© 1997 American Heart Association, Inc.
Articles |
Coagulation Factor VII and the Risk of Coronary Heart Disease in Healthy Men
From the Institut für Klinische Chemie und Laboratoriumsmedizin, Westfälische Wilhelms-Universität Münster, Münster (R.J., G.A.); the Städtisches Klinikum Solingen, Solingen (J.H.); the Institut für Arterioskleroseforschung an der Westfälischen Wilhelms-Universität Münster, Münster (H.S., G.A.); and Medizinische Klinik A, Westfälische Wilhelms-Universität Münster, Münster (J. van de L.), Germany.
Correspondence to Dr med Ralf Junker, Institut für Klinische Chemie und Laboratoriumsmedizin, Westfälische Wilhelms-Universität Münster, Albert Schweitzer-Straße 33, 48129 Münster, Germany. E-mail junkerr{at}uni-muenster.de
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Abstract |
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Abstract Numerous investigations have demonstrated the role of thrombus formation in the pathogenesis of coronary heart disease (CHD). A tendency to thrombosis may also be indicated by elevated levels of coagulation factor VII clotting activity (FVIIc). Significant associations of FVIIc with increased coronary risk, however, have been found only in the Northwick Park Heart Study. Here we present the results of the 8-year follow-up of FVIIc measurements in 2780 healthy men of the Prospective Cardiovascular Münster study. In the study population (age at entry, 49.3±6.1 years, mean±SD), 130 CHD events occurred during follow-up. FVIIc was significantly higher in subjects with coronary events than in those without (112.4±20.1% vs 108.7±21.4%, P=.023). Compared with individuals without coronary events, FVIIc was not significantly higher in men with nonfatal events (111.7±20.4%; P=.196, n=93), but there was a tendency toward higher FVIIc activity in subjects with fatal events (114.6±19.5%; P=.076, n=37). In the multiple logistic regression analysis, we did not find FVIIc to be an independent risk factor for CHD, and the significance of FVIIc disappeared after total cholesterol, LDL-cholesterol, and triglycerides were taken into account. The increase in the number of CHD events through higher levels of FVIIc was more pronounced in the presence of additional cardiovascular risk factors: smoking; myocardial infarction events in family; angina pectoris; high levels of fibrinogen, total cholesterol, LDL cholesterol, and triglycerides; and a low level of HDL cholesterol. We conclude that FVIIc is a risk factor for CHD, especially in the presence of additional risk factors, and must be taken into account when assessing cardiovascular risk in men.
Key Words: prospective study • myocardial infarction • coronary risk factors
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Diseases of the cardiovascular system are the major cause of morbidity and mortality in Western countries. The development of atherosclerosis, MI, and sudden cardiac death is at least partly due to increased activity of the coagulation system. Several investigations have demonstrated the role of thrombus formation in the pathogenesis of atherosclerosis and acute cardiovascular events.1 2 3 4 The NPHS has indicated that FVIIc is independently associated with the risk of CHD.5 In addition, in several cross-sectional studies, elevated plasma levels of FVIIc have been shown to be associated with CHD.6 7 8 Nevertheless, not all studies have confirmed FVIIc as an independent risk factor. Hence, the significance of FVIIc in CHD remains unclear.9 10
In 1994 we published the results of the 6-year follow-up of the PROCAM Study, which showed that there was a tendency for plasma levels of FVIIc to be higher in subjects who had experienced a CHD event.11 Here we present the results of the 8-year follow-up of FVIIc measurements in 2780 healthy men.
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Methods |
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Study Design and Subjects
The PROCAM Study started in 1979. Apparently healthy employees of Westphalian companies were examined specifically for cardiovascular risk factors and then kept under observation to record mortality, subsequent MI, and stroke. The initial baseline examination included each participant's medical history, physical examination, ECG at rest, and a comprehensive laboratory blood analysis. In 1981 determination of plasma fibrinogen and FVIIc levels was included. A total of 10 581 subjects (7540 men and 3041 women) were recruited up to 1985. From 1981 onward, significant numbers of MIs or CHD deaths occurred only in men aged 40 and older. Statistical analysis was therefore confined to the 2780 male participants between 40 and 65 years of age with no prior history of MI or stroke who had completed the 8-year follow-up (Table 1
).
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Diagnostic criteria and the definition of end points have been published in detail.12 Two end points were considered: definite nonfatal MI and definite CHD death, including sudden cardiac death and fatal MI. Definite nonfatal MI was diagnosed if one or more of the following conditions were fulfilled: diagnostic ECG at the time of the event; ischemic cardiac pain plus diagnostic enzyme levels; ischemic cardiac pain plus equivocal enzyme levels and equivocal ECG; or an ECG that was diagnostic for MI while a previous one was not. Sudden cardiac death was diagnosed if an apparently well subject was observed to have died within 1 hour of onset of symptoms or within 1 hour of having last been seen without them and the cause of death could not be reasonably attributed (on the basis of complete clinical information) to violence, trauma, or some potentially lethal disease other than CHD. Fatal MI was diagnosed when a death certificate or hospital record described the cause of death accordingly or when an autopsy finding of acute MI was available. The members of the Critical Event Committee (see "Appendix") verified the diagnoses and causes of death in all event cases.
Blood Samples
Blood was drawn by venipuncture in the morning after
a 12-hour fast. Blood samples for coagulation tests were collected into
plastic tubes containing 1/10 of the volume with 3.13% trisodium
citrate. Within 60 minutes of blood collection, the plasma was
separated by centrifugation at room temperature for 15
minutes at 2500g. Serum from blood samples was prepared
without additives for clinical chemistry by
centrifugation for 10 minutes at 3000g.
After aliquots were placed in plastic tubes, plasma and serum were kept
in liquid N2 until they were stored in the laboratory at
-70°C.
Blood Analysis
FVIIc and fibrinogen were measured on a KC10 coagulation
analyzer (Amelung). FVIIc was determined in a one-step assay
using thromboplastin (Thromborel S) and factor VII–deficient plasma
(both from Behringwerke). Fibrinogen was determined according to the
Clauss method using thrombin (Multifibren), control plasma (both from
Behringwerke), and pooled plasma. Measurement of TGs and total
cholesterol in serum was performed on a Hitachi 737
autoanalyzer (Boehringer Mannheim). HDL-C
concentrations were determined after precipitation with phosphotungstic
acid/MgCl2 (Boehringer Mannheim), and LDL-C was
calculated using the Friedewald formula.
Statistical Analysis
Continuous variables were compared by the t test
(TGs after logarithmic transformation), and discrete
parameters were compared by the 
2
test. In all analyses except where age was included as an
independent variable in the multiple logistic regression, results
were adjusted for age by using regressions derived from the entry data.
For additional description of the relation between a specific
variable and the probability of suffering a CHD event, the number
of CHD events in tertiles of the variable is given. In addition, a
multiple logistic regression analysis was performed; the
variables included age, systolic blood pressure, diabetes
mellitus, smoking, MI in the family, angina pectoris, total
cholesterol, LDL-C, HDL-C, and TGs. ORs were calculated for
the lower and upper tertiles of variables. The statistical
analysis was done with the software packages
SPSSx and SAS.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Incidence and Mortality
In the 2780 subjects studied (age at entry, 49.3±6.1 years; range, 40 to 65), a total of 130 CHD events (15 sudden cardiac deaths, 22 fatal MIs, and 93 nonfatal MIs) occurred during the observation period of 96 months, which corresponds to an annual incidence of 0.62%. Sixty-nine patients died from causes other than CHD (8 from other diseases of the circulatory system, 33 from malignant neoplasms, 16 from accidents and violence, and 12 from other diseases). In addition, 20 nonfatal strokes were observed (Table 2
).
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Comparison of Subjects With and Without CHD Events
After adjustment for age, mean values for fibrinogen, FVIIc, total
cholesterol, LDL-C, the LDL-C to HDL-C ratio, TGs, and
systolic and diastolic blood pressure were revealed
to be significantly higher in the event group, whereas HDL-C was higher
in subjects without CHD events. There was no significant difference in
BMI between the two groups (Table 3).
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Incidences by tertiles of variables are demonstrated in Table 4. The strongest associations were
observed for tertiles of the LDL-C to HDL-C ratio (OR, 6.3) and LDL-C
(OR, 4.9). The weakest association was found for BMI (OR, 1.5) and
FVIIc (OR, 1.6).
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Comparison of Subjects With Fatal and Nonfatal CHD Events and Those
Without CHD Events
As shown in Table 5, no significant
differences in fibrinogen were found between subjects with nonfatal
(mean fibrinogen level, 2.91±0.57 g/L) and fatal (mean
fibrinogen level, 2.92±0.64 g/L) CHD events. Compared with the
no-event group (mean fibrinogen level, 2.59±0.57 g/L),
fibrinogen was significantly higher in patients with nonfatal
(P<.001, n=93) as well as fatal (P=.004, n=37)
events.
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For FVIIc, there was a tendency to higher FVIIc activities in individuals with fatal events after the CHD group was divided into subgroups with nonfatal versus fatal events. The mean FVIIc value was 111.7±20.4% in subjects with nonfatal CHD events and 114.6±19.5% in subjects with fatal events. Compared with subjects without any coronary events, FVIIc (mean, 108.7±21.4%) was not significantly higher in patients with nonfatal events (mean, 111.7±20.4%; P=.196, n=37), but a borderline significant difference appeared when the no-event group was compared with the fatal-event group (mean, 114.6±19.5%; P=.076, n=93).
Results of Multiple Logistic Regression Analysis
To consider the independence of FVIIc as a predictor of CHD, a
multiple logistic regression analysis was performed. As shown
in Table 6, FVIIc remained a significant
predictor of CHD events after adjustment for age, systolic
blood pressure, smoking, diabetes mellitus, angina pectoris, MI events
in the family, fibrinogen, and HDL-C. After total
cholesterol, LDL-C, and TGs were taken into account,
however, this significance was lost.
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Incidence of CHD Events for Combined Tertiles of FVIIc and
Nonlaboratory Variables
The combination of nonlaboratory parameters
(systolic blood pressure, smoking habit, diabetes mellitus,
angina pectoris, and MI in the family) and tertiles of FVIIc and the
resulting incidence are summarized in Table 7. On the one hand, for subjects with MI
in the family or angina pectoris and for smokers, there was a higher OR
with increasing levels of FVIIc than for subjects without the
additional risk factor (smoker-to-nonsmoker OR, 2.1/1.3;
with-to-without MI in the family OR, 3.6/1.4; angina pectoris-to-no
angina pectoris OR, 2.4/1.6). On the other hand, the coronary
risk of smokers and subjects with MI in the family was more pronounced
in the upper than the lower tertile of FVIIc (ORs of the upper-to-lower
tertiles of FVIIc: for smokers, 2.5/1.6; for those with MI in the
family, 1.8/0.7; and for those with angina pectoris, 6.8/4.5).
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Incidence of CHD Events for Combined Tertiles of FVIIc and Other
Laboratory Variables
Incidences for combinations of tertiles of FVIIc and fibrinogen,
total cholesterol, LDL-C, HDL-C, and TGs are summarized in
Table 8. For all parameters
the OR was higher within the upper than the lower tertile of the
corresponding risk factor (although vice versa for HDL-C). The ORs of
FVIIc varied between 1.1 (within the lower tertiles of total
cholesterol and TGs and the lower and middle tertiles of
LDL-C) and 1.9 (within the upper tertile of fibrinogen and the lower
tertile of HDL-C). On the other hand, the importance of fibrinogen,
total cholesterol, LDL-C, HDL-C, and TGs as risk factors
for CHD was greater in the presence of high levels of FVIIc (ORs within
the upper to lower tertiles of FVIIc: for fibrinogen, 2.8/2.0; for
total cholesterol, 3.2/2.4; for LDL-C, 6.3/4.5; for HDL-C,
2.9/2.0; and for TGs, 2.0/1.4).
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As displayed in the Figure, the highest incidence values
(111.8 per 1000 men) were due to the combination of high FVIIc and
LDL-C. When compared with the lower tertiles of both
parameters (incidence, 16.4 per 1000 men), this value is a
nearly 7-fold increase in risk. The lowest number of events within the
upper tertiles and the lowest increase in risk compared with the low
tertiles were found for FVIIc and TGs (lower tertiles, 35.4 per 1000
men; upper tertiles, 79.0 per 1000 men; 2.2-fold increase).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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The results delineated in this article confirm and extend the results of the 6-year follow-up of the PROCAM Study. The annual incidence was nearly unchanged (0.65% versus 0.62%) and low when compared with the results of the NPHS (0.8%, 5-year follow-up).5 11 Our recent results confirm fibrinogen as an independent risk factor for CHD.13 Owing to a longer observation period and a greater CHD incidence, FVIIc now also appears to be significantly higher in subjects suffering coronary events than in those without such events (mean FVIIc, 112.4±20.1% versus 108.7±21.4%; P<.05).
However, as shown in Table 4
, the incidence of CHD was 1.6-fold higher
in the upper tertile of FVIIc than in the lower tertile. Compared with
the other risk factors, eg, LDL-C with an OR of 4.9, 1.6
represents only a slight increase in incidence. In the NPHS,
FVIIc was found to be much more strongly associated with
coronary risk (117.4% versus 107.0%; P<.001,
5-year follow-up).5
As shown by the results of a laboratory comparison, the FVIIc assay used in the NPHS is more sensitive to the activated form of coagulation factor VII (ie, FVIIa) than is the PROCAM assay. Plasma samples enriched with FVIIa expressed a proportionately greater FVIIc in the NPHS assay using mixed human and bovine thromboplastin than in the PROCAM pure human thromboplastin system. It was also true that the converse held in samples that were relatively deficient in FVIIa. Therefore, the clear-cut association of FVIIc with CHD in the NPHS may be due to the ability of their assay to detect increased circulating levels of the two-chain form of FVII.14 To our knowledge, there are no differences between the NPHS and PROCAM sample collecting protocols that may have contributed to the discrepant results concerning FVIIc.
Table 5 displays the results for MI survivors and those who died of MI
or sudden cardiac death. In contrast to the entire group, the
significance of FVIIc was lost within the subgroups because of fewer
individuals. Nevertheless, differences in FVIIc were still found. FVIIc
showed a borderline significance when individuals with fatal events
were compared with subjects without events (114.6% versus 108.7%,
P=.076). In subjects with nonfatal events, FVIIc was not
significantly different from both of the other groups (111.7%,
P=.169 and .451, respectively). Contrastingly, the
difference in FVIIc between subjects suffering fatal events and those
suffering nonfatal events was significant in the NPHS
(P=.008).5 However, both sets of results
support the assumption of an activated coagulation system,
which increases the risk of fatal events due to the enhanced size and
stability of the occlusive thrombus.15
After performing multiple logistic regression analysis, we
could not confirm FVIIc as an independent risk factor for CHD, as
demonstrated in the NPHS.5 As shown in Table 6, no
significance was found after accounting for total
cholesterol, LDL-C, and TGs. This finding was confirmed by
the data displayed in Table 8 and the Figure: within the lower and the
middle tertiles of LDL-C, the increase in incidence through higher
levels of FVIIc was negligible. These findings were similar but less
pronounced for the combination of tertiles of FVIIc and tertiles of
total cholesterol and TGs. In contrast, after adjustment
for age, fibrinogen, HDL-C, and nonlaboratory parameters
(systolic blood pressure, angina pectoris, smoking, diabetes
mellitus, and MI events in the family), FVIIc remained significant.
Activation of FVII and the subsequent increase in FVIIc is partly due to an elevation of the hemostatic balance by interactions between lipoproteins and coagulation factors. A correlation between FVIIc levels and TGs as well as total cholesterol has been shown in several studies.16 17 18 19 20 21 Dietary fat intake increased FVIIc, whereas treatment of hypertriglyceridemia with lipid-lowering drugs resulted in a decrease of FVIIc.18 19 On the one hand, higher levels of FVIIc in hyperlipidemic patients may be due to enhanced synthesis of FVII; on the other hand, this may be due to a larger proportion of the activated form of FVIIc.17 21 The correlation between FVIIc and lipoproteins may be explained by the binding of FVII to TG-rich particles.22 23 However, these results support our finding that FVIIc is not independently associated with coronary risk. Higher ORs for FVIIc in the presence of other laboratory and nonlaboratory risk factors (and vice versa) may be explained by additive effects of the two risk factors on atherosclerotic progress. Moreover, direct interaction between the coagulation system and lipids contributes to the elevation of risk for CHD.
Subjects included in this study were apparently healthy. Nevertheless, already-existing minimal atherosclerotic lesions could not be excluded. This factor may be especially relevant for subjects with high levels of laboratory risk factors as well as the nonlaboratory risk factors. The release of tissue factor during rupture of an atheromatous plaque is associated with CHD by means of a dramatically enhanced activation of coagulation factor X by FVIIa in the presence of tissue factor. Therefore, even minimal lesions of atherosclerosis may lead to activation of the coagulation system, which contributes to atherosclerotic progress.15 24 25 26 The assumption that the coagulation system plays a major role in thrombus formation in patients with already-existing CHD is further supported by our findings in patients suffering angina pectoris, who had the highest risk of developing CHD. The OR of FVIIc was higher for subjects suffering from angina pectoris than for those without. Additionally, the OR of angina pectoris was higher within the upper tertile of FVIIc then in the lower tertile. For tertiles of systolic blood pressure and FVIIc, we found the OR of FVIIc to be higher within the lower tertile of systolic blood pressure than the middle and upper tertiles. Furthermore, patients suffering from diabetes mellitus showed a lower OR than did those without. Both findings may be due to the low number of cases and need further investigation.
On the whole, FVIIc is a risk factor for CHD and has to be taken into account when estimating cardiovascular risk in men. The increase in cardiovascular risk through elevated levels of FVIIc depends mainly on the presence of additional risk factors. Consequently, interaction between FVIIc and other risk factors requires further investigation.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported by the Bundesministerium für Forschung und Technologie, Ministerium für Wissenschaft und Forschung NRW, Deutsche Forschungsgemeinschaft, Landesversicherungsanstalt Westfalen, and Landesversicherungsanstalt Rheinprovinz. The excellent technical cooperation of J. Bailey, M. Käse, and C. Sandau is gratefully acknowledged.
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Appendix 1 |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Members of the Critical Event Committee included K. Kochsiek, MD, Würzburg; B.E. Strauer, MD, Düsseldorf; U. Gleichmann, MD, Bad Oeynhausen; and R. Uebis, MD, Aachen, Germany.
Received August 2, 1996; accepted October 21, 1996.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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 E.M. Bladbjerg, S.O. Skouby, L.F. Andersen, and J. Jespersen Effects of different progestin regimens in hormone replacement therapy on blood coagulation factor VII and tissue factor pathway inhibitor Hum. Reprod., December 1, 2002; 17(12): 3235 - 3241. [Abstract] [Full Text] [PDF]
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V. Stangl, G. Baumann, and K. Stangl Coronary atherogenic risk factors in women Eur. Heart J., November 2, 2002; 23(22): 1738 - 1752. [Full Text] [PDF]
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 P. Marques-Vidal, E. Mazoyer, V. Bongard, P. Gourdy, J.-B. Ruidavets, L. Drouet, and J. Ferrieres Prevalence of Insulin Resistance Syndrome in Southwestern France and Its Relationship With Inflammatory and Hemostatic Markers Diabetes Care, August 1, 2002; 25(8): 1371 - 1377. [Abstract] [Full Text] [PDF]
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 J. B. Braunstein, D. W. Kershner, P. Bray, G. Gerstenblith, S. P. Schulman, W. S. Post, and R. S. Blumenthal Interaction of Hemostatic Genetics With Hormone Therapy : New Insights To Explain Arterial Thrombosis in Postmenopausal Women Chest, March 1, 2002; 121(3): 906 - 920. [Abstract] [Full Text] [PDF]
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 A. K. Olsen, E. M. Bladbjerg, A. K. Hansen, and P. Marckmann A High Fat Meal Activates Blood Coagulation Factor VII in Rats J. Nutr., March 1, 2002; 132(3): 347 - 350. [Abstract] [Full Text] [PDF]
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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. S. Williams and P. F. Bray Genetics of Arterial Prothrombotic Risk States Experimental Biology and Medicine, May 1, 2001; 226(5): 409 - 419. [Abstract] [Full Text]
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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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 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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D. A. Lane and P. J. Grant Role of hemostatic gene polymorphisms in venous and arterial thrombotic disease Blood, March 1, 2000; 95(5): 1517 - 1532. [Full Text] [PDF]
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L. F. Larsen, J. Jespersen, and P. Marckmann Are olive oil diets antithrombotic? Diets enriched with olive, rapeseed, or sunflower oil affect postprandial factor VII differently Am. J. Clinical Nutrition, December 1, 1999; 70(6): 976 - 982. [Abstract] [Full Text] [PDF]
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L. I Mennen, M. P. de Maat, G. Meijer, P. Zock, D. E Grobbee, F. J Kok, C. Kluft, and E. G Schouten Postprandial response of activated factor VII in elderly women depends on the R353Q polymorphism Am. J. Clinical Nutrition, October 1, 1999; 70(4): 435 - 438. [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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F. M. van 't Hooft, A. Silveira, P. Tornvall, A. Iliadou, E. Ehrenborg, P. Eriksson, and A. Hamsten Two Common Functional Polymorphisms in the Promoter Region of the Coagulation Factor VII Gene Determining Plasma Factor VII Activity and Mass Concentration Blood, May 15, 1999; 93(10): 3432 - 3441. [Abstract] [Full Text] [PDF]
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 J. Danesh, R. Collins, P. Appleby, and R. Peto Association of Fibrinogen, C-reactive Protein, Albumin, or Leukocyte Count With Coronary Heart Disease: Meta-analyses of Prospective Studies JAMA, May 13, 1998; 279(18): 1477 - 1482. [Abstract] [Full Text] [PDF]
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L. I. Mennen, M. P. M. de Maat, E. G. Schouten, C. Kluft, J. C. M. Witteman, A. Hofman, and D. E. Grobbee Dietary Effects on Coagulation Factor VII Vary across Genotypes of the R/Q353 Polymorphism in Elderly People J. Nutr., May 1, 1998; 128(5): 870 - 874. [Abstract] [Full Text]
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 D. R. Stauffer, B. N. Chukwumezie, J. A. Wilberding, E. D. Rosen, and F. J. Castellino Characterization of Transcriptional Regulatory Elements in the Promoter Region of the Murine Blood Coagulation Factor VII Gene J. Biol. Chem., January 23, 1998; 273(4): 2277 - 2287. [Abstract] [Full Text] [PDF]
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