(Circulation. 1997;96:1102-1108.)
© 1997 American Heart Association, Inc.
Articles |
Prospective Study of Hemostatic Factors and Incidence of Coronary Heart Disease
The Atherosclerosis Risk in Communities (ARIC) Study
From the Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis (A.R.F.); Division of Hematology, University of Texas Medical School, Houston (K.K.W.); Collaborative Studies Coordinating Center, Chapel Hill, NC (W.D.R., L.E.C.); and NHLBI, NIH, Bethesda, Md (A.R.S.).
Correspondence to Dr Aaron R. Folsom, Division of Epidemiology, School of Public Health, University of Minnesota, Suite 300, 1300 S 2nd St, Minneapolis, MN 55454-1015. E-mail folsom{at}epivax.epi.umn.edu
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Abstract |
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Background Although hemostatic factors contribute to acute coronary syndromes and atherogenesis, few studies have prospectively evaluated the association between multiple hemostatic factors and coronary heart disease incidence.
Methods and Results The Atherosclerosis
Risk in Communities Study recruited 14 477 adults from 45 to 64 years
of age who were initially free of coronary heart disease.
Coronary disease risk factors and several plasma hemostatic
factors were measured, and incidence of coronary heart disease
was ascertained during an average follow-up of 5.2 years. Age-, race-,
and field center–adjusted relative risks of coronary heart
disease were significantly elevated (P
.05) per higher
value of fibrinogen (relative risk: men, 1.76; women, 1.54), white
blood cell count (men, 1.68; women, 2.23), factor VIII coagulant
activity (women, 1.25), and von Willebrand factor antigen (men,
1.20; women, 1.18). Adjustment for other risk factors attenuated these
associations for fibrinogen (adjusted relative risk: men, 1.48; women,
1.21), and it eliminated the white blood cell count, factor VIII, and
von Willebrand factor associations, consistent with the
other risk factors either confounding or partly operating through their
effects on the hemostatic variables. Adjusted standardized relative
risks of total mortality, ranging from 1.13 to 1.37, were also elevated
(P<.05) in relation to these four factors. There was no
association of coronary disease incidence with factor VII,
protein C, antithrombin III, or platelet count.
Conclusions Elevated levels of fibrinogen, white blood cell count, factor VIII, and von Willebrand factor are risk factors and may play causative roles in coronary heart disease. However, their measurement in healthy adults appears to add little to prediction of coronary events beyond that of more established risk factors.
Key Words: coagulation • coronary disease • von Willebrand factor • fibrinogen • leukocytes
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Introduction |
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Considerable evidence indicates that the hemostatic system plays an important role in the pathogenesis of atherosclerotic vascular diseases. Yet few prospective epidemiological studies have examined whether plasma levels of hemostatic factors among initially healthy individuals can predict the subsequent incidence of CHD. An increased plasma fibrinogen concentration1 2 3 4 5 6 and WBC4 7 8 9 are consistent risk factors for cardiovascular disease, and WBC effects may interact with the effects of fibrinogen.4 Prospective evidence for roles in CHD of factor VII,2 5 10 factor VIII,2 10 von Willebrand factor,10 11 12 platelet count,13 aPTT, and two anticoagulation factors, protein C 10 and AT-III,14 15 is more limited and inconsistent. Few prior studies have included women or ethnically diverse populations.
The ARIC Study16 measured hemostatic factors in a large sample of middle-aged adults. This report details the association of these factors with CHD incidence after an average follow-up of 5 years.
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Methods |
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Study Population
The ARIC Study16 17 included a cohort totaling 15 792 persons between 45 and 64 years of age at recruitment in 1987 through 1989. Population samples were selected from Forsyth County, North Carolina; Jackson, Miss (blacks only); the northwest suburbs of Minneapolis, Minn; and Washington County, Maryland. Participants underwent reexamination in 1990 through 1992 (93% return rate) and in 1993 through 1995 (86% return rate).
Baseline Measurements
Blood was drawn after an 8-hour fasting period with minimal
trauma from an antecubital vein. Detailed methods for hemostatic
variables have been published.18 19 In brief,
fibrinogen was measured by the thrombin-time titration
method20 with reagents and calibration materials
(Fibriquik) obtained from General Diagnostics
(Organon-Technika Co). Factor VII and VIII activities were measured by
determining the ability of the tested sample to correct the clotting
time of human factor VII– or factor VIII–deficient plasma obtained
from George King Biomedical Inc. von Willebrand factor antigen
and protein C antigen were determined by ELISA kits from American
Bioproducts Co. AT-III activity was measured by a
chromogenic substrate method. aPTT was measured on an
automated coagulometer (Coag-A-Mate X-2, General
Diagnostics). The reference material for assays was the
Universal Coagulation Reference Plasma (Thromboscreen, Pacific
Hemostasis, Curtin Matheson Scientific, Inc). Reliability coefficients
(method variance plus intraindividual variance divided by total
variance) obtained from repeated testing of individuals over several
weeks were 0.72 for fibrinogen, 0.78 for factor VII, 0.86 for factor
VIII, 0.68 for von Willebrand factor, 0.56 for protein C, 0.42
for AT-III, and 0.92 for aPTT.21
Plasma total cholesterol22 and
triglycerides23 were measured by enzymatic
methods, and LDL cholesterol was calculated.24
HDL cholesterol was measured after dextran-magnesium
precipitation of non-HDL lipoproteins.25 Prevalent
diabetes mellitus was defined as a fasting glucose level 
140 mg/dL,
nonfasting glucose level 200 mg/dL, and/or a history of or treatment
for diabetes. Platelet counts and WBCs were measured by Coulter
counters in laboratories in each study community.
The ratio of waist (umbilical level) and hip (maximum buttocks) circumferences was calculated as a measure of fat distribution. Three blood pressure measurements were taken with a random-zero sphygmomanometer. The mean of the last two measurements was used. Physical activity was expressed as a sport index ranging from 0 (low) to 5 (high).26 Average carotid intima-media thickness was assessed by use of a standardized B-mode ultrasonographic technique.27 28 Prevalent CHD at baseline was defined, for exclusion, as a reported history of a physician-diagnosed heart attack, prior MI by ECG, or prior cardiovascular surgery or coronary angioplasty. Persons with exertional angina by questionnaire29 (4% of the cohort) were not excluded because doing so had no impact on results.
Ascertainment of Incident Events
CHD incidence in ARIC was identified as previously
described.17 30 For hospitalized patients, trained
abstractors recorded the presenting signs and symptoms,
including chest pain, cardiac enzymes, and related clinical
information. Up to three 12-lead ECGs were visually coded with the
Minnesota Code,31 and waveform evolution was evaluated by
use of side-by-side comparisons. Out-of-hospital deaths were
investigated by means of the death certificate and, in most cases, an
interview with next of kin and questionnaires completed by the
patient's physicians. Coroner reports and autopsy reports, when
available, were used for validation.
CHD incidence was defined for this article as a definite, probable, or silent MI or definite CHD death by use of published criteria.30 Unrecognized MI was defined by the appearance between the first and subsequent ARIC examinations of a major Q wave or a minor Q wave with ischemic ST-T changes or an MI by computerized NOVACODE32 criteria confirmed by side-by-side visual ECG comparison.
Data Analysis
Of the 15 792 ARIC participants, 14 477 were free of CHD at
baseline, were not taking anticoagulants, and had at least one
hemostatic factor measured. Sex-specific and age-, race-, and ARIC
field center–adjusted mean baseline values of hemostatic factors were
compared by ANCOVA for participants who did versus did not develop an
incident CHD event during follow-up. Incidence rates were calculated by
dividing the number of events by the person-years of follow-up, within
thirds of the distributions of hemostasis variables, on the basis
of tertiles of the entire sample distribution. Quintiles were also used
sometimes. Length of follow-up was calculated for clinically recognized
cases as the time elapsed from the baseline examination to the first
CHD event. The date of unrecognized MI, being unknown, was assigned
arbitrarily as the midpoint between the ARIC examination at which an
ECG revealed it and the immediately prior examination. For noncases,
follow-up continued until the date of death, date of last contact (if
lost), or through December 31, 1993. Age-, race-, and field
center–adjustment of rates was accomplished by use of sex-specific
Poisson regression models using 5-year age groupings.
Multivariate modeling to obtain relative risks of
incident CHD and total mortality in relation to hemostasis factors was
performed by use of proportional hazards regression. Hemostatic factors
were stratified by thirds or treated as continuous variables.
Curvilinear associations were tested by including a quadratic term in
each continuous variable model, retaining it when significant
(P<.05). Correlates of hemostatic factors, which might
serve as determinants of the effects of hemostatic factors or as
potential confounders in the analysis, had been detailed in
previous ARIC publications.33 34 35 36 37 38 We chose to adjust for
age, race (black, other), ARIC field center (three dummy
variables), LDL cholesterol, HDL
cholesterol, systolic blood pressure,
antihypertensive medication use (yes, no), diabetes (yes, no),
cigarette smoking (current, former, never), pack-years of cigarettes,
waist-to-hip ratio, and sport index. Relative risks and 95% CIs were
computed for the highest versus lowest third or per SD of study
variables (standardized relative risks). In the case of a quadratic
association, the standardized relative risk was calculated for an
increment of 1 SD centered at the mean of the study variable. In a
supplemental analysis, we also corrected standardized relative
risks for measurement error in hemostatic factors with the formula
SSRcorrected=e
(SD)/R,
where ß is the regression coefficient and R is the reliability
coefficient. Reliability data were not available for WBC and
platelet count.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The ARIC cohort included 27% blacks; almost all other participants were white. Several of the baseline hemostatic factors were interrelated: factor VIII with von Willebrand factor (Pearson r=.71), factor VIII or von Willebrand factor with aPTT (r=-.31 and -.46), factor VIII or von Willebrand factor with fibrinogen (r=.26 and .29), WBC with fibrinogen (r=.29), WBC with platelet count (r=.24), and factor VII with protein C (r=.40).
Over the 4 to 7 years of follow-up, 238 men developed incident CHD
events (169 nonfatal or fatal clinically recognized MI, 40 other fatal
CHD, 29 "silent" MI), as did 110 women (87 clinical MI, 11 fatal
CHD, and 12 "silent" MI). Men who developed incident CHD had
higher (P<.05) age-, race-, and ARIC field center–adjusted
mean baseline values of fibrinogen, von Willebrand factor, and
WBCs than did men who remained free of CHD (Table 1
).
Women who developed CHD also had elevations in these three
parameters and in mean factor VII and VIII coagulant
activities. The adjusted mean values of these variables in those
who developed CHD were approximately 1/5 to 1/2 SD higher
than in those who did not develop CHD. There was no significant
difference in mean protein C, AT-III, aPTT, or platelet count
between these two groups.
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Age-, race-, and field center–adjusted incidence rates of CHD rose
significantly from the lowest to highest thirds of the fibrinogen
distribution: 2.77-fold in men and 2.63-fold in women (the
Figure). For the highest versus lowest fifth of the
fibrinogen distribution (not shown), relative risks were 3.66 and 3.50,
respectively. Relative risks of CHD rose 1.22- to 1.53-fold across
thirds of factor VIII or von Willebrand factor in men and women
(the Figure). Relative risks for the highest versus lowest third of
platelet count were 1.28 in men and 1.52 in women, although neither
trend was statistically significant. Relative risks were significantly
elevated for the highest versus lowest third of WBC: 2.62 in men and
4.24 in women. Incidence rates of CHD were not appreciably associated
with factor VII, protein C, AT-III, or aPTT. Although some of the
associations depicted in the Figure appeared to differ between men and
women, sex differences in relative risks were not statistically
significant.
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The Figure
also provides the relative risks of CHD per each SD-higher
level of the hemostatic factors (standardized relative risks) derived
from proportional hazards regression analysis. For three
associations that required a quadratic term in addition to a linear
term (fibrinogen in men and WBC in both sexes), the standardized
relative risk is for an increment of 1 SD centered at the mean. Thus,
in women, the age-, race-, and field center–adjusted incidence of CHD
was 54% higher per SD increment (65 mg/dL) of fibrinogen. In men, CHD
incidence was 76% higher for a fibrinogen of 335 versus 270 mg/dL. CHD
incidence was 10% to 25% higher per each SD increment in factor VIII
or von Willebrand factor. These standardized relative risks
were somewhat higher when corrected for measurement error. CHD
incidence was 68% higher in men and 123% higher in women for a WBC of
7000 versus 5100 cells/mm3. Although the factor VII
standardized relative risk in women was 1.25 (P=.02), there
was no evidence of a monotonic trend in incidence across thirds (the
Figure) or fifths (not shown) of the factor VII distribution.
Furthermore, after adjustment for other major risk factors, there was
no statistically significant association of factor VII with CHD
incidence or CHD mortality (data not shown).
Table 2 shows that for the most part, fibrinogen and WBC
were CHD risk factors in blacks and whites, older and younger
participants, smokers and nonsmokers, and in those individuals above
and below the median carotid intima-media wall thickness. Although CIs
mostly overlapped 1.0, relative risks for factor VIII and von
Willebrand factor were also elevated for these subgroups and
were especially elevated for blacks compared with whites. These
associations also generally held within strata on the basis of a median
split of other major risk factors (not shown). Tests for two-way
interactions (and specifically of fibrinogen with WBC4 and
LDL cholesterol5 12 ) were not statistically
significant.
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A number of accepted CHD risk factors, eg, cigarette smoking,
hypertension, diabetes, and physical inactivity, may exert their
effects through elevations of plasma fibrinogen, factor VIII, von
Willebrand factor, or WBCs. To determine whether this could
have occurred in these data, we computed
multivariate-adjusted relative risks (Table 3) for comparison with the age-, race-, and field
center–adjusted relative risks (the Figure). The
multivariate-adjusted relative risks of CHD per
SD-higher fibrinogen concentration were 1.48 in men and 1.21 in women
(P<.05). The standardized relative risks for factor VIII,
von Willebrand factor, and WBC were no longer statistically
significantly different from 1.0 after multivariate
adjustment. Attenuation of the relative risks with adjustment suggests
that the accepted risk factors partially accounted for the positive
association of fibrinogen with CHD and almost totally accounted for the
factor VIII, von Willebrand factor, and WBC associations. The
risk factor covariates that most attenuated the associations of
fibrinogen and WBC with CHD were smoking (both sexes), HDL
cholesterol (men), and LDL cholesterol (women);
the factor VIII and von Willebrand factor associations with CHD
were attenuated most by the inclusion of diabetes.
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Higher levels of plasma fibrinogen, factor VIII, von Willebrand factor, and WBC were also associated with increased all-cause mortality. Adjusted relative risks of death ranged from 1.13 to 1.37 per SD increment of these factors. Insufficient numbers precluded detailed analyses by underlying cause of death, but generally all four hemostatic factors were associated positively with cardiovascular deaths and noncancer/noncardiovascular deaths, and fibrinogen was associated with cancer deaths.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The ARIC Study assessed whether levels of hemostatic factors in middle-aged adults free of CHD predict the incidence of CHD during an average of 5.2 years of follow-up. We found that CHD incidence was associated positively with fibrinogen, WBC, factor VIII, and von Willebrand factor. This was true for women and men and for blacks and whites. CHD was not associated with factor VII, AT-III, protein C, or platelet count.
The associations of fibrinogen with CHD were moderately strong in both
men and women. Smaller studies, primarily of men, also have found
fibrinogen associated positively with CHD incidence1 2 3 4 5 6 and
with other atherosclerotic vascular diseases.6 In a pooled
analysis,6 the odds ratio of CHD for the highest
versus lowest tertile of fibrinogen among six studies was 2.3 (95% CI,
1.9 to 2.8) versus age-, race-, and field center–adjusted relative
risks of 2.77 and 2.63 in ARIC men and women, respectively. Fibrinogen
is correlated positively with most other CHD risk
factors.33 Thus, in ARIC, as in other studies,
multivariate adjustment reduced the relative risks.
This suggests that fibrinogen could mediate some of the effect of other
risk factors (in ARIC, primarily smoking and plasma lipids). However,
even in nonsmokers and most other subgroups (Table 2), fibrinogen
proved to be a CHD risk factor.
Elevated fibrinogen could predict incident CHD because it may reflect the inflammatory activity of progressing atherosclerosis. Yet there are also direct mechanisms by which fibrinogen may contribute to acute coronary events.2 Fibrinogen stimulates smooth muscle migration and proliferation, is a component of atherosclerotic plaques, promotes platelet aggregation, and is a major contributor to blood viscosity and thrombi,2 all of which may contribute to coronary disease.
The association of WBC with CHD was moderately strong in ARIC,
corroborating prior studies,4 7 8 9 but it was reduced
substantially by controlling for other risk factors (primarily smoking
and lipids). We did not find a statistical interaction between the
association of fibrinogen and WBC with CHD incidence as was reported
previously.4 Oxidant-generating stimuli (eg, smoking) may
raise the WBC, but WBC proved to be a CHD risk factor even in
nonsmokers and most other subgroups (Tables 2 and 3). WBC contributes
to blood viscosity and participates in endothelial
injury,9 both of which may increase risk of CHD. However,
as with fibrinogen, WBC elevations also may reflect the inflammatory
activity of atherosclerosis.
A few prospective clinical studies have linked higher von Willebrand factor antigen levels with a greater risk of acute events among patients with CHD.10 11 12 However, to the best of our knowledge, no previous prospective study of healthy adults has reported a positive association between von Willebrand factor and subsequent CHD incidence. Elevated von Willebrand factor levels are believed to indicate endothelial dysfunction and vascular inflammation,39 may promote platelet adhesion to damaged arterial walls, and may enhance platelet aggregation under sheer stress.40 In women, factor VIII was also positively associated with CHD incidence, which might be expected because factor VIII is bound to von Willebrand factor in plasma and there is a correlation of 0.71 between these two factors. The Northwick Park Heart Study also reported a positive association of factor VIII with CHD in men during early follow-up,41 but it did not persist with longer follow-up.2 Despite their univariate predictions, which were especially strong in blacks, neither von Willebrand factor nor factor VIII was associated independently with CHD in ARIC. The likely risk factor, diabetes, elevates von Willebrand factor and factor VIII.35
We found that fibrinogen, factor VIII, von Willebrand factor, and WBC also were associated positively with total mortality; this appeared to include both noncardiovascular and cardiovascular deaths. Others have reported similar associations between these factors and mortality.2 41 A number of chronic conditions elevate hemostatic factors, especially those that are acute-phase reactants, so the observed associations with total mortality may not be totally causal.
The Northwick Park Heart Study reported a strong positive association between factor VII coagulant activity and CHD incidence in middle-aged men.2 The Prospective Cardiovascular Münster Study also found a positive association, although it did not quite achieve statistical significance.5 In contrast, other investigators have found no association of factor VII with CHD.4 42 A role for factor VII is plausible because it plays a key role in coagulation. A possible reason for discrepancies among studies is the factor VII assay used. The Northwick Park Heart Study used a factor VII assay that seems to be more sensitive than the assay used in ARIC Study in detecting the activated form of factor VII.43
The Northwick Park Heart Study investigators reported a significant
U-shaped association between AT-III, an inhibitor of
thrombin, and CHD; risks were elevated for both low and high AT-III
levels.14 In contrast, AT-III activity was associated
inversely with cardiac events in patients with angina.15
We found a U-shaped association only in women (the Figure), but it was
not statistically significant. Protein C, an inhibitor of
factors V and VIII, also was not associated with CHD. Measurement
error, however, is excessive for AT-III and protein C,21
substantially reducing our chances of showing an association with CHD,
if one exists.
A previous study found platelet count to be associated positively with CHD incidence,3 but Meade et al41 did not. We observed a suggestive but statistically insignificant positive association in both men and women. Four separate laboratories, using automated methods, measured the platelet counts in ARIC participants; nonstandardization could have obscured associations of the platelet count with CHD.
Other potential limitations of this study warrant consideration. ARIC
made a single assessment of hemostatic factors, which may lead to
misclassification of the habitual hemostatic factor levels of some
individuals. Correction for measurement unreliability strengthens the
relative risk estimates (the Figure). The accumulated follow-up was
relatively short, and there were too few CHD events for the detection
of small effects, especially in subgroup analyses. Although
participants with clinical CHD at baseline were excluded, a large
number of participants may have had alterations of hemostasis because
of subclinical disease. Although this could weaken cause-effect
inferences from these data, it does not diminish the predictive
capacity of elevated levels of fibrinogen and WBC, particularly for
CHD. Finally, the interpretation of the weaker associations of
hemostatic factors with CHD after multivariate
adjustment is complicated. If the adjusting factors were merely
confounding variables, then the multivariate
relative risks are the most informative. However, if, as is suspected,
several risk factors operate through hemostatic mechanisms, then the
relative risks adjusted only for age, race, and field center
represent the mechanistic aspects of these hemostatic
variables on CHD.
From a preventive-medicine point of view, only measurement of
fibrinogen (and not the other hemostatic factors) contributed anything
beyond traditional risk factors in the prediction of CHD. A fibrinogen
measurement costs approximately the same as a lipid profile, so it
could be considered for risk factor screening. However, there is no
universal standardization system for the fibrinogen assay, and the
independent contribution of fibrinogen to prediction of risk appears to
be modest (Table 3). There also has been no clinical trial yet to
demonstrate that lowering fibrinogen will prevent CHD. These facts
suggest that routine screening for elevated fibrinogen in healthy
adults is currently not warranted.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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The ARIC study was funded by NHLBI contracts N01-HC-55015, N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021, and N01-HC-55022. We appreciate the important contributions of the following ARIC personnel: Phyllis Johnson, Marilyn Knowles, Catherine Paton, Dawn Scott, Nadine Shelton, Carol Smith, and Pamela Williams from the University of North Carolina, Chapel Hill; Betty Warren, Dorothy Washington, Mattye Watson, and Nancy Wilson from the University of Mississippi Medical Center, Jackson; Paul McGovern, Fangzi Liao, Susan Winkhart, Laura Kemmis, Maxine Dammen, Caryl DeYoung, Jaci Dion, and Lowell Hedquist from the University of Minnesota, Minneapolis; Joyce Chabot, Carol Christman, Mary Ann Cocodrilli, and Dorrie Costa from Johns Hopkins University, Baltimore, Md; Valarie Stinson, Pam Pfile, Hoang Pham, and Teri Trevino from the University of Texas Medical School, Houston; Wanda Alexander, Doris Harper, Charlie Rhodes, and Selma Soyal from the Atherosclerosis Clinical Laboratory, Methodist Hospital, Houston, Tex; Mary Lauffer, Suzanne Pillsbury, Tiffany Robertson, and Anne Safrit from the Ultrasound Reading Center, Bowman-Gray School of Medicine, Winston-Salem, NC; and Debbie Rubin-Williams, Climmon Walker, Louis Wijnberg, and Kiduk Yang from the ARIC Coordinating Center, University of North Carolina, Chapel Hill.
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Footnotes |
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Guest editor for this article was James H. Chesebro, MD, Cardiovascular Institute, New York, NY.
Received September 24, 1996; revision received March 25, 1997; accepted March 26, 1997.
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V. Salomaa, V. Rasi, S. Kulathinal, E. Vahtera, M. Jauhiainen, C. Ehnholm, and J. Pekkanen Hemostatic Factors as Predictors of Coronary Events and Total Mortality: The FINRISK '92 Hemostasis Study Arterioscler Thromb Vasc Biol, February 1, 2002; 22(2): 353 - 358. [Abstract] [Full Text] [PDF]
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M. Pahor, L. V. Franse, S. R. Deitcher, W. C. Cushman, K. C. Johnson, R. I. Shorr, K. Kottke-Marchant, R. P. Tracy, G. W. Somes, and W. B. Applegate Fosinopril Versus Amlodipine Comparative Treatments Study: A Randomized Trial to Assess Effects on Plasminogen Activator Inhibitor-1 Circulation, January 29, 2002; 105(4): 457 - 461. [Abstract] [Full Text] [PDF]
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J. Borawski and M. Mysiwiec Effects of Recombinant Erythropoietin Therapy on Circulating Endothelial Markers in Hemodialysis Patients Clinical and Applied Thrombosis/Hemostasis, January 1, 2002; 8(1): 77 - 84. [Abstract] [PDF]
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 J. D Mills and P. J Grant Insulin resistance, haemostatic factors and cardiovascular risk The British Journal of Diabetes & Vascular Disease, January 1, 2002; 2(1): 19 - 26. [Abstract] [PDF]
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V. Palmieri, A. Celentano, M. J. Roman, G. de Simone, M. R. Lewis, L. Best, E. T. Lee, D. C. Robbins, B. V. Howard, and R. B. Devereux Fibrinogen and Preclinical Echocardiographic Target Organ Damage: The Strong Heart Study Hypertension, November 1, 2001; 38(5): 1068 - 1074. [Abstract] [Full Text] [PDF]
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C. D. Lee, A. R. Folsom, F. J. Nieto, L. E. Chambless, E. Shahar, and D. A. Wolfe White Blood Cell Count and Incidence of Coronary Heart Disease and Ischemic Stroke and Mortality from Cardiovascular Disease in African-American and White Men and Women: Atherosclerosis Risk in Communities Study Am. J. Epidemiol., October 15, 2001; 154(8): 758 - 764. [Abstract] [Full Text] [PDF]
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 J. Borawski, B. Naumnik, K. Pawlak, and M. Mysliwiec Endothelial dysfunction marker von Willebrand factor antigen in haemodialysis patients: associations with pre-dialysis blood pressure and the acute phase response Nephrol. Dial. Transplant., July 1, 2001; 16(7): 1442 - 1447. [Abstract] [Full Text] [PDF]
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K. Yano, J. S. Grove, R. Chen, B. L. Rodriguez, J. D. Curb, and R. P. Tracy Plasma Fibrinogen as a Predictor of Total and Cause-Specific Mortality in Elderly Japanese-American Men Arterioscler Thromb Vasc Biol, June 1, 2001; 21(6): 1065 - 1070. [Abstract] [Full Text] [PDF]
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P. W. Kamphuisen, J. C. J. Eikenboom, and R. M. Bertina Elevated Factor VIII Levels and the Risk of Thrombosis Arterioscler Thromb Vasc Biol, May 1, 2001; 21(5): 731 - 738. [Full Text] [PDF]
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K. K. Wu, N. Aleksic, C. Ahn, E. Boerwinkle, A. R. Folsom, and H. Juneja Thrombomodulin Ala455Val Polymorphism and Risk of Coronary Heart Disease Circulation, March 13, 2001; 103(10): 1386 - 1389. [Abstract] [Full Text] [PDF]
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M. Cushman, J. P. Costantino, R. P. Tracy, K. Song, L. Buckley, J. D. Roberts, and D. N. Krag Tamoxifen and Cardiac Risk Factors in Healthy Women : Suggestion of an Anti-inflammatory Effect Arterioscler Thromb Vasc Biol, February 1, 2001; 21(2): 255 - 261. [Abstract] [Full Text] [PDF]
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D. F. Geffken, M. Cushman, G. L. Burke, J. F. Polak, P. A. Sakkinen, and R. P. Tracy Association between Physical Activity and Markers of Inflammation in a Healthy Elderly Population Am. J. Epidemiol., February 1, 2001; 153(3): 242 - 250. [Abstract] [Full Text] [PDF]
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J. A. Cooper, G. J. Miller, K. A. Bauer, J. H. Morrissey, T. W. Meade, D. J. Howarth, S. Barzegar, J. P. Mitchell, and R. D. Rosenberg Comparison of Novel Hemostatic Factors and Conventional Risk Factors for Prediction of Coronary Heart Disease Circulation, December 5, 2000; 102(23): 2816 - 2822. [Abstract] [Full Text] [PDF]
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E. M. Bladbjerg, A.-M. Munster, P. Marckmann, N. Keller, and J. Jespersen Dietary Factor VII Activation Does Not Increase Plasma Concentrations of Prothrombin Fragment 1+2 in Patients With Stable Angina Pectoris and Coronary Atherosclerosis Arterioscler Thromb Vasc Biol, November 1, 2000; 20(11): 2494 - 2499. [Abstract] [Full Text] [PDF]
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N. Aleksic, H. Juneja, A. R. Folsom, C. Ahn, E. Boerwinkle, L. E. Chambless, and K. K. Wu Platelet PlA2 Allele and Incidence of Coronary Heart Disease : Results From the Atherosclerosis Risk In Communities (ARIC) Study Circulation, October 17, 2000; 102(16): 1901 - 1905. [Abstract] [Full Text] [PDF]
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 D. Girelli, C. Russo, P. Ferraresi, O. Olivieri, M. Pinotti, S. Friso, F. Manzato, A. Mazzucco, F. Bernardi, and R. Corrocher Polymorphisms in the Factor VII Gene and the Risk of Myocardial Infarction in Patients with Coronary Artery Disease N. Engl. J. Med., September 14, 2000; 343(11): 774 - 780. [Abstract] [Full Text] [PDF]
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S. Sato, M. Nakamura, M. Iida, Y. Naito, A. Kitamura, T. Okamura, Y. Nakagawa, H. Imano, M. Kiyama, H. Iso, et al. Plasma Fibrinogen and Coronary Heart Disease in Urban Japanese Am. J. Epidemiol., September 1, 2000; 152(5): 420 - 423. [Abstract] [Full Text] [PDF]
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L. F. Bielak, G. G. Klee, P. F. Sheedy II, S. T. Turner, R. S. Schwartz, and P. A. Peyser Association of Fibrinogen With Quantity of Coronary Artery Calcification Measured by Electron Beam Computed Tomography Arterioscler Thromb Vasc Biol, September 1, 2000; 20(9): 2167 - 2171. [Abstract] [Full Text] [PDF]
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C. R. Isasi, T. J. Starc, R. P. Tracy, R. Deckelbaum, L. Berglund, and S. Shea Inverse Association of Physical Fitness with Plasma Fibrinogen Level in Children The Columbia University BioMarkers Study Am. J. Epidemiol., August 1, 2000; 152(3): 212 - 218. [Abstract] [Full Text] [PDF]
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J. C. Souto, L. Almasy, E. Muniz-Diaz, J. M. Soria, M. Borrell, L. Bayen, J. Mateo, P. Madoz, W. Stone, J. Blangero, et al. Functional Effects of the ABO Locus Polymorphism on Plasma Levels of von Willebrand Factor, Factor VIII, and Activated Partial Thromboplastin Time Arterioscler Thromb Vasc Biol, August 1, 2000; 20(8): 2024 - 2028. [Abstract] [Full Text] [PDF]
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I. Saito, A. R. Folsom, F. L. Brancati, B. B. Duncan, L. E. Chambless, and P. G. McGovern Nontraditional Risk Factors for Coronary Heart Disease Incidence among Persons with Diabetes: The Atherosclerosis Risk in Communities (ARIC) Study Ann Intern Med, July 18, 2000; 133(2): 81 - 91. [Abstract] [Full Text] [PDF]
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G. Montalescot, J. P. Collet, L. Lison, R.e. Choussat, A. Ankri, E. Vicaut, K. Perlemuter, F. Philippe, G.e. Drobinski, and D. Thomas Effects of various anticoagulant treatments on von Willebrand factor release in unstable angina J. Am. Coll. Cardiol., July 1, 2000; 36(1): 110 - 114. [Abstract] [Full Text] [PDF]
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M. Kumari, M. Marmot, and E. Brunner Social Determinants of von Willebrand Factor : The Whitehall II Study Arterioscler Thromb Vasc Biol, July 1, 2000; 20(7): 1842 - 1847. [Abstract] [Full Text] [PDF]
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R. Klein, A. R. Sharrett, B. E. K. Klein, L. E. Chambless, L. S. Cooper, L. D. Hubbard, and G. Evans Are Retinal Arteriolar Abnormalities Related to Atherosclerosis? : The Atherosclerosis Risk in Communities Study Arterioscler Thromb Vasc Biol, June 1, 2000; 20(6): 1644 - 1650. [Abstract] [Full Text] [PDF]
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M. Pinotti, R. Toso, D. Girelli, D. Bindini, P. Ferraresi, M. L. Papa, R. Corrocher, G. Marchetti, and F. Bernardi Modulation of factor VII levels by intron 7 polymorphisms: population and in vitro studies Blood, June 1, 2000; 95(11): 3423 - 3428. [Abstract] [Full Text] [PDF]
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J. M. Soria, L. Almasy, J. C. Souto, I. Tirado, M. Borell, J. Mateo, S. Slifer, W. Stone, J. Blangero, and J. Fontcuberta Linkage analysis demonstrates that the prothrombin G20210A mutation jointly influences plasma prothrombin levels and risk of thrombosis Blood, May 1, 2000; 95(9): 2780 - 2785. [Abstract] [Full Text] [PDF]
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D. Feng, G. H. Tofler, M. G. Larson, C. J. O’Donnell, I. Lipinska, C. Schmitz, P. A. Sutherland, M. T. Johnstone, J. E. Muller, R. B. D’Agostino, et al. Factor VII Gene Polymorphism, Factor VII Levels, and Prevalent Cardiovascular Disease : The Framingham Heart Study Arterioscler Thromb Vasc Biol, February 1, 2000; 20(2): 593 - 600. [Abstract] [Full Text] [PDF]
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A. R. Folsom, K. K. Wu, M. Rasmussen, L. E. Chambless, N. Aleksic, and F. J. Nieto Determinants of Population Changes in Fibrinogen and Factor VII Over 6 Years : The Atherosclerosis Risk in Communities (ARIC) Study Arterioscler Thromb Vasc Biol, February 1, 2000; 20(2): 601 - 606. [Abstract] [Full Text] [PDF]
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J. B. Meigs, M. A. Mittleman, D. M. Nathan, G. H. Tofler, D. E. Singer, P. M. Murphy-Sheehy, I. Lipinska, R. B. D'Agostino, and P. W. F. Wilson Hyperinsulinemia, Hyperglycemia, and Impaired Hemostasis: The Framingham Offspring Study JAMA, January 12, 2000; 283(2): 221 - 228. [Abstract] [Full Text] [PDF]
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A. Jager, V. W. M. van Hinsbergh, P. J. Kostense, J. J. Emeis, J. S. Yudkin, G. Nijpels, J. M. Dekker, R. J. Heine, L. M. Bouter, and C. D. A. Stehouwer von Willebrand Factor, C-Reactive Protein, and 5-Year Mortality in Diabetic and Nondiabetic Subjects : The Hoorn Study Arterioscler Thromb Vasc Biol, December 1, 1999; 19(12): 3071 - 3078. [Abstract] [Full Text] [PDF]
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M. Cushman, C. Legault, E. Barrett-Connor, M. L. Stefanick, C. Kessler, H. L. Judd, P. A. Sakkinen, and R. P. Tracy Effect of Postmenopausal Hormones on Inflammation-Sensitive Proteins : The Postmenopausal Estrogen/Progestin Interventions (PEPI) Study Circulation, August 17, 1999; 100(7): 717 - 722. [Abstract] [Full Text] [PDF]
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A. R. Folsom, W. D. Rosamond, E. Shahar, L. S. Cooper, N. Aleksic, F. J. Nieto, M. L. Rasmussen, and K. K. Wu Prospective Study of Markers of Hemostatic Function With Risk of Ischemic Stroke Circulation, August 17, 1999; 100(7): 736 - 742. [Abstract] [Full Text] [PDF]
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G. Mariani, J. Conard, F. Bernardi, R. Bertina, V. V. Garcia, H. Prydz, M. Samama, P. M. Sandset, M. Puopolo, M. V. Ciarla, et al. Oral Contraceptives Highlight the Genotype-Specific Association Between Serum Phospholipids and Activated Factor VII Arterioscler Thromb Vasc Biol, August 1, 1999; 19(8): 2024 - 2028. [Abstract] [Full Text] [PDF]
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R. P. Tracy, A. M. Arnold, W. Ettinger, L. Fried, E. Meilahn, and P. Savage The Relationship of Fibrinogen and Factors VII and VIII to Incident Cardiovascular Disease and Death in the Elderly : Results From the Cardiovascular Health Study Arterioscler Thromb Vasc Biol, July 1, 1999; 19(7): 1776 - 1783. [Abstract] [Full Text] [PDF]
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G. Maresca, A. Di Blasio, R. Marchioli, and G. Di Minno Measuring Plasma Fibrinogen to Predict Stroke and Myocardial Infarction : An Update Arterioscler Thromb Vasc Biol, June 1, 1999; 19(6): 1368 - 1377. [Abstract] [Full Text] [PDF]
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S. P. Wamala, M. A. Murray, M. Horsten, M. Eriksson, K. Schenck-Gustafsson, A. Hamsten, A. Silveira, and K. Orth-Gomer Socioeconomic Status and Determinants of Hemostatic Function in Healthy Women Arterioscler Thromb Vasc Biol, March 1, 1999; 19(3): 485 - 492. [Abstract] [Full Text] [PDF]
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