© 1999 American Heart Association, Inc.
Brief Reviews |
Measuring Plasma Fibrinogen to Predict Stroke and Myocardial Infarction
An Update
From the Clinica Medica, Dipartimento di Medicina Clinica e Sperimentale (G.M.), Ateneo "Federico II" Napoli; Laboratoro di Epidemiologia Clinica Cardiovascolare, Istituto di Ricerche Farmacologiche Mario Negri (A.D.B., R.M.), Consorzio Mario Negri Sud, S. Maria Imbaro (CH); Istituto di Medicina Interna e Geriatria (G.D.M.), Università di Palermo, Italy.
Correspondence to Giovanni Di Minno, MD, Clinica Medica, Dipartimento di Medicina, Clinica e Sperimentale, Via S. Pansini 5, 80131 Napoli, Italy. E-mail diminno{at}unina.it
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsReferences |
|---|
Abstract—Plasma fibrinogen is a major determinant of platelet aggregation and blood viscosity. The decrease in plasma fibrinogen by bezafibrate is associated with a decrease in the risk of reinfarctions. To strengthen the predictive value of plasma fibrinogen with respect to cardiovascular risk, we performed a meta-analysis of studies conducted between 1984 and 1998. Emphasis has been put on the relationship between high levels of plasma fibrinogen and fatal and/or nonfatal cardiovascular events in both the general population and in patients with previous cardiovascular events. Twenty-two studies (13 prospective, 5 cross-sectional, and 4 case-control) addressing the association between fibrinogen plasma concentrations and cardiovascular disease were analyzed. The overall estimate of risk of cardiovascular event in subjects with plasma fibrinogen levels in the higher tertile, was twice as high as that of subjects in the lower one (odds ratio, 1.99; 95% confidence interval, 1.85 to 2.13). High plasma fibrinogen levels were associated with an increased risk of cardiovascular disease in healthy as much as in high-risk individuals. A metaregression showed no confounding effects attributable to selected characteristics of retrieved studies. A subgroup analysis (study design, follow up, mean fibrinogen levels, percentage of smokers, and mean age) allowed us to conclude that fibrinogen is an independent risk factor for cardiovascular disease; that it interacts with major determinants of myocardial and cerebrovascular ischemia; and that, in secondary prevention studies, it enhances by 8% the prediction of future events by established risk factors. Thus, fibrinogen measurements should be encouraged to refine the overall risk profiles of individuals and to better tailor preventive interventions.
Key Words: fibrinogen • risk factor • stroke • myocardial ischemia • meta-analysis
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsReferences |
|---|
Stroke and myocardial infarction are major thrombotic complications of atherosclerosis and leading causes of morbidity and mortality in western countries. Many studies have established the involvement in atherosclerosis of blood lipids and lipoproteins, hypertension, diabetes mellitus, and smoking, as well as the active role of endothelial injury, smooth muscle cell proliferation, and inflammation.1 2 3 The role of hypercoagulability and of plasma fibrinogen, the central protein of the coagulation system, in this complex scenario has been suspected for many years, and has recently been documented by experimental and clinical evidence: human gelatinous and fibrous plaques are rich in fibrinogen and its degradation products4 5 6 7 8 9 ; thrombin, fibrinogen, and fibronectin are involved in cell proliferation3 7 8 9 10 ; fibrinogen is involved in mechanisms (platelet aggregation, endothelial cell injury, and plasma viscosity) that play a central role in the formation of thrombi10 ; and thrombosis is a major determinant of myocardial ischemia.11 12 13 Early epidemiological evidence has associated high levels of plasma fibrinogen with cardiovascular disease (CVD).10 14 15 Moreover, drugs that lower the progression of coronary heart disease also reduce plasma fibrinogen levels in young postinfarction males.16
Recommendations for the management of CVD in the general population as well as for people with previous cardiovascular events were recently formulated jointly by various medical associations. These recommendations focus on preventive interventions based on the summation of risks rather than addressing the individual who is a carrier of an isolated high-risk factor (the philosophy being that individuals with a combination of borderline risks may actually be at considerably greater risk than subjects with a single very high risk factor). Thus, these recommendations for the primary prevention of coronary heart disease in clinical practice focus only on cholesterol, hypertension, and smoking habits.17 18 19 Because patients at risk for the development of fibrinogen-related ischemic complications of atherosclerosis can be easily identified and treatment strategies have been developed to protect against these complications, clinically oriented prevention recommendations should consider the role of fibrinogen in CVD. In an effort to strengthen the clinical impact of measuring plasma fibrinogen, we performed a meta-analysis to answer the following questions: (1) Is epidemiological evidence still supporting plasma fibrinogen as an independent risk factor for cardiovascular disease? (2) Is plasma fibrinogen measurement improving prediction of future ischemic events by established risk factors? (3) What areas of uncertainty remain with respect to the association between fibrinogen and CVD?
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsReferences |
|---|
Twenty-two studies20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 (MEDLINE search from 1984 to September 1998) (Tables 1
and 2), in which the association of plasma
fibrinogen concentrations with the risk of CVD had been evaluated, were
scrutinized. Other relevant studies were identified by resuming recent
reviews.10 14 15 42 Studies not providing enough
information as to the criteria adopted for the present
meta-analysis (ie, odds ratios [ORs], confidence intervals
[CIs], and/or the possibility of recalculating crude ORs) were
not used.
|
|
Statistical Analysis
Data from different studies were combined using the
general variance-based method.43 44 45 46 47 48 49 50 51 52 53 This method requires
only information on the OR estimate and 95% CI of each
study.44 95% CIs were used to assess the variance of each
study effect. When provided by the authors, adjusted ORs and their CIs
were preferred. Crude ORs and their 95% CIs were used when an adjusted
estimate was not provided. These estimates were used to carry out the
overview for all studies as well as for the subgroups. To examine the
strength of the association between total
cardiovascular events and the different subgroups, we
fitted a multivariate inverse variance–weighed linear
regression of the logarithmic ORs for total events as dependent
variable against the variables. The weights that were obtained
with the variance-based method were adopted for the regression
analysis.
2 was used to assess the magnitude of
heterogeneity among studies, ie, the within-group
heterogeneity (Het-w).44 The
2 with degrees of freedom 1 less than the
number of groups was used to assess the magnitude of the
heterogeneity of the ORs between the subgroups of
studies, ie, the between-group heterogeneity
(Het-b).45 46
Subgroup Analysis
Duration of follow-up, mean plasma fibrinogen values at
baseline, percentage of current smokers, mean age of the study
population, and study design (prospective, cross-sectional, and
case-control) were taken into consideration to stratify for potential
confounders (subgroup analyses). Continuous variables were
dichotomized according to their approximate median values. The criteria
used for subgroup analysis according to different study designs
(prospective, cross-sectional, and case-control) are given below.
Prospective Studies
Cardiovascular events were presented
according to tertiles of fibrinogen in the majority of the
studies.20 22 23 24 25 26 28 32 The relationship between
fibrinogen levels and cardiovascular events was
determined by comparing higher and lower tertiles of fibrinogen. The
results of 3 prospective studies (Gothenburg and Scottish Heart Health
Study, Caerphilly-Speedwell)20 25 26 published as
quintiles were recalculated into tertiles using a conservative approach
that assumes a linear increase in events within quintiles. This method
tends to underestimate the risk associated to fibrinogen
tertiles.15
Cross-Sectional Studies
The effect of fibrinogen level in cross-sectional studies was
evaluated by comparing upper and lower quartiles. Three studies
presented their results as quartiles of
fibrinogen.33 34 37 In the Prevention Cardiovasculaire en
Medecine du Travail study, tertiles of fibrinogen were used because the
results were presented only as unadjusted estimates of the OR
of the higher tertile of plasma fibrinogen level compared with the
lower one.35 Sharp et al36 presented
their results as quintiles of fibrinogen. These were recalculated.
Case-Control Studies
OR and 95% CI values were computed by comparing higher
quartiles of fibrinogen to lower ones38 40 41 In 1 case,
it was not possible to recalculate risk estimates into quartiles; thus
the unadjusted estimate according to the median value, as
presented by the authors, was used.39
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsReferences |
|---|
Is the Epidemiological Evidence Still Supporting Plasma Fibrinogen as an Independent Risk Factor for Cardiovascular Disease?
Of the 22 studies contributing to this analysis, 63 736 individuals were included and 5712 cardiovascular (CV) events were observed. The end points available for the analysis were fatal and nonfatal coronary heart disease (CHD) for 10 studies,20 22 24 26 27 28 31 32 34 36 fatal and nonfatal CV events for 4 studies,23 37 38 39 arterial plaque progression for 2 studies,35 40 deep vein thrombosis for 1 study,41 and myocardial infarction for 4 studies.21 25 29 33
Thirteen prospective studies evaluated a total of 47 323 subjects
(Table 1
); 5 cross-sectional and 4 case-control studies
recruited 15 537 and 1625 subjects, respectively (Table 2).
Figure 1 summarizes of OR estimates and
their 95% CIs. The overall OR estimate from all studies was 1.99 (95%
CI, 1.85 to 2.13). The Het-w test was statistically significant
(P<0.05).
|
When all the prospective studies were considered, a total of 2581 events in 47 323 subjects was observed and the estimate of risk of CVD was more than doubled when comparing the higher tertile to the lower one. Eight prospective studies were conducted in general populations and 1910 CV events were found in 37 684 subjects.20 21 22 23 24 25 26 27 The overall estimate of risk of cardiovascular events in subjects in the higher tertile of fibrinogen was more than doubled compared with that of subjects in the lower tertile.
Eight prospective studies were carried out on healthy men and a total of 1587 CV events in 24 983 subjects was observed.20 21 22 23 24 25 26 27 Three studies on healthy women reported 404 CV events in 13 803 individuals.20 23 26 No difference in the estimate of CV risk was found after separate analyses for men and women (Het-b test, not significant [NS]). Five prospective studies on high-risk subjects recruited 9639 individuals who experienced 671 events.26 29 31 32 Subjects in the higher tertile of fibrinogen had a 92% greater risk of CV events. No difference in CV risk was evident between studies in the general population and those in high-risk subjects (Het-b test, NS). No effect modification emerged from studies on subjects with or without previous CVD.
In cross-sectional and case-control studies, the overall estimates of risk in subjects with higher levels of fibrinogen compared with those in the lower tertile were 1, 5, and 3 times higher, respectively.
Subgroup Analysis
Duration of follow-up was analyzed only for
prospective studies (Figure 2A). Studies
with duration of follow-up above and below 5.2 years had comparable ORs
(2.5 versus 2.24; Het-b, NS). Similar results were obtained by
examining the effect of duration of follow-up in studies that recruited
high-risk subjects. In studies in general populations, subjects had an
6.0 year (median) follow-up. Studies with duration of follow up
above and below the median value had a similar risk of CV events (OR,
2.40 versus 2.70). Duration of follow up did not influence the results
of studies in healthy men as well as in high-risk subjects.
|
Mean fibrinogen values of the subjects recruited in each study
were used as rough estimates of the fibrinogen level of the population
of origin (Figure 2B). When all the studies were taken into
consideration, the risk of CV events was almost twice as high in
studies with mean fibrinogen values above 303 mg/dL. No difference in
the estimates of risk were apparent when mean fibrinogen values
measured in the patients recruited were examined according to study
design (ie, cross-sectional and case-control studies).
The percentage of smokers in each study was used as an index of
the interplay between smoking habits and fibrinogen levels in
determining the level of CV risk (Figure 2C). No difference was
apparent between studies according to the prevalence of smokers above
and below the median value of 36% when all studies were considered.
Similar results were obtained by evaluating all prospective studies or
prospective studies on males, on the general population or high risk
populations alone.
The prevalence of smoking in cross-sectional studies did not change the estimate of risk attributable to fibrinogen levels. It was not possible to evaluate the role of smoking habits in case-control studies.
Mean age of subjects recruited in each study was used to evaluate the
role of fibrinogen levels in younger and older patients (Figure 2D).
Comparable results were found in the whole study group, in
prospective studies of general populations, in prospective studies of
high-risk individuals, in cross-sectional studies, and in case-control
studies, all of which showed no effect modification.
Meta Regression
To examine the strength of the association between total
cardiovascular events and the selected subgroups, an
inverse variance-weighed multiple linear regression of the logarithmic
ORs for total events were used as dependent variables against study
design, percentage of smokers, age, and mean plasma fibrinogen values
as explanatory variables (Table 3).
Cross-sectional studies behaved differently. Mean fibrinogen values and
percentage of smokers at baseline did not influence the risk
estimates.
|
Limitations of the Present Meta-Analysis
Publication biases and different study designs may have
overestimated the risk related to high plasma fibrinogen levels. The
somewhat lower estimates of CV risk in cross-sectional studies is
likely to be caused by inherent selection biases. This can be because
of specific characteristics of this type of study (ie, selection of
subjects with better prognosis). Conversely, because of the type of
studies or the use of fibrinogen values measured close to the index
event (ie, more representative of the hemostatic state
before the event), there might have been emphasis in the role of
fibrinogen as a CV risk factor in case-control studies. However, the
results of the present meta-analysis are strengthened by
those of the Scottish Heart Health Study,25 in which no
interaction between fibrinogen levels and other
cardiovascular risk factors occurs. On the other hand,
despite differences in the analytical procedures used for their
meta-analysis, Danesh et al42 achieved results
similar to ours. Finally, on the bases of meta-regression
analysis, it is unlikely that the selection characteristics of
the studies retrieved (mean age, healthy/high-risk subjects, smoking
habits, duration of follow-up, and mean plasma fibrinogen values) may
have affected the estimates of the risk associated with quantiles of
fibrinogen values.
Because different methods with differences in variability,
accuracy, precision, and agreement among different laboratories have
been used to measure plasma fibrinogen in the studies retrieved (Table 4). This may have hampered the accuracy
of the risk estimates. However, the net results of each study–the
association between high plasma fibrinogen and stroke and myocardial
infarction–were unequivocal. Each method used different cutoff values
(see legend of Figure 1). However, comparisons between higher
and lower figures (as in the present analysis) reduce the
disadvantages inherent to the differences in the methods used.
|
Is Plasma Fibrinogen Measurement Improving Prediction of Future
Ischemic Events By Established Risk Factors?
1. Fibrinogen Interaction With Other Risk Factors
In the Prospective Cardiovascular Muster
study, fibrinogen plasma levels of 277 mg/dL increased by 2-fold the
risk of myocardial infarction in subjects with LDL
cholesterol >163 mg/dL.23 In the Framingham
study, fibrinogen levels of 312 mg/dL increased by 6-fold the risk of
myocardial infarction in smokers.22 In the Gotheburg
study, fibrinogen levels >500 mg/dL increased by 12-fold the risk of
stroke in subjects with systolic blood pressure >180
mm Hg.20
2. Attributable Risk
In the Atherosclerosis Risk in Communities
study, the role of fibrinogen was marginal, albeit significant, when
the data were corrected for major cardiovascular risk
factors.27 However in the Scottish Heart Health Study,
which examined various factors, fibrinogen was the second most
important factor for predicting causes of death in men and the sixth
most important factor for women.61 Based on the data from
>1300 individuals who had experienced recurrence of a
coronary event, the Gruppo Italiano per lo Studio della
Sopravvivenza Nell'Infarto Miocardico (GISSI) Prevention Group
prepared a Coronary Risk Chart for the secondary prevention of
CHD. In addition to using fibrinogen levels to determine the overall
risk of individual patients, this chart assesses attributable risks for
established CV risk factors.62 Fibrinogen levels higher
than median values (371 mg/dL) predicted myocardial reinfarction in
younger as much as in older individuals. The prognostic role of
fibrinogen for the evaluation of the global risk for CVD was comparable
with that of major CV risk factors. Furthermore, prediction of CVD by
established factors was improved by 8% when fibrinogen was added to
the analysis. Under the same conditions of analysis,
cholesterol improved prediction by 5%, hypertension by
5%, and diabetes mellitus by 7% (Figure 3).
|
What Areas of Uncertainty Remain With Respect to the Association
Between Fibrinogen and CVD?
1. Methods to Measure Plasma Fibrinogen
Taking into account accuracy (as evaluated with reference to
the gravimetric method), precision (as evaluated by determining the
inter- and intra-assay coefficients of variations), and agreement of
methods (among different laboratories), the (semiquantitative) Clauss
clotting method has been suggested to be a reliable manner of measuring
very low and very high plasma fibrinogen levels in short- and long-term
studies of repeatability.10 Recent data support the notion
that the nephelometric method may provide a prediction comparable to
that of the Clauss method.63 Although requiring further
confirmation, these observations raise the possibility that commonly
recognized reference methods other than the Clauss may be recommended
for future epidemiological studies. However, the potential availability
of a simpler, easier, and more reproducible method by no means hampers
the clinical impact of measuring plasma fibrinogen levels.
2. Pathogenetic Significance
Similar to other acute-phase proteins, expression of
fibrinogen (ie, its plasma level) is regulated by interleukin-6 and
impaired by transforming growth factor-ß.10 64 65
C-reactive protein (CRP) is also an acute-phase reactant; its baseline
levels predicted the risk of a first myocardial infarction and stroke
independently of other risk factors in apparently healthy men as well
as in patients with unstable angina.42 66 67 68 Fibrinogen
correlates with CRP both in men and women.42 Thus, the
question is whether raised plasma fibrinogen is the epiphenomenon of
the severity of the vascular damage taking place. Vascular injury,
response to vascular injury, and plaque rupture and fissuring are major
stages of the development and progression of
atherosclerosis.1 2 3 Presently, it is
unclear whether plasma fibrinogen is related to 1 or more of these
stages. However, although relevant from a therapeutic point of view
(ie, measuring plasma fibrinogen to identify subjects in whom
interventions on established risk factors affecting specific stages in
atherosclerosis have to be greatest), the question is
of little relevance from a prognostic point of view.
3. Gene–Environment Interaction
High fibrinogen levels have been reported to be accounted
for by environmental and genetic differences.69 70 71 72 73 74 75 Some
polymorphisms modulate the response of genes to environmental
stimuli, ie, the same stimulus may cause different levels of fibrinogen
in subjects with different polymorphisms.76 This is
consistent with the possibility that a theoretical level
(determined by genes) and a real level (because of the interaction of
genes with the environment) of fibrinogen may play a role in the intra-
and inter-population variability of fibrinogen levels and may explain,
at least in part, differences in CVD frequency and
cardiovascular death between Japan and USA. However,
despite its pathophysiological relevance, this
information is unlikely to affect the clinical impact of plasma
fibrinogen levels.
Areas of Future Research
The gradient of CHD death rate across European countries has
been associated with a different distribution of some genotypes
affecting plasma levels of factor VII.77 78 Similar to
fibrinogen, the latter is a known determinant of hypercoagulability and
of the risk of CVD.21 23 79 Whether a similar gradient for
fibrinogen is also present also is unclear.
In 2 studies,70 74 molecular variations of plasma fibrinogen have been related to arterial thrombosis regardless of their effect on plasma fibrinogen. Whether the analysis of these markers should be included in the cardiovascular risk factor profile regardless of plasma fibrinogen measurements remains to be clarified. Interleukin-6 gene variants have been reported.80 Their effect on plasma fibrinogen levels and, in turn, CVD, deserves proper investigation.
With 1 exception,16 the lack of clinical trials
demonstrating the effectiveness of lowering fibrinogen levels on hard
clinical end points is hampering the clinical impact of measuring
plasma fibrinogen levels. Plasma levels of fibrinogen are lowered by
drugs commonly used in clinical practice (Table 5). Clinical trials with these drugs
should be encouraged to implement knowledge on the correlation between
fibrinogen and CVD.
|
Within the area of cerebrovascular disease, it is presently possible to identify groups of subjects who will take advantage of therapies, including antiplatelet agents, antihypertensive therapy (or a combination of both), carotid endoarteriectomy, and anticoagulation. To improve the impact of plasma fibrinogen and address some of the issues raised above, future prospective observational or interventional studies in vascular medicine should include the measurement of fibrinogen (and its genotypes) at the beginning of and at some time during the trials. This would be particularly relevant in large studies, with appropriate statistical power, that include individuals from different geographic areas. We believe that this attitude may refine the overall individual risk, and provide the individual patient with a tailor-made intervention based on a specific mechanism and/or stage of the atherosclerotic vascular disease.
|
Acknowledgments |
|---|
We thank Drs Giovanni de Gaetano, Maria Benedetta Donati, and Licia Iacoviello for their help during the preparation of the manuscript; and Rosa Maria Marfisi and Anna Polidoro for assistance with data analysis and figure elaboration.
Received August 14, 1998; accepted December 1, 1998.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsReferences |
|---|
1. Munro JM, Costran RS. The pathogenesis of atherosclerosis: Atherogenesis and inflammation. Lab Invest. 1988;58:249–261.[Medline] [Order article via Infotrieve]
2. Fuster V, Badimon L, Badimon J, Chesebro J. The pathogenesis of coronary artery disease and the acute coronary syndromes. N Engl J Med. 1992;326:242–250.[Medline] [Order article via Infotrieve]
3. Ross R. The pathogenesis of atherosclerosis. In: Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine. 5th ed. Philadelphia: Saunders; 1997:1105–1125.
4. Henschen A, McDonagh J. Fibrinogen, fibrin and factor XIII. In: Zwaal RFA, Hemker HC, eds. Blood Coagulation. Amsterdam: Elsevier Science Pub Co; 1986:171–241.
5. Atherosclerosis Risk in Community Study. Operation Manual, No. 9: Hemost Determinations. Bethesda, MD: National Heart, Lung, and Blood Institute; April 28, 1987. Version 1.0.
6. Bini A, Kudrik BJ. Fibrin and its derivatives in the normal and disease vessel wall. In: Plasminogen activation in fibrinolysis, in tissue remodeling and in development. Ann N Y Acad Sci. 1992;667:112–126.[Medline] [Order article via Infotrieve]
7. Constantinides P. Cause of thrombosis in human atherosclerotic arteries. Ann J Cardiol. 1990;66:37G–40G.
8. Smith EL, Thompson WD. Fibrin as cofactor in atherogenesis. Thromb Res. 1994;73:1–19.[Medline] [Order article via Infotrieve]
9. Schwartz CJ, Valente AJ, Kelley JL, Sprague EA, Edwards EH. Thrombosis and development of atherosclerosis: Rokitansky revisited. Semin Thromb Hemost. 1988;14:189–195.[Medline] [Order article via Infotrieve]
10.
Di Minno G, Mancini M. Measuring plasma fibrinogen to
predict stroke and myocardial infarction.
Arteriosclerosis. 1990;10:1–7.
11.
Falk E. Unstable angina with fatal outcome: Dynamic
coronary thrombosis leading to infarction and/or sudden death.
Autopsy evidence of recurrent mural thrombosis with
peripheral embolization culminating in total vascular
occlusion. Circulation. 1985;71:699–708.
12.
Davies MJ, Thomas CA. Plaque fissuring: The cause
of acute myocardial infarction, sudden ischaemic death, and crescendo
angina. Br Heart J. 1985;53:363–373.
13. Saffitz JE, Schwartz CJ. Coronary atherosclerosis and thrombosis underlying acute myocardial infarction. Cardiol Clin. 1987;5:21–30.[Medline] [Order article via Infotrieve]
14. Cook NS, Ubben D. Fibrinogen as a major risk factor for cardiovascular disease. Trends Pharmacol Sci. 1990;11:444–451.[Medline] [Order article via Infotrieve]
15.
Ernst E., Resch K. L. Fibrinogen as a
cardiovascular risk factor: A meta-analysis and
review of the literature. Ann Intern Med. 1993;118:956–963.
16. Ericsson CG, Hamsten A, Nilsson J, Grip L, Svane B, de Faire U. Angiographic assessment of effects of bezafibrate on progression of coronary artery disease in young male postinfarction patients. Lancet. 1996;347:849–853.[Medline] [Order article via Infotrieve]
17.
Anderson KM, Wilson PWF, Odell PM, Kannel WB. An
updated coronary risk profile: A Statement for health
professionals. Circulation. 1991;83:356–362.
18.
Pyorala K, De Baker G, Graham I, Poole-Wilson P, Wood D
on behalf of the Task Force: Prevention of coronary heart
disease in clinical practice: Recommendations of the Task Force of the
European Society of Cardiology, European
Atherosclerosis Society and European Society of
Hypertension. Eur Heart J. 1994;15:1300–1331.
19. 27th Bethesda Conference. Matching the intensity of risk factor management with the hazard for coronary disease events. J Am Coll Cardiol. 1996;27:957–1047.[Medline] [Order article via Infotrieve]
20. Wilhelmsen L, Svardsudd K, Korsan-Bengtsen K, Larsson B, Welin L, Tibblin G. Fibrinogen as risk factor for stroke and myocardial infarction. N Engl J Med. 1984;311:501–505.[Abstract]
21. Meade TW, Brozovic M, Chakrabarti RR, Haines AP, Iameson JD, Mellows S, Miller GJ, North WRS, Striling Y, Thompson SG. Haemostatic function and ischemic heart disease: The Northwick park heart study. Lancet. 1986;I:533–537.
22.
Kannel WB, Wolf PA, Castelli WP, D'Agostino RB.
Fibrinogen and risk of cardiovascular disease: The
Framingham study. JAMA. 1987;258:1183–1186.
23.
Heinrich J, Balleisen L, Schulte H, Assmann G, van de
Loo J. Fibrinogen and factor VII in the prediction of coronary
risk: Results from the PROCAM study in healthy men. Arterioscler
Thromb. 1994;14:54–59.
24. Cremer P, Nagel D, Labrot B, Mann H, Muche R, Elster H, Seidel D. Lipoprotein Lp(a) as predictor of myocardial infarction in comparison to fibrinogen, LDL Cholesterol and other risk factors: Results from the prospective Gottingen Risk Incidence and Prevalence Study (GRIPS). Europ J Clin Invest.. 1994;24:444–453.[Medline] [Order article via Infotrieve]
25.
Woodward M, Lowe GDO, Rumley A, Tunstall-Pedoe.
Fibrinogen as a risk factor for coronary heart disease and
mortality in middle-aged men and women: Scottish Heart Health Study.
Eur Heart J. 1998;19:55–62.
26.
Sweetnam PM, Thomas HF, Yarnell JWG, Beswick AD,
Baker IA, Elwood PC. Fibrinogen viscosity and the ten year incidence of
ischaemic heart disease: The Caerphilly and Speedwell Studies.
Eur Heart J. 1996;17:1814–1820.
27.
Folsom AR, Wu KK, Rosamond WD, Sharrett AR, Chambless
LE. Prospective study of hemostatic factors and incidence of
coronary heart disease: The Atherosclerosis
Risk in Communities (ARIC) Study. Circulation. 1997;96:1102–1108.
28. Fowkes FGR, Lowe GDO, Housley E, Rattray A, Rumley A, Elton RA, MacGregor IR, Dawes J. Cross-linked fibrin degradation products, progression of peripheral arterial disease, and risk of coronary heart disease. Lancet. 1993;342:84–86.[Medline] [Order article via Infotrieve]
29.
Thompson SG, Kienast J, Pyke SDM, Haverkate F, van de
Loo J, for the European Concerted Action on Thrombosis, and
Disabilities Angina Pectoris Study Group. Hemostatic factors and the
risk of myocardial infarction or sudden death in patients with angina
pectoris. N Engl J Med. 1995;332:635–641.
30. Thompson SG, Calori G, Thomson JM, Haverkate F, Duckert F. The Impact of Sequential quality assessment exercises on laboratory performance: The Multicentre ECAT Angina Pectoris Study. Report from the European Concerted Action on Thrombosis, and Disabilities (ECAT). Thromb Haemost. 1991;65:149–152.[Medline] [Order article via Infotrieve]
31.
Benderly M, Graff E, Reicher-Reiss H, Behar S, Brunner
D, Goldbourt U, for the Benzafibrate Infarction Prevention (BIP) Study
Group. Fibrinogen is a predictor of mortality in coronary heart
disease patients. Arterioscler Thromb Vasc Biol. 1996;16:351–356.
32.
Toss H, Lindahl B, Siegbahn A, Wallentin L. Prognostic
influence of increased fibrinogen and C-reactive protein levels in
unstable coronary artery disease. Circulation. 1997;96:4204–4210.
33.
Lee A. J., Lowe GDO, Woodward M., Tunstall-Pedoe
H. Fibrinogen in relation to history of prevalent hypertension,
diabetes, stroke, intermittent claudicatio, coronary heart
disease and family history: The Scottish Heart Health Study. Br
Heart J. 1993;69:338–342.
34.
Salomaa V, Rasi V, Pekkanen J, Vahtera E, Jauhiainen M,
Vartiainen E, Myllyla G, Ehnholm C. Haemostatic factors and prevalent
coronary heart disease: The FINRISK haemostasis study.
Eur Heart J. 1994;15:1293–1299.
35.
Levenson J, Giral P, Raziavian M, Gariepy J, Simon A.
Fibrinogen and silent atherosclerosis in subjects with
cardiovascular risk factors. Arterioscler Thromb
Vasc Biol. 1995;15:1263–1268.
36.
Sharp DS, Abbott RD, Burchfiel CM, Rodriguez BL, Tracy
RP, Yano K, Curb D. Plasma fibrinogen and coronary heart
disease in elderly Japanese-American men. Arterioscler Thromb
Vasc Biol. 1996;16:262–268.
37. Woodward M, Lowe GDO, Rumley A, Tunstall-Pedoe H, Philippou H, Lane DA, Morrison CE. Epidemiology of coagulation factors, inhibitors and activation markers: The Third Glasgow MONICA Survey II. Relationships to cardiovascular disease. Br J Haematol. 1997;97:785–797.[Medline] [Order article via Infotrieve]
38. Qizilbash N, Jones L, Warlow C, Mann J. Fibrinogen and lipid concentrations as risk factors for transient ischemic attacks and minor ischemic strokes. BMJ. 1991;303:605–609.
39. Resch KL, Ernst E, Matrai A, Paulsen HF. Fibrinogen and viscosity as risk factors for subsequent cardiovascular events in stroke survivors. Ann Intern Med. 1992;117:371–375.
40. Wu KK, Folsom AR, Heiss G, Davis CE, Conlan MG, Barnes R, for the ARIC Study Investigators. Association of coagulation factors and inhibitors with carotid Artery Atherosclerosis Risk in Communities (ARIC) Study. Ann Epidemiol. 1992;2:471–480.[Medline] [Order article via Infotrieve]
41. Koster T, Rosendaal FR, Reitsma PH, van der Valden PA, Briet E, Vandenbroucke JP. Factor VII and fibrinogen levels as risk factors for venous thrombosis: A case-control study of plasma levels and DNA polymorphisms: the Leiden Thrombophilia Study (LETS). Thromb Haemost. 1994;71:719–722.[Medline] [Order article via Infotrieve]
42.
Danesh J, Collins R, Appleby P, Peto R. Association of
fibrinogen, C-reactive protein, albumin, or leukocyte count
with coronary heart disease: Meta-analysis of
prospective studies. JAMA. 1998;279:1477–1482.
43. Petitti DB. Meta-Analysis, Decision Analysis, and Cost-effectiveness Analysis. Oxford, England: Oxford University Press; 1994.
44. Greenland S. Quantitative methods in the review of epidemiologic literature. Epidemiol Rev. 1987;39:1–30.
45. D'Agostino RB, Weintraub M. Meta-analysis: A method for synthesizing research. Clin Pharmacol Ther. 1995;58:605–616.[Medline] [Order article via Infotrieve]
46.
Greenland S, Longnecker MP. Methods for trend
estimation from summarized dose-response data, with applications to
Meta-analysis. Am J Epidemiol. 1992;135:1301–1309.
47.
Laird NM, Mosteller F. Some statistical methods for
combining experimental results. Epidemiol Rev. 1987;9:1–30.
International Journal of Technology Assessment in Health Care
1990;6:5–30.
48. Jenicek M. Meta-analysis in medicine where we are and where we want to go. J Clin Epidemiol. 1989;42:34–44.
49. Greenland S, Salvan A. Bias in the one-step method for pooling study results. Stat Med. 1991;9:247–252.
50.
Olkin I. A critical look at some popular meta-analytic
methods [Invited commentary]. Am J Epidemiol. 1994;140:297–299.
51.
Rosner B, Spiegelman D, Willet WC. Correction of
logistic regression relative risk estimates and confidence intervals
for random within-person measurement error. Am J
Epidemiol. 1992;136:1400–1413.
52. Gibaldi M. Meta-analysis: a review of its place in therapeutic decision making. Drugs. 1993;46:805–818.[Medline] [Order article via Infotrieve]
53. L'Abbè KA, Detsky AS, O'Rourke K. Meta-analysis in clinical research. Ann Intern Med. 1987;107:224–233.
54. Ingram GIC. The determination of plasma fibrinogen by the clot-weight method. Biochem J. 1952;51:583–585.[Medline] [Order article via Infotrieve]
55. Ellis BC, Stransky A. A quick and accurate method for the determination of fibrinogen in plasma. J Lab Clin Med. 1961;58:477–488.[Medline] [Order article via Infotrieve]
56. Blomback B, Blomback M. Purification of human bovine fibrinogan. Arkh Kem. 1956;10:415–443.
57. von Clauss A. Gerinnungphysiologische Schnellmethode zur bestimmung des fibrinogen. Acta Haematol. 1957;17:237–246.[Medline] [Order article via Infotrieve]
58. Brittin GM, Rafinia H, Ravel D, Werner M, Brown B. Evaluationof single radial immunodiffusion for quantitation of plasma fibrinogen. Am J Pathol. 1972;57:89–94.
59.
Ernst E, Resch KL, Saradeth T, Maier A, Matrai A. A
viscometric method of measuring plasma fibrinogen concentrations.
J Clin Pathol. 1992;45:534–535.
60. Dessert J, Bocquet P, Belleville J, Later R, Quincy C. An automated immunonephelometric method for the quatitiative determination of plasma fibrinogen. Hamostasis. 1973;1:215.
61.
Tunstall-Pedoe H, Woodward M, Taverdale R, A'Brook R,
McCluskey MK. Comparison of the prediction by 27 different factors of
coronary heart disease and death in men and women of the
Scottish Heart Health Study: Cohort study. BMJ. 1997;315:722–729.
62. Marchioli R, Bomba E, Di Pasquale A, Geraci E, Giannuzzi C, Marfisi RM, Pede S, Schweiger C, Tavazzi L, Tognoni G, Valagussa F, a nome dei Ricercatori GISSI-Prevenzione. La carta del rischio post-IMA: Risultati dei primi 18 mesi di follow-up del GISSI-Prevenzione. G Ital Cardiol. 1998;28:416–433.[Medline] [Order article via Infotrieve]
63. Sweetnam PM, Yarnell WG, Lowe GDO, Baker LA, O'Brein JR, Rumley A, Etherinton MD, Whitehead PJ, Elwood PC. The relative power of heat-precipitation nephelometric and clottable (Clauss) fibrinogen in the prediction of ischaemic heart disease: The Caerphilly and Speedwell Studies. Br J Haematol. 1998;100:552–558.
64. Fey GH, Fuller GM. Regulation of the acute phase gene expression by inflammatory mediators. Mol Biol Med. 1987;4:323–328.[Medline] [Order article via Infotrieve]
65. Hassan J, Chelucci C, Peschle C, Sorrentino V. Transforming growth factor b (TGF-b) inhibits expression of fibrinogen and factor VII in a hepatoma cell line. Thromb Haemost. 1992;67:478–483.[Medline] [Order article via Infotrieve]
66. Haverkate F, Thompson SG, Pyke SDM, Gallimore JR, Pepys MB, for the ECAT Study Group. Production of C-reactive protein and risk of coronary events in stable and unstable angina. Lancet. 1997;349:462–466.[Medline] [Order article via Infotrieve]
67.
Maseri A. Inflammation,
atherosclerosis, and ischemic events: Exploring
the hidden side of the moon. N Engl J Med. 1997;336:1014–1016.
68.
Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens
CH. Inflammation, aspirin and the risk of
cardiovascular disease in apparently healthy men.
N Engl J Med. 1997;336:973–979.
69. Thomas AE, Green FR, Kelleher CH, Wilkes HC, Brennan PJ, Meade TW, Humphries SE. Variation in the promoter region of the b fibrinogen gene is associated with plasma fibrinogen levels in smokers and in non-smokers. Thromb Haemost. 1991;65:487–490.[Medline] [Order article via Infotrieve]
70. Fowkes FGR, Connor JM, Smith FB, Wood J, Donnan PT, Lowe GDO. Fibrinogen genotype and risk of peripheral atherosclerosis. Lancet. 1992;339:693–696.[Medline] [Order article via Infotrieve]
71. Connor JM, Fowkers FGR, Wood J, Smith FB, Donnan PT, Lowe GDO. Genetic variation at fibrinogen loci and plasma fibrinogen levels. J Med Genet. 1992;29:480–482.[Medline] [Order article via Infotrieve]
72.
Scarabin PY, Bara L, Ricard S, Poirier O, Cambou JP,
Arveiler D, Luc G, Evans AE, Samama MM, Cambien F. Genetic variation at
the b-fibrinogen locus in relation to plasma fibrinogen concentrations
and risk of myocardial infarction: The ECTIM study. Arterioscler
Thromb. 1993;13:886–891.
73.
de Maat MPM, de Knijff P, Green FR, Thomas AE,
Jespersen J, Kluft C. Gender-related association between b-fibrinogen
genotype and plasma fibrinogen levels and linkage
disequilibrium at the fibrinogen locus in Greenland Inuit.
Arterioscler Thromb Vasc Biol. 1995;15:856–860.
74.
Behague I, Poirier O, Nicaud V, Evans A, Arveiler D,
Luc G, Cambou JP, Scarabin PY, Bara L, Green F, Cambien F.
Beta-fibrinogen gene polymorphisms are associated with plasma
fibrinogen and coronary artery disease in patients with
myocardial infarction: The ECTIM study. Circulation. 1996;93:440–449.
75. Margaglione M, Cappucci G, Colaizzo D, Pirro L, Vecchione G, Grandone E, Di Minno G. Fibrinogen plasma levels in an apparently healthy general population: Relation to environmental and genetic determinants. Thromb Haemost. 1998;80:805–810.[Medline] [Order article via Infotrieve]
76. Di Minno G, Grandone E, Margaglione M. Clinical relevance of polymorphic markers of arterial thrombosis. Thromb Haemost. 1997;78:462–466.[Medline] [Order article via Infotrieve]
77.
Bernardi F, Arcieri P, Bertina RM, Chiarotti F, Corral
J, Pinotti M, Prydz H, Samama M, Sanset PM, Strom R, Vincente Garcia V,
Mariani G. Contribution of factor VII genotype to
activated FVII levels: Differences in genotype
frequencies between northern and southern European populations.
Arterioscler Thromb Vasc Biol. 1997;17:2548–2553.
78.
Iacoviello L, Di Castelnuovo A, De Knijff P, D'Orazio
A, Amore C, Arboretti R, Kluft C, Donati MB. Polymorphisms in the
coagulation factor VII gene and the risk of myocardial infarction.
N Engl J Med. 1998;338:79–85.
79. Ballestein L, Bailey J, Epping PH, Schulte H, van de Loo J. Epidemiological study on factor VII, Factor VIII and fibrinogen in an industrial population: I Baseline data on the relation to age, gender, body-weight, smoking, alcohol, pill-using and menopause. Thromb Haemost. 1985;54:475–479.[Medline] [Order article via Infotrieve]
80. Fishman D, Foulds G, Jeffery R, Mohamed-Ali V, Yudkin JS, Humphries S, Woo D. The effect of novel polymorphisms in the Interleukin-6 (IL-6) gene on IL-6 transcription and plasma IL-6 levels, and an association with systemic- onset juvenile chronic arthritis. J Clin Invest. 1998;102:1369–1376.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  D. S. Frankel, J. B. Meigs, J. M. Massaro, P. W.F. Wilson, C. J. O'Donnell, R. B. D'Agostino, and G. H. Tofler Von Willebrand Factor, Type 2 Diabetes Mellitus, and Risk of Cardiovascular Disease: The Framingham Offspring Study Circulation, December 9, 2008; 118(24): 2533 - 2539. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Koch, P. Hoppmann, J. Biele, J. C. Mueller, A. Schomig, and A. Kastrati Fibrinogen Genes and Myocardial Infarction: A Haplotype Analysis Arterioscler. Thromb. Vasc. Biol., April 1, 2008; 28(4): 758 - 763. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O Rogowski, I Shapira, A Shirom, S Melamed, S Toker, and S Berliner Heart rate and microinflammation in men: a relevant atherothrombotic link Heart, August 1, 2007; 93(8): 940 - 944. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Pilote, K. Dasgupta, V. Guru, K. H. Humphries, J. McGrath, C. Norris, D. Rabi, J. Tremblay, A. Alamian, T. Barnett, et al. A comprehensive view of sex-specific issues related to cardiovascular disease Can. Med. Assoc. J., March 13, 2007; 176(6): S1 - S44. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. J. Maxwell, E. Westein, W. S. Nesbitt, S. Giuliano, S. M. Dopheide, and S. P. Jackson Identification of a 2-stage platelet aggregation process mediating shear-dependent thrombus formation Blood, January 15, 2007; 109(2): 566 - 576. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Y.-P. Ho, M.-J. Chen, W. H.-H. Sheu, Y.-C. Yi, A. C.-W. Tsai, H.-F. Guu, and E. S.-C. Ho Differential effects of oral conjugated equine estrogen and transdermal estrogen on atherosclerotic vascular disease risk markers and endothelial function in healthy postmenopausal women Hum. Reprod., October 1, 2006; 21(10): 2715 - 2720. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Sato, H. Iso, H. Noda, A. Kitamura, H. Imano, M. Kiyama, T. Ohira, T. Okada, M. Yao, T. Tanigawa, et al. Plasma Fibrinogen Concentrations and Risk of Stroke and Its Subtypes Among Japanese Men and Women Stroke, October 1, 2006; 37(10): 2488 - 2492. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. von Kanel, U. Hepp, C. Buddeberg, M. Keel, L. Mica, K. Aschbacher, and U. Schnyder Altered Blood Coagulation in Patients With Posttraumatic Stress Disorder Psychosom Med, July 1, 2006; 68(4): 598 - 604. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Ziakas, S. Gavrilidis, G. Giannoglou, E. Souliou, K. Gemitzis, D. Kalampalika, M. A. Vayona, I. Pidonia, G. Parharidis, and G. Louridas In-Hospital and Long-Term Prognostic Value of Fibrinogen, CRP, and IL-6 Levels in Patients with Acute Myocardial Infarction Treated with Thrombolysis Angiology, May 1, 2006; 57(3): 283 - 293. [Abstract] [PDF]
|
|
|
|
 |
|
 A. A. Quyyumi Women and Ischemic Heart Disease: Pathophysiologic Implications From the Women's Ischemia Syndrome Evaluation (WISE) Study and Future Research Steps J. Am. Coll. Cardiol., February 7, 2006; 47(3_Suppl_S): S66 - S71. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. M C. S M Leao, M. P. C Duarte, D. M. B Silva, P. R. V Bahia, C. M. Coeli, and M. L. F. de Farias Influence of methyltestosterone postmenopausal therapy on plasma lipids, inflammatory factors, glucose metabolism and visceral fat: a randomized study Eur. J. Endocrinol., January 1, 2006; 154(1): 131 - 139. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Smith, C. Patterson, J. Yarnell, A. Rumley, Y. Ben-Shlomo, and G. Lowe Which Hemostatic Markers Add to the Predictive Value of Conventional Risk Factors for Coronary Heart Disease and Ischemic Stroke?: The Caerphilly Study Circulation, November 15, 2005; 112(20): 3080 - 3087. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Fibrinogen Studies Collaboration* Plasma Fibrinogen Level and the Risk of Major Cardiovascular Diseases and Nonvascular Mortality: An Individual Participant Meta-analysis JAMA, October 12, 2005; 294(14): 1799 - 1809. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Feinbloom and K. A. Bauer Assessment of Hemostatic Risk Factors in Predicting Arterial Thrombotic Events Arterioscler. Thromb. Vasc. Biol., October 1, 2005; 25(10): 2043 - 2053. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. D. Smith, R. Harbord, J. Milton, S. Ebrahim, and J. A.C. Sterne Does Elevated Plasma Fibrinogen Increase the Risk of Coronary Heart Disease?: Evidence from a Meta-Analysis of Genetic Association Studies Arterioscler. Thromb. Vasc. Biol., October 1, 2005; 25(10): 2228 - 2233. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Woodward, G. D.O. Lowe, D. J. Campbell, S. Colman, A. Rumley, J. Chalmers, B. C. Neal, A. Patel, A. J. Jenkins, B. E. Kemp, et al. Associations of Inflammatory and Hemostatic Variables With the Risk of Recurrent Stroke Stroke, October 1, 2005; 36(10): 2143 - 2147. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. I. Paraskevas, S. S. Daskalopoulou, M. E. Daskalopoulos, and C. D. Liapis Secondary Prevention of Ischemic Cerebrovascular Disease. What Is the Evidence? Angiology, September 1, 2005; 56(5): 539 - 552. [Abstract] [PDF]
|
|
|
|
|
|
H. J. Milionis, E. Rizos, J. Goudevenos, K. Seferiadis, D. P. Mikhailidis, and M. S. Elisaf Components of the Metabolic Syndrome and Risk for First-Ever Acute Ischemic Nonembolic Stroke in Elderly Subjects Stroke, July 1, 2005; 36(7): 1372 - 1376. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Elosua, B. Bartali, J. M. Ordovas, A. M. Corsi, F. Lauretani, L. Ferrucci, and on Behalf of the InCHIANTI Investigators Association Between Physical Activity, Physical Performance, and Inflammatory Biomarkers in an Elderly Population: The InCHIANTI Study J. Gerontol. A Biol. Sci. Med. Sci., June 1, 2005; 60(6): 760 - 767. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. Soria, L. Almasy, J. C. Souto, A. Buil, M. Lathrop, J. Blangero, and J. Fontcuberta A Genome Search for Genetic Determinants That Influence Plasma Fibrinogen Levels Arterioscler. Thromb. Vasc. Biol., June 1, 2005; 25(6): 1287 - 1292. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Arikan and S. Sen Endothelial Damage and Hemostatic Markers in Patients with Uncomplicated Mild-to-Moderate Hypertension and Relationship with Risk Factors Clinical and Applied Thrombosis/Hemostasis, April 1, 2005; 11(2): 147 - 159. [Abstract] [PDF]
|
|
|
|
|
|
A M Smith, K M English, C J Malkin, R D Jones, T H Jones, and K S Channer Testosterone does not adversely affect fibrinogen or tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) levels in 46 men with chronic stable angina Eur. J. Endocrinol., February 1, 2005; 152(2): 285 - 291. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. J. Kullo and C. M. Ballantyne Conditional Risk Factors for Atherosclerosis Mayo Clin. Proc., February 1, 2005; 80(2): 219 - 230. [Abstract] [PDF]
|
|
|
|
 |
|
 M P J van Goor, E B Gomez-Garcia, F W G Leebeek, G J Brouwers, P J Koudstaal, and D W J Dippel The - 148 C/T fibrinogen gene polymorphism and fibrinogen levels in ischaemic stroke: a case-control study J. Neurol. Neurosurg. Psychiatry, January 1, 2005; 76(1): 121 - 123. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. M. Rothwell, S. C. Howard, D. A. Power, S. A. Gutnikov, A. Algra, J. van Gijn, T. G. Clark, M. F.G. Murphy, C. P. Warlow, and for the Cerebrovascular Cohort Studies Collaborati Fibrinogen Concentration and Risk of Ischemic Stroke and Acute Coronary Events in 5113 Patients With Transient Ischemic Attack and Minor Ischemic Stroke Stroke, October 1, 2004; 35(10): 2300 - 2305. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. F Viles-Gonzalez, V. Fuster, and J. J Badimon Atherothrombosis: A widespread disease with unpredictable and life-threatening consequences Eur. Heart J., July 2, 2004; 25(14): 1197 - 1207. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. J Baer, J. T Judd, B. A Clevidence, and R. P Tracy Dietary fatty acids affect plasma markers of inflammation in healthy men fed controlled diets: a randomized crossover study Am. J. Clinical Nutrition, June 1, 2004; 79(6): 969 - 973. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D Zeltser, O Rogowski, S Berliner, T Mardi, D Justo, J Serov, M Rozenblat, D Avitzour, and I Shapira Sex differences in the expression of haemorheological determinants in individuals with atherothrombotic risk factors and in apparently healthy people Heart, March 1, 2004; 90(3): 277 - 281. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Kang, K. Chu, and J.-K. Roh POEMS Syndrome, Fibrinogen, and Ischemic Stroke: A Critical Point of View--Reply Arch Neurol, January 1, 2004; 61(1): 155 - 156. [Full Text] [PDF]
|
|
|
|
|
|
E. Lutgens, R.-J. van Suylen, B. C. Faber, M. J. Gijbels, P. M. Eurlings, A.-P. Bijnens, K. B. Cleutjens, S. Heeneman, and M. J.A.P. Daemen Atherosclerotic Plaque Rupture: Local or Systemic Process? Arterioscler. Thromb. Vasc. Biol., December 1, 2003; 23(12): 2123 - 2130. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. von Kanel and J. E. Dimsdale Hemostatic Alterations in Patients With Obstructive Sleep Apnea and the Implications for Cardiovascular Disease Chest, November 1, 2003; 124(5): 1956 - 1967. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Kamath and G.Y.H. Lip Fibrinogen: biochemistry, epidemiology and determinants QJM, October 1, 2003; 96(10): 711 - 729. [Full Text] [PDF]
|
|
|
|
 |
|
 V. Palmieri, R. P. Tracy, M. J. Roman, J. E. Liu, L. G. Best, J. N. Bella, D. C. Robbins, B. V. Howard, and R. B. Devereux Relation of Left Ventricular Hypertrophy to Inflammation and Albuminuria in Adults With Type 2 Diabetes: The Strong Heart Study Diabetes Care, October 1, 2003; 26(10): 2764 - 2769. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. E. Bojesen, K. Juul, P. Schnohr, A. Tybjaerg-Hansen, and B.o. G. Nordestgaard Platelet glycoprotein IIb/IIIa PlA2/PlA2 homozygosity associated with risk of ischemic cardiovascular disease and myocardial infarction in young men: The Copenhagen City Heart Study J. Am. Coll. Cardiol., August 20, 2003; 42(4): 661 - 667. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. G. Hackam and S. S. Anand Emerging Risk Factors for Atherosclerotic Vascular Disease: A Critical Review of the Evidence JAMA, August 20, 2003; 290(7): 932 - 940. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C.J. Malkin, P.J. Pugh, T.H. Jones, and K.S. Channer Testosterone for secondary prevention in men with ischaemic heart disease? QJM, July 1, 2003; 96(7): 521 - 529. [Full Text] [PDF]
|
|
|
|
 |
|
 K. Kain, J. M. Blaxill, A. J. Catto, P. J. Grant, and A. M. Carter Increased Fibrinogen Levels among South Asians versus Whites in the United Kingdom Are Not Explained by Common Polymorphisms Am. J. Epidemiol., July 15, 2002; 156(2): 174 - 179. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. G.C. Spencer, D. Gurney, A. D. Blann, D. G. Beevers, and G. Y.H. Lip Von Willebrand Factor, Soluble P-Selectin, and Target Organ Damage in Hypertension: A Substudy of the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) Hypertension, July 1, 2002; 40(1): 61 - 66. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Acevedo, G. L. Pearce, K. Kottke-Marchant, and D. L. Sprecher Elevated Fibrinogen and Homocysteine Levels Enhance the Risk of Mortality in Patients From a High-Risk Preventive Cardiology Clinic Arterioscler. Thromb. Vasc. Biol., June 1, 2002; 22(6): 1042 - 1045. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P R J Ames, A Margarita, J D. Alves, C Tommasino, L Iannaccone, and V Brancaccio Anticardiolipin antibody titre and plasma homocysteine level independently predict intima media thickness of carotid arteries in subjects with idiopathic antiphospholipid antibodies Lupus, April 1, 2002; 11(4): 208 - 214. [Abstract] [PDF]
|
|
|
|
|
|
R Marchioli, F Avanzini, F Barzi, C Chieffo, A Di Castelnuovo, M.G Franzosi, E Geraci, A.P Maggioni, R.M Marfisi, N Mininni, et al. Assessment of absolute risk of death after myocardial infarction by use of multiple-risk-factor assessment equations; GISSI-Prevenzione mortality risk chart Eur. Heart J., November 2, 2001; 22(22): 2085 - 2103. [Abstract] [PDF]
|
|
|
|
|
|
L. Iacoviello, M. Vischetti, F. Zito, and M. Benedetta Donati Genes Encoding Fibrinogen and Cardiovascular Risk Hypertension, November 1, 2001; 38(5): 1199 - 1203. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. J. Milionis, E. Rizos, and D. P. Mikhailidis Smoking Diminishes the Beneficial Effect of Statins: Observations from the Landmark Trials Angiology, September 1, 2001; 52(9): 575 - 587. [Abstract] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
 |
|
 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]
|
|
|
|
|
|
S. C. Clarke, P. M. Schofield, A. A. Grace, J. C. Metcalfe, and H. L. Kirschenlohr Tamoxifen Effects on Endothelial Function and Cardiovascular Risk Factors in Men With Advanced Atherosclerosis Circulation, March 20, 2001; 103(11): 1497 - 1502. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||