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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1995;15:1094-1097.)
© 1995 American Heart Association, Inc.

Articles

Determinants of Fibrin D-Dimer in the Edinburgh Artery Study

Amanda J. Lee; F. Gerald R. Fowkes; Gordon D. O. Lowe; Ann Rumley

From the Wolfson Unit for Prevention of Peripheral Vascular Diseases, Department of Public Health Sciences, University of Edinburgh, and the Haemostasis, Thrombosis, and Vascular Medicine Unit (G.D.O.L., A.R.), University Department of Medicine, Glasgow Royal Infirmary, Glasgow, UK.

	Abstract

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Abstract There is growing evidence that fibrin D-dimer is associated with coronary and peripheral atherosclerosis. Using data from the Edinburgh Artery Study, we examined the distribution of fibrin D-dimer in 1592 men and women 55 to 74 years old and assessed its relationship with a range of cardiovascular risk factors. Fibrin D-dimer levels were higher in women than in men (P.05) and increased with age (P.001). Current cigarette smokers had higher levels than ex-smokers, who, in turn, had higher levels than those who had never smoked. On multiple regression analyses with age and plasma fibrinogen as covariates, only lifetime smoking in men and systolic blood pressure in women were independent predictors of fibrin D-dimer levels. Since fibrin D-dimer does not appear to be independently related to many of the common cardiovascular risk factors, it may be a useful index of the thrombotic contribution to arterial disease.

Key Words: fibrin D-dimer • risk factors • atherosclerosis

	Introduction

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Both population and case-control studies have shown an increased risk of cardiovascular events associated with variations in several coagulation and fibrinolytic factors.^{1 2 3 4 5} Activation of coagulation as well as activation of the fibrinolytic system generates increased plasma levels of fibrin degradation products. In particular, fibrin D-dimer (a characteristic breakdown product of cross-linked fibrin) has been associated with arterial disease and atrial fibrillation and is both a primary and a secondary predictor of coronary events.^{6 7 8 9 10 11 12 13} However, there have been very few reports on the epidemiology of fibrin D-dimer. Therefore, using data from the cross-sectional Edinburgh Artery Study, the aims of this report were to (1) examine the distribution of fibrin D-dimer in the older population and (2) assess the interrelationships between fibrin D-dimer and a range of cardiovascular risk factors.

	Methods

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The Edinburgh Artery Study is a cross-sectional survey of 1592 men and women 55 to 74 years old selected from the age/sex registers of 10 general practices with catchment populations spread geographically and socioeconomically throughout the city of Edinburgh. The sample was selected randomly within sex-specific 5-year age groups to produce equal numbers in each group. Subjects attended a university clinic in which they completed an extensive questionnaire and had a comprehensive medical examination. The response rate was 65%, and a follow-up of nonresponders did not show any significant bias. Details of the study population, recruitment, and prevalence of peripheral arterial disease have been described elsewhere.¹⁴

The questionnaire included validated questions on social class, smoking history, alcohol intake, and exercise. A food frequency questionnaire was used to obtain nutrient information,¹⁵ and multiple regression analysis was used to calculate energy-adjusted nutrient intakes for this population.¹⁶ Right arm blood pressure (systolic and diastolic phase V) was taken with a Hawksley random-zero sphygmomanometer with the subject lying supine after a 10-minute rest. Ankle systolic pressures were measured on the right and left legs with a Doppler probe and a random-zero sphygmomanometer. The ankle-brachial pressure index, which is the ratio of ankle to arm systolic pressure, was then calculated. In clinical practice, this measure is widely used to assess peripheral arterial disease and appears to be an adequate measure of both symptomatic and asymptomatic disease in populations.¹⁷ Standing height was measured without shoes to the nearest 5 mm with a free-standing metal rule on a heavy base. Weight was measured without shoes and outer clothing to the nearest 100 g on digital scales (Soehnle).

From a fasting blood sample, total cholesterol, HDL cholesterol, glucose, triglycerides, uric acid, thiocyanate, and -glutamyltransferase were estimated on a Cobas Bio analyzer by use of standard kits. Fibrinogen was measured in citrated plasma by a thrombin-clotting turbidimetric method in a centrifugal analyzer.¹⁸ Fibrin D-dimer antigen was measured in citrated plasma by an enzyme-linked immunosorbent assay (AGEN) based on a monoclonal antibody. A variety of other hemostatic factors, including urinary fibrinopeptide A by radioimmunoassay, were also measured as part of the Edinburgh Artery Study.

Statistical Methods
Data were analyzed on the Edinburgh University mainframe computer with SPSS-X and BMDP statistical packages. Of the 1592 participants of the Edinburgh Artery Study (809 men and 783 women), fibrin D-dimer was measured in 1437 subjects (737 men and 700 women), who form the basis of this report. The distributions of fibrin D-dimer, glucose, triglycerides, -glutamyltransferase, dietary fat, saturated fat, polyunsaturated fat, protein, cereal fiber, -tocopherol, retinol, ß-carotene, and linoleic acid were all highly skewed; thus, a logarithmic transformation was used in the analyses. As a measure of lifetime cigarette smoking, the number of years smoked multiplied by average number of packs smoked per day (pack-years) was calculated. The distribution of pack-years and of units of alcohol consumed in the previous week were both skewed; thus, a square-root transformation was used. Body mass index was calculated as weight divided by the square of height (kg/m²).

Overall difference of fibrin D-dimer between the sexes was assessed with Student's t test. Differences between the 5-year age groups were examined by analysis of variance. Partial correlation coefficients (after age adjustment) reflected the linear association between fibrin D-dimer and each of the continuous risk factors. It should be noted that because of the large sample size, even small correlations reached statistical significance. Levels of fibrin D-dimer across smoking, social class, and leisure activity groups were examined by analysis of covariance with age as the covariate.

Stepwise multiple linear regression with fibrin D-dimer as the dependent variable was used to examine the independence of those risk factors that had shown a significant univariate relationship. A forward stepping procedure was used, with age having forced entry. The model was then repeated with both age and fibrinogen having forced entry. The residuals for the multiple regression models were approximately normally distributed.

	Results

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Fibrin D-dimer levels were significantly higher in women and showed a trend of increasing values across the four 5-year age groups in both sexes (Table 1). The age-adjusted correlation coefficients between fibrin D-dimer and a range of cardiovascular risk factors are shown in Table 2 for men and women separately. Among men, fibrin D-dimer showed a significantly positive correlation with pack-years, uric acid, body mass index, and systolic blood pressure and a significantly negative correlation with HDL cholesterol and cereal fiber. For women, alcohol consumption and HDL cholesterol were significantly negatively correlated with fibrin-D dimer, whereas pack-years, triglycerides, uric acid, body mass index, blood pressure, and retinol showed statistically significant positive correlations. In addition, fibrin D-dimer was significantly associated with plasma fibrinogen in both sexes.

View this table: [in this window] [in a new window]   Table 1. Geometric Mean (95% Confidence Interval) Fibrin D-Dimer Levels by Age and Sex

View this table: [in this window] [in a new window]   Table 2. Age-Adjusted Correlation Coefficients Between Fibrin D-Dimer and Cardiovascular Risk Factors

Among the men, 26.1% were current cigarette smokers, 50.2% were ex–cigarette smokers, and 23.7% reported having never smoked cigarettes. The corresponding percentages among the women were 25.6%, 25.2%, and 49.2%, respectively. As shown in the Figure, male current smokers had higher fibrin D-dimer levels than male ex-smokers who, in turn, had higher levels than the male never-smokers. In women, current smokers had higher fibrin D-dimer levels than either the ex- or never-smokers, although never-smokers had slightly higher levels than the ex-smokers. Furthermore, the male current light smokers (1 to 9 cigarettes per day) had lower fibrin D-dimer levels than the current heavy smokers (30 or more cigarettes per day), whereas the moderate smokers (10 to 19 and 20 to 29 cigarettes per day) had intermediate fibrin D-dimer levels. Among the women, current light smokers had the highest fibrin D-dimer levels of all the current smoking groups.

View larger version (54K): [in this window] [in a new window]   Figure 1. Bar graph showing age-adjusted geometric mean fibrin D-dimer level (in nanograms per milliliter) by smoking status. Error bars indicate upper 95% confidence limit. Probability values for difference between current smoking groups (1 to 9, 10 to 19, etc, cigarettes [cigs] per day) were P.05 in men and P.001 in women. Probability values for difference between current, ex-, and never-smoking groups were P.001 in both sexes.

Table 3 shows evidence of a trend of increasing fibrin D-dimer levels across nonmanual to manual social classes in both sexes. In addition, those subjects who reported having taken no leisure activity in the previous week had elevated fibrin D-dimer levels compared with subjects who reported having taken some exercise. The group who partook in the most strenuous types of leisure activity showed the lowest levels of fibrin D-dimer.

View this table: [in this window] [in a new window]   Table 3. Age-Adjusted Geometric Mean (95% Confidence Interval) Fibrin D-Dimer by Social Class and Leisure Activity in Previous Week

Table 4 summarizes the results of the stepwise multiple regression analyses, which were used to identify any statistically independent determinants of fibrin D-dimer level. Age was used as a covariate in the initial model, whereas both age and fibrinogen were used as covariates in the second model. Among men, the major determinants of fibrin D-dimer were age, social class, pack-years, and HDL cholesterol. In the second model, age, fibrinogen, and pack-years had an independent effect on fibrin D-dimer level. Among women, age, systolic blood pressure, pack-years, and alcohol consumption had an independent effect in the first model, whereas in the second model, age, fibrinogen, and systolic blood pressure had an independent effect. In both sexes, addition of all the other variables did not significantly change the power of predicting fibrin D-dimer (multiple R=.44, R²=.19 for men and multiple R=.43, R²=.19 for women).

View this table: [in this window] [in a new window]   Table 4. Stepwise Regression Models of Fibrin D-Dimer and Cardiovascular Risk Factors

	Discussion

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Fibrin D-dimer is a characteristic degradation product of cross-linked fibrin. Elevated plasma D-dimer levels have been reported in subjects with either coronary and peripheral atherosclerosis^{7 8 9 10 19} or atrial fibrillation.¹² In addition, elevated D-dimer levels correlate with disease severity.^{7 20 21} However, there is little published information on the distribution and determinants of plasma D-dimer levels in the general population. The present analysis is based on the largest population sample of plasma fibrin D-dimer levels to date and, unlike some studies, includes data on both sexes. Our results indicate univariate associations of fibrin D-dimer with a range of cardiovascular risk factors. However, on multiple regression analyses with age and fibrinogen as covariates, only lifetime smoking among men and systolic blood pressure among women were independently associated with fibrin D-dimer levels.

In the present study, women had significantly higher fibrin D-dimer levels than men. This has previously been found in an Italian study²² and in a Scottish study among premenopausal women only (G. Lowe, personal communication). In contrast, Al-Zahrani et al⁷ found no sex differential in plasma D-dimer levels. Several reports have shown an increase in fibrin D-dimer levels with age,^{7 22} which may reflect an increase in the turnover of fibrin associated with age-related increases in endothelial disturbance and worsening atherosclerosis.

Consistent with a previous study,²² current smokers had higher fibrin D-dimer levels than ex- or never-smokers, although others have reported no difference between smokers and nonsmokers.^{6 7} In addition, there seemed to be some evidence of a dose-response effect of increasing fibrin D-dimer level with increasing amount smoked among male current smokers. This was not seen in another study (G. Lowe, personal communication). The stronger effect of smoking in men persisted on multivariate analyses, with pack-years being an independent determinant of fibrin D-dimer levels. One case-control study has suggested that smoking caused part of the increased fibrin formation in peripheral arterial disease.⁹ We also noted an interaction between smoking status and age in both sexes, with increases in fibrin D-dimer level across all four age groups in all smoking categories (current, ex, and never). Smoking over a long time most likely induces vascular modifications, which may lead to increased fibrin turnover.

Hypertensive patients have been reported to have higher fibrin D-dimer levels than normotensive individuals.^{22 23} In the present study, correlations between blood pressure and fibrin D-dimer levels were noted, which were of the same magnitude as in previous articles.^{7 24} However, no other study has reported an independent effect of blood pressure on fibrin D-dimer levels, as in the women in our study.

Several other studies have observed a correlation between fibrin D-dimer level and plasma fibrinogen level.^{7 9 22} This is possibly due to fibrin degradation products, such as D-dimer, stimulating fibrinogen synthesis by hepatocytes via the stimulation of the release of interleukin-6²⁵ or, alternatively, to increased fibrinogen levels causing hypercoagulability with increased fibrin turnover. Fibrinogen levels have been correlated with hypercoagulability, as measured by urinary fibrinopeptide A levels (r=.07, P.01 in the present study).

The relationship of fibrin D-dimer to both symptomatic and asymptomatic prevalent peripheral arterial disease in the Edinburgh Artery Study population has been reported elsewhere.²⁶ A linear relationship of increasing fibrin D-dimer across categories of increasing severity of peripheral vascular disease was found. In addition, after adjustment for a range of cardiovascular risk factors, fibrin D-dimer remained independently related both to the risk of intermittent claudication and to the degree of arterial disease (as measured by the ankle-brachial pressure index). Such results support previous, smaller studies^{7 8 9 19} and suggest a role for intravascular fibrin deposition in the development of peripheral atherosclerosis.

We can conclude that fibrin D-dimer does not seem to be highly correlated with the major cardiovascular risk factors, other than age, smoking, blood pressure, and plasma fibrinogen. Thus, it may be a useful index of the thrombotic contribution to arterial disease. It seems likely that increased intravascular fibrin formation found in subjects with coronary and peripheral atherosclerosis is related to the extent of arterial disease^{20 21} independently of major risk factors. Finally, since only about a quarter of the variation in fibrin D-dimer levels could be explained by known risk factors, further studies are needed to search for other genetic and/or environmental factors that affect fibrinolysis.

	Acknowledgments

 
This study was supported by a grant from the British Heart Foundation. We also thank the research staff: M. Apps, E. Cawood, J. Dunbar, P. Farquhar, S.E. Lennie, I. McGinley, E. Kerracher, A. Rattray, and F. Smith; also P. Griffiths, M. Orr, and C. Stewart for technical assistance.

	Footnotes

 
Reprint requests to Dr A.J. Lee, Wolfson Unit for Prevention of Peripheral Vascular Diseases, Department of Public Health Sciences, University of Edinburgh, Teviot Place, Edinburgh EH8 9AG, UK.

Received March 9, 1995; accepted May 5, 1995.

	References

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This Article Abstract Submit a response Alert me when this article is cited Alert me when eLetters are posted 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 Lee, A. J. Articles by Rumley, A. Search for Related Content PubMed PubMed Citation Articles by Lee, A. J. Articles by Rumley, A.