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Effects of warfarin therapy on plasma fibrinogen, von Willebrand factor, and fibrin D-dimer in left ventricular dysfunction secondary to coronary artery disease with and without aneurysms

Cardiac impairment in patients is associated with intracardiac thrombus formation and thromboembolism. A high prothrombotic state may exist in such patients, and abnormalities in plasma markers of thrombogenesis may be indicative of such a state. The aim of this study was to determine the associatio... Full description

Journal Title: The American journal of cardiology 1995, Vol.76 (7), p.453-458
Main Author: Lip, Gregory Y.H
Other Authors: Lowe, Gordon D.O , Metcalfe, Malcolm J , Rumley, Ann , Dunn, Francis G
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: New York, NY: Elsevier Inc
ID: ISSN: 0002-9149
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title: Effects of warfarin therapy on plasma fibrinogen, von Willebrand factor, and fibrin D-dimer in left ventricular dysfunction secondary to coronary artery disease with and without aneurysms
format: Article
creator:
  • Lip, Gregory Y.H
  • Lowe, Gordon D.O
  • Metcalfe, Malcolm J
  • Rumley, Ann
  • Dunn, Francis G
subjects:
  • Abridged Index Medicus
  • Analysis
  • Analysis of Variance
  • Aneurysms
  • Biological and medical sciences
  • Blood. Blood coagulation. Reticuloendothelial system
  • Cardiac patients
  • Cardiology
  • Cardiovascular disease
  • Coronary Disease - blood
  • Coronary Disease - complications
  • Coronary heart disease
  • Cross-Sectional Studies
  • Drug therapy
  • Female
  • Fibrin
  • Fibrin Fibrinogen Degradation Products - metabolism
  • Fibrinogen - metabolism
  • Heart Aneurysm - blood
  • Heart Aneurysm - drug therapy
  • Heart Aneurysm - etiology
  • Heart Ventricles
  • Humans
  • Longitudinal Studies
  • Male
  • Medical research
  • Medical sciences
  • Middle Aged
  • Pharmacology. Drug treatments
  • Prospective Studies
  • Thromboembolism
  • Thromboembolism - etiology
  • Thromboembolism - prevention & control
  • Ventricular Dysfunction, Left - blood
  • Ventricular Dysfunction, Left - drug therapy
  • Ventricular Dysfunction, Left - etiology
  • Von Willebrand factor
  • von Willebrand Factor - metabolism
  • Warfarin
  • Warfarin - therapeutic use
ispartof: The American journal of cardiology, 1995, Vol.76 (7), p.453-458
description: Cardiac impairment in patients is associated with intracardiac thrombus formation and thromboembolism. A high prothrombotic state may exist in such patients, and abnormalities in plasma markers of thrombogenesis may be indicative of such a state. The aim of this study was to determine the associations of left ventricular (LV) aneurysm formation and dysfunction with plasma fibrinogen, von Willebrand factor, and fibrin D-dimer, which are markers associated with thrombus formation (thrombogenesis) and to investigate the effects of warfarin given to patients with LV aneurysms on fibrinogen and D-dimer levels. A cross-sectional study of 112 patients with coronary artery disease was initially performed: 34 patients had normal LV function (group 1); 30 had LV dysfunction without aneurysm formation (group 2); 29 had LV aneurysms without anticoagulation (group 3a); and 19 patients had LV aneurysms with warfarin therapy (group 3b). Results were compared with 158 population controls from a random population sample. A longitudinal study of 10 patients given warfarin was also performed. In group 1, plasma fibrinogen (median difference 0.36 g/L; p = 0.0009) and von Willebrand factor (median difference 17 IU/dl; p = 0.04) were elevated, whereas plasma D-dimer levels (median difference 23.0 ng/ml; p = 0.001) were lower than those in population control subjects. There were no significant differences in plasma fibrinogen, von Willebrand factor, or D-dimer levels between groups 1 and 2. In group 3a, plasma fibrinogen was elevated when compared with group 1 (median difference 0.6 g/L; p = 0.0001), with a trend toward high von Willebrand factor levels. In these patients, plasma D-dimer levels were also elevated when compared with group 1 (median difference 55 ng/ml; p = 0.0007). In similar patients taking warfarin (group 3b), there was no significant difference in plasma fibrinogen, but there was a lower plasma fibrin D-dimer level when compared with group 3a (median difference 65.5 ng/ml; p = 0.0003). In the longitudinal study, there was a reduction in median plasma fibrin D-dimer levels 2 months after administering warfarin (148 vs 61 ng/ml; paired Wilcoxon test, p = 0.01). This reduction in plasma fibrin D-dimer with warfarin is consistent with the beneficial effect of warfarin therapy in reducing thromboembolic risk. The measurement or plasma fibrin D-dimer may thus be useful as a marker of ongoing intravascular thrombogenesis, allowing identification of high-risk patients
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0002-9149
fulltext: fulltext
issn:
  • 0002-9149
  • 1879-1913
url: Link


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titleEffects of warfarin therapy on plasma fibrinogen, von Willebrand factor, and fibrin D-dimer in left ventricular dysfunction secondary to coronary artery disease with and without aneurysms
sourceAlma/SFX Local Collection
creatorLip, Gregory Y.H ; Lowe, Gordon D.O ; Metcalfe, Malcolm J ; Rumley, Ann ; Dunn, Francis G
creatorcontribLip, Gregory Y.H ; Lowe, Gordon D.O ; Metcalfe, Malcolm J ; Rumley, Ann ; Dunn, Francis G
descriptionCardiac impairment in patients is associated with intracardiac thrombus formation and thromboembolism. A high prothrombotic state may exist in such patients, and abnormalities in plasma markers of thrombogenesis may be indicative of such a state. The aim of this study was to determine the associations of left ventricular (LV) aneurysm formation and dysfunction with plasma fibrinogen, von Willebrand factor, and fibrin D-dimer, which are markers associated with thrombus formation (thrombogenesis) and to investigate the effects of warfarin given to patients with LV aneurysms on fibrinogen and D-dimer levels. A cross-sectional study of 112 patients with coronary artery disease was initially performed: 34 patients had normal LV function (group 1); 30 had LV dysfunction without aneurysm formation (group 2); 29 had LV aneurysms without anticoagulation (group 3a); and 19 patients had LV aneurysms with warfarin therapy (group 3b). Results were compared with 158 population controls from a random population sample. A longitudinal study of 10 patients given warfarin was also performed. In group 1, plasma fibrinogen (median difference 0.36 g/L; p = 0.0009) and von Willebrand factor (median difference 17 IU/dl; p = 0.04) were elevated, whereas plasma D-dimer levels (median difference 23.0 ng/ml; p = 0.001) were lower than those in population control subjects. There were no significant differences in plasma fibrinogen, von Willebrand factor, or D-dimer levels between groups 1 and 2. In group 3a, plasma fibrinogen was elevated when compared with group 1 (median difference 0.6 g/L; p = 0.0001), with a trend toward high von Willebrand factor levels. In these patients, plasma D-dimer levels were also elevated when compared with group 1 (median difference 55 ng/ml; p = 0.0007). In similar patients taking warfarin (group 3b), there was no significant difference in plasma fibrinogen, but there was a lower plasma fibrin D-dimer level when compared with group 3a (median difference 65.5 ng/ml; p = 0.0003). In the longitudinal study, there was a reduction in median plasma fibrin D-dimer levels 2 months after administering warfarin (148 vs 61 ng/ml; paired Wilcoxon test, p = 0.01). This reduction in plasma fibrin D-dimer with warfarin is consistent with the beneficial effect of warfarin therapy in reducing thromboembolic risk. The measurement or plasma fibrin D-dimer may thus be useful as a marker of ongoing intravascular thrombogenesis, allowing identification of high-risk patients. This may aid in decision-making when warfarin therapy is being considered.
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0ISSN: 0002-9149
1EISSN: 1879-1913
2DOI: 10.1016/S0002-9149(99)80129-5
3PMID: 7653443
4CODEN: AJCDAG
languageeng
publisherNew York, NY: Elsevier Inc
subjectAbridged Index Medicus ; Analysis ; Analysis of Variance ; Aneurysms ; Biological and medical sciences ; Blood. Blood coagulation. Reticuloendothelial system ; Cardiac patients ; Cardiology ; Cardiovascular disease ; Coronary Disease - blood ; Coronary Disease - complications ; Coronary heart disease ; Cross-Sectional Studies ; Drug therapy ; Female ; Fibrin ; Fibrin Fibrinogen Degradation Products - metabolism ; Fibrinogen - metabolism ; Heart Aneurysm - blood ; Heart Aneurysm - drug therapy ; Heart Aneurysm - etiology ; Heart Ventricles ; Humans ; Longitudinal Studies ; Male ; Medical research ; Medical sciences ; Middle Aged ; Pharmacology. Drug treatments ; Prospective Studies ; Thromboembolism ; Thromboembolism - etiology ; Thromboembolism - prevention & control ; Ventricular Dysfunction, Left - blood ; Ventricular Dysfunction, Left - drug therapy ; Ventricular Dysfunction, Left - etiology ; Von Willebrand factor ; von Willebrand Factor - metabolism ; Warfarin ; Warfarin - therapeutic use
ispartofThe American journal of cardiology, 1995, Vol.76 (7), p.453-458
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01995 Excerpta Medica, Inc. All rights reserved under the United States, International, and Pan-American Copyright Conventions.
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1Lowe, Gordon D.O
2Metcalfe, Malcolm J
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title
0Effects of warfarin therapy on plasma fibrinogen, von Willebrand factor, and fibrin D-dimer in left ventricular dysfunction secondary to coronary artery disease with and without aneurysms
1The American journal of cardiology
addtitleAm J Cardiol
descriptionCardiac impairment in patients is associated with intracardiac thrombus formation and thromboembolism. A high prothrombotic state may exist in such patients, and abnormalities in plasma markers of thrombogenesis may be indicative of such a state. The aim of this study was to determine the associations of left ventricular (LV) aneurysm formation and dysfunction with plasma fibrinogen, von Willebrand factor, and fibrin D-dimer, which are markers associated with thrombus formation (thrombogenesis) and to investigate the effects of warfarin given to patients with LV aneurysms on fibrinogen and D-dimer levels. A cross-sectional study of 112 patients with coronary artery disease was initially performed: 34 patients had normal LV function (group 1); 30 had LV dysfunction without aneurysm formation (group 2); 29 had LV aneurysms without anticoagulation (group 3a); and 19 patients had LV aneurysms with warfarin therapy (group 3b). Results were compared with 158 population controls from a random population sample. A longitudinal study of 10 patients given warfarin was also performed. In group 1, plasma fibrinogen (median difference 0.36 g/L; p = 0.0009) and von Willebrand factor (median difference 17 IU/dl; p = 0.04) were elevated, whereas plasma D-dimer levels (median difference 23.0 ng/ml; p = 0.001) were lower than those in population control subjects. There were no significant differences in plasma fibrinogen, von Willebrand factor, or D-dimer levels between groups 1 and 2. In group 3a, plasma fibrinogen was elevated when compared with group 1 (median difference 0.6 g/L; p = 0.0001), with a trend toward high von Willebrand factor levels. In these patients, plasma D-dimer levels were also elevated when compared with group 1 (median difference 55 ng/ml; p = 0.0007). In similar patients taking warfarin (group 3b), there was no significant difference in plasma fibrinogen, but there was a lower plasma fibrin D-dimer level when compared with group 3a (median difference 65.5 ng/ml; p = 0.0003). In the longitudinal study, there was a reduction in median plasma fibrin D-dimer levels 2 months after administering warfarin (148 vs 61 ng/ml; paired Wilcoxon test, p = 0.01). This reduction in plasma fibrin D-dimer with warfarin is consistent with the beneficial effect of warfarin therapy in reducing thromboembolic risk. The measurement or plasma fibrin D-dimer may thus be useful as a marker of ongoing intravascular thrombogenesis, allowing identification of high-risk patients. This may aid in decision-making when warfarin therapy is being considered.
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0Abridged Index Medicus
1Analysis
2Analysis of Variance
3Aneurysms
4Biological and medical sciences
5Blood. Blood coagulation. Reticuloendothelial system
6Cardiac patients
7Cardiology
8Cardiovascular disease
9Coronary Disease - blood
10Coronary Disease - complications
11Coronary heart disease
12Cross-Sectional Studies
13Drug therapy
14Female
15Fibrin
16Fibrin Fibrinogen Degradation Products - metabolism
17Fibrinogen - metabolism
18Heart Aneurysm - blood
19Heart Aneurysm - drug therapy
20Heart Aneurysm - etiology
21Heart Ventricles
22Humans
23Longitudinal Studies
24Male
25Medical research
26Medical sciences
27Middle Aged
28Pharmacology. Drug treatments
29Prospective Studies
30Thromboembolism
31Thromboembolism - etiology
32Thromboembolism - prevention & control
33Ventricular Dysfunction, Left - blood
34Ventricular Dysfunction, Left - drug therapy
35Ventricular Dysfunction, Left - etiology
36Von Willebrand factor
37von Willebrand Factor - metabolism
38Warfarin
39Warfarin - therapeutic use
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titleEffects of warfarin therapy on plasma fibrinogen, von Willebrand factor, and fibrin D-dimer in left ventricular dysfunction secondary to coronary artery disease with and without aneurysms
authorLip, Gregory Y.H ; Lowe, Gordon D.O ; Metcalfe, Malcolm J ; Rumley, Ann ; Dunn, Francis G
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0Abridged Index Medicus
1Analysis
2Analysis of Variance
3Aneurysms
4Biological and medical sciences
5Blood. Blood coagulation. Reticuloendothelial system
6Cardiac patients
7Cardiology
8Cardiovascular disease
9Coronary Disease - blood
10Coronary Disease - complications
11Coronary heart disease
12Cross-Sectional Studies
13Drug therapy
14Female
15Fibrin
16Fibrin Fibrinogen Degradation Products - metabolism
17Fibrinogen - metabolism
18Heart Aneurysm - blood
19Heart Aneurysm - drug therapy
20Heart Aneurysm - etiology
21Heart Ventricles
22Humans
23Longitudinal Studies
24Male
25Medical research
26Medical sciences
27Middle Aged
28Pharmacology. Drug treatments
29Prospective Studies
30Thromboembolism
31Thromboembolism - etiology
32Thromboembolism - prevention & control
33Ventricular Dysfunction, Left - blood
34Ventricular Dysfunction, Left - drug therapy
35Ventricular Dysfunction, Left - etiology
36Von Willebrand factor
37von Willebrand Factor - metabolism
38Warfarin
39Warfarin - therapeutic use
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jtitleThe American journal of cardiology
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date1995
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pages453-458
issn0002-9149
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codenAJCDAG
abstractCardiac impairment in patients is associated with intracardiac thrombus formation and thromboembolism. A high prothrombotic state may exist in such patients, and abnormalities in plasma markers of thrombogenesis may be indicative of such a state. The aim of this study was to determine the associations of left ventricular (LV) aneurysm formation and dysfunction with plasma fibrinogen, von Willebrand factor, and fibrin D-dimer, which are markers associated with thrombus formation (thrombogenesis) and to investigate the effects of warfarin given to patients with LV aneurysms on fibrinogen and D-dimer levels. A cross-sectional study of 112 patients with coronary artery disease was initially performed: 34 patients had normal LV function (group 1); 30 had LV dysfunction without aneurysm formation (group 2); 29 had LV aneurysms without anticoagulation (group 3a); and 19 patients had LV aneurysms with warfarin therapy (group 3b). Results were compared with 158 population controls from a random population sample. A longitudinal study of 10 patients given warfarin was also performed. In group 1, plasma fibrinogen (median difference 0.36 g/L; p = 0.0009) and von Willebrand factor (median difference 17 IU/dl; p = 0.04) were elevated, whereas plasma D-dimer levels (median difference 23.0 ng/ml; p = 0.001) were lower than those in population control subjects. There were no significant differences in plasma fibrinogen, von Willebrand factor, or D-dimer levels between groups 1 and 2. In group 3a, plasma fibrinogen was elevated when compared with group 1 (median difference 0.6 g/L; p = 0.0001), with a trend toward high von Willebrand factor levels. In these patients, plasma D-dimer levels were also elevated when compared with group 1 (median difference 55 ng/ml; p = 0.0007). In similar patients taking warfarin (group 3b), there was no significant difference in plasma fibrinogen, but there was a lower plasma fibrin D-dimer level when compared with group 3a (median difference 65.5 ng/ml; p = 0.0003). In the longitudinal study, there was a reduction in median plasma fibrin D-dimer levels 2 months after administering warfarin (148 vs 61 ng/ml; paired Wilcoxon test, p = 0.01). This reduction in plasma fibrin D-dimer with warfarin is consistent with the beneficial effect of warfarin therapy in reducing thromboembolic risk. The measurement or plasma fibrin D-dimer may thus be useful as a marker of ongoing intravascular thrombogenesis, allowing identification of high-risk patients. This may aid in decision-making when warfarin therapy is being considered.
copNew York, NY
pubElsevier Inc
pmid7653443
doi10.1016/S0002-9149(99)80129-5