for stroke in Copenhagen, Denmark. Stroke. 1988;19:1345–1353.[Abstract/Free Full Text]

26. Kawachi I, Colditz G, Stampfer M. Smoking cessation and decreased risk of stroke in women. JAMA. 1993;269:232–236.[Abstract/Free Full Text]

27. Sacco RL, Kargman DE, Gu Q, Boden-Albala B, Paik M, Shea S, Hauser WA, Ginsberg HN. Predictors of carotid plaque in a multi-ethnic cohort. Stroke. 1995;26:170. Abstract.

28. Sacco RL, Ellenberg JH, Mohr JP, Tatemichi TK, Hier DB, Price TR, Wolf PA. Infarcts of undetermined cause: the NINCDS Stroke Data Bank. Ann Neurol. 1989;25:382–390.[Medline] [Order article via Infotrieve]

This article has been cited by other articles:

				R. M. Samuelson, J. Yamamoto, E. I. Levy, A. H. Siddiqui, and L. N. Hopkins The Argument to Support Broader Application of Extracranial Carotid Artery Stent Technology Circulation, October 2, 2007; 116(14): 1602 - 1610. [Full Text] [PDF]

				K. I. Paraskevas, D. P. Mikhailidis, and C. D. Liapis Internal Carotid Artery Occlusion: Association With Atherosclerotic Disease in Other Arterial Beds and Vascular Risk Factors Angiology, June 1, 2007; 58(3): 329 - 335. [Abstract] [PDF]

				R. L. Sacco, R. Adams, G. Albers, M. J. Alberts, O. Benavente, K. Furie, L. B. Goldstein, P. Gorelick, J. Halperin, R. Harbaugh, et al. Guidelines for Prevention of Stroke in Patients With Ischemic Stroke or Transient Ischemic Attack: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association Council on Stroke: Co-Sponsored by the Council on Cardiovascular Radiology and Intervention: The American Academy of Neurology affirms the value of this guideline. Circulation, March 14, 2006; 113(10): e409 - e449. [Abstract] [Full Text] [PDF]

				R. L. Sacco, R. Adams, G. Albers, M. J. Alberts, O. Benavente, K. Furie, L. B. Goldstein, P. Gorelick, J. Halperin, R. Harbaugh, et al. Guidelines for Prevention of Stroke in Patients With Ischemic Stroke or Transient Ischemic Attack: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association Council on Stroke: Co-Sponsored by the Council on Cardiovascular Radiology and Intervention: The American Academy of Neurology affirms the value of this guideline. Stroke, February 1, 2006; 37(2): 577 - 617. [Abstract] [Full Text] [PDF]

				C. Hajat, K. Tilling, J. A. Stewart, N. Lemic-Stojcevic, and C. D.A. Wolfe Ethnic Differences in Risk Factors for Ischemic Stroke: A European Case-Control Study Stroke, July 1, 2004; 35(7): 1562 - 1567. [Abstract] [Full Text] [PDF]

				A. J. Grau, C. Weimar, F. Buggle, A. Heinrich, M. Goertler, S. Neumaier, J. Glahn, T. Brandt, W. Hacke, and H.-C. Diener Risk Factors, Outcome, and Treatment in Subtypes of Ischemic Stroke: The German Stroke Data Bank Stroke, November 1, 2001; 32(11): 2559 - 2566. [Abstract] [Full Text] [PDF]

				J Forsblad, A Gottsater, T Matzsch, and F Lindgarde Predictors of carotid endarterectomy in middle-aged individuals Vascular Medicine, May 1, 2001; 6(2): 81 - 85. [Abstract] [PDF]

				O. Fustinoni and J. Biller Ethnicity and Stroke : Beware of the Fallacies Stroke, May 1, 2000; 31(5): 1013 - 1015. [Full Text] [PDF]

				G. W. Petty, R. D. Brown Jr, J. P. Whisnant, J. D. Sicks, W. M. O’Fallon, and D. O. Wiebers Ischemic Stroke Subtypes : A Population-Based Study of Incidence and Risk Factors Stroke, December 1, 1999; 30(12): 2513 - 2516. [Abstract] [Full Text] [PDF]

				P. B. Gorelick, R. L. Sacco, D. B. Smith, M. Alberts, L. Mustone-Alexander, D. Rader, J. L. Ross, E. Raps, M. N. Ozer, L. M. Brass, et al. Prevention of a First Stroke: A Review of Guidelines and a Multidisciplinary Consensus Statement From the National Stroke Association JAMA, March 24, 1999; 281(12): 1112 - 1120. [Abstract] [Full Text] [PDF]

				R. Zidovetzki, P. Chen, M. Fisher, F. M. Hofman, and F. M. Faraci Nicotine Increases Plasminogen Activator Inhibitor-1 Production by Human Brain Endothelial Cells via Protein Kinase C–Associated Pathway • Editorial Comment Stroke, March 1, 1999; 30(3): 651 - 655. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) 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 Mast, H. Articles by Sacco, R. L. Search for Related Content PubMed PubMed Citation Articles by Mast, H. Articles by Sacco, R. L.