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Erschienen in: BMC Cardiovascular Disorders 1/2020

Open Access 01.12.2020 | Research article

Prognostic value of plasma von Willebrand factor levels in major adverse cardiovascular events: a systematic review and meta-analysis

verfasst von: Mengge Fan, Xia Wang, Xun Peng, Shuo Feng, Junyu Zhao, Lin Liao, Yong Zhang, Yinglong Hou, Ju Liu

Erschienen in: BMC Cardiovascular Disorders | Ausgabe 1/2020

Abstract

Background

Prediction of major adverse cardiovascular events (MACEs) may offer great benefits for patients with coronary artery disease (CAD). Von Willebrand factor (vWF) is stored in endothelial cells and released into blood plasma upon vascular dysfunction. This meta-analysis was performed to evaluate the prognostic value of plasma vWF levels in CAD patients with MACEs.

Methods

A total of 15 studies were included in this meta-analysis through the search in PubMed, Embase and CNKI. Data were collected from 960 patients who had MACEs after CAD and 3224 controls nested without the adverse events. The standard mean difference (SMD) and 95% confidence intervals (95% CI) were calculated using random-effects model.

Results

The plasma vWF levels examined at 24 h and 48 h after admission were significantly higher in CAD patients with MACEs than those without. The pooled SMD among the MACEs group and the non-MACEs group was 0.55 (95% CI = 0.30–0.80, P < 0.0001) and 0.70 (95% CI = 0.27–1.13, P = 0.001), respectively. However, no significant difference was found in plasma vWF levels on admission between the two groups.

Conclusion

Plasma vWF level in CAD patients examined at 24 h and 48 h after admission might be an independent prognostic factor for MACE.
Hinweise

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Abkürzungen
95%CI
95% confidence intervals
ACS
Acute coronary syndromes
AMI
Acute myocardial infarction
CAD
Coronary artery disease
CK-MB
Creatine kinase MB ECG: electro cardio graph
IQR
Inter quartile range
MACEs
Major adverse cardiac events
non-STEMI
Non-ST-elevated myocardial infarction
NOS
Newcastle-Ottawa quality assessment scale
PCI
Percutaneous coronary intervention
SD
Standard deviation
SE
Standard error
SMD
Standard mean difference
STMI
ST-elevated myocardial infarction
vWF
von Willebrand factor

Background

Coronary artery disease (CAD) is characterized by the occlusion or stenosis of coronary artery mostly caused by atherosclerosis, and is one of the leading causes of mortality in humans [1, 2]. Patients with CAD are vulnerable in development of major cardiovascular events (MACEs) including nonfatal acute myocardial infarction, unstable angina, stroke, transient ischemic attack, peripheral arterial occlusive disorder, and death [3]. According to previous long-term follow-up studies, the incidence of MACEs development after CAD ranges from 21 to 49% [4], while the recurrence rates of MACEs are up to 75% within 3 years [5]. These events are typically caused by the formation of thrombus and insufficient blood supply. Identifying risk factors for the development of MACEs is of great value in the prognosis of CAD patients.
Von Willebrand factor (vWF) is a large multimeric glycoprotein required for the formation of hemostatic plugs and arterial thrombi [6]. vWF adheres platelets to the blood vessel wall, and acts as a plasma carrier for factor VIII to prevent its degradation in the blood circulation [7, 8]. After synthesis, vWF is stored in the Weibel-Palade bodies of endothelial cells and the α-granules of platelets [9, 10]. The stored vWF is rapidly released at moments of endothelial cell damage, thus it is considered as a promised biomarker for endothelial dysfunction [11]. In addition, studies have shown that the plasma vWF derived from coronary vascular endothelial cells is significantly elevated when coronary artery injury occurs [12], indicating a pathogenesis role of vWF in the progression of CAD. Increased level of vWF has been recognized as an independent predictor of CAD in general population [9]. However, the prognostic role of vWF in CAD patients remains controversial. Several studies demonstrate a weak association between elevated vWF level and adverse outcomes in patients with CAD [13]. The current meta-analysis was performed to evaluate the prognostic value of plasma vWF in patients with CAD, in terms of MACEs.

Methods

Search strategy

We searched for all publications concerning the association between vWF and CAD up to July 2018. The literatures were searched in PubMed, Embase database and CNKI. The search strategy was composed by the following search terms (vWF OR Willebrand Protein OR von Willebrand Factor OR Factor VIIIR-Ag) AND (Coronary Disease OR coronary artery disease OR CAD OR CHD OR Myocardial Infarction OR AMI OR Acute coronary syndrome OR ACS OR angina) AND (major adverse cardiac events OR mortality OR death OR prognosis).

Study selection

Inclusion criteria were as follows: (1) cohort studies enrolling patients with CAD (myocardial Infarction, acute coronary syndrome and stable CAD); (2) data on plasma vWF was reported; (3) MACEs or mortality following CAD were recorded; (4) studies written in English or Chinese. Exclusion criteria are as follows: (1) patients without CAD; (2) there is no definitive value of plasma vWF.

Data extraction

Two independent reviewers extracted the following data from each eligible studies: first author’s name, year of publication, mean age, sample size, gender, mean and standard deviation (mean ± SD) or mean and standard error (mean ± SE) of plasma vWF concentration, definition of MACEs, mean or median follow-up duration, treatment modality, data regarding baseline and follow-up concentrations of vWF. Moreover, if the articles provide the data of median and interquartile range (IQR) format or mean and p value, we calculated the SMD according to the formulations recommended by Cochrane Handbooks. Any discrepancy in data extraction was resolved through discussion with a third reviewer.

Quality assessment

Two independent authors assessed the methodological quality according to the Newcastle-Ottawa Quality Assessment scale (NOS) for cohort study. Total NOS score ranged from 0 to 9 stars. Those scored ≥7 stars were considered as high quality and those scored ≤5 as low quality.

Statistical analysis

Meta-analyses were conducted on Review Manager software (RevMan5.3, Cochrane Collaboration, Oxford, UK, http://​community.​cochrane.​org) and STATA software (Stata Corp, College Station, Texas, USA). The SMD and 95% confidence intervals were calculated using a generic inverse variance approach. The overall effects were determined by Z-test and P-value < 0.05 were considered as statistically significant.
The heterogeneity across studies was tested by CochranQ statistics and I2 statistics. A random-effects model was used due to significant heterogeneity. Subgroup analyses were conducted to identify the source of potential heterogeneity based on the duration of follow-up, PCI, and severity of CAD. Meta-regression was also conducted to explore the potential heterogeneity. P < 0.05 was considered statistically significant. Sensitivity analysis was performed by removing studies one by one to estimate the stability of meta-analysis.

Results

Search results and characteristics of included studies

A total of 1382 publications were identified by the search strategy, and 1324 publications remained in this study after removal of duplicates. After carefully reviewing the titles and abstracts, 44 candidate articles were screened out for further full-text reading, and 1280 unrelated articles were excluded. In addition, 27 full-text reviewed articles were excluded due to disqualification of inclusion criteria, 15 studies were included in this meta-analysis. Search progress was shown in Fig. 1. Of these 15 studies, 4 studies were conducted in China, 3 in Austria, 3 in UK, 2 in Germany, 1 in USA, 1 in Norway and 1 in France. A total of 4184 patients with CAD were identified and analyzed. Individual study sample sizes varied from 58 to 1045, and the duration of follow-up ranged from 30 days to 13 years. The included studies provided the plasma level of vWF at different time points after CAD (on admission, 24 h, 48 h). The main characteristics of the studies were shown in Table 1.
Table 1
Characteristics of the studies included in the meta-analysis
Year
Author
Blood Sampling Schedule
Patients
Age, y C/CTL
Sample size C/CTL
Treatment modality
Definition of MACEs
Measuring Methods
Rates of HF C/CTL
Follow up
2016
HAMID
24 h
STEMI
57/53
17/61
PCI, Thrombolytic
All-cause mortality, recurrent nonfatal MI, or HF and the secondary endpoint of early adverse LV remodeling
ELISA
NR
30 days
2015
Liu
Admission
STEMI
58/60
30/102
PCI
Recurrent MI, heart failure readmission, unplanned repeat revascularization, malignant dysrhythmia, stroke, or pulmonary embolism
ELISA
NR
1 year
2013
Leu
Admission
CAD
68/67
33/42
Antiplatelet
CV death, nonfatal AMI, unstable angina, stroke, transient ischemic attack, or peripheral arterial occlusive disorder
ELISA
NR
40 months
2013
Hyseni
Admission
ACS
67.5/ 76.8
293/46
PCI, Antithrombotic
All-cause mortality
ELISA
NR
4 years
2008
Yu
Admission, 12 h, 48 h
ACS
68/64
22/48
Anticoagulation
Death, MI or recurrent MI, and recurrent angina
ELISA
NR
30 days
2008
BOOS
24 h
ACS
69/60.6
42/169
Thrombolysis, PCI
CV death, non-fatal MI, readmission with acute HF and stroke, and CV death separately.
ELISA
28.6 / 7.6
338 days
2006
Fuchs
24 h
ACS
60/57
58/150
PCI, Thrombolysis
Recurrent non-fatal MI (STEMI and NSTE-MI)
Turbidometry
NR
28 months
2006
An
24 h
ACS
NR
21/59
NR
Non-fatal reinfarction, non-fatal heart failure, recurrent angina attacks, drug intensification or emergency revascularization, and cardiac death
ELISA
NR
30 days
2005
Lee
Admission, 48 h
ACS
67/70
24/34
Antiplatelet, Anticoagulation
Death, MI, and refractory angina requiring revascularisation
ELISA
8 /6
30 days
2005
Warlo
24 h
CAD
NR
73/927
Antiplatelet
Unstable angina pectoris, MI, non haemorrhagic stroke and death
NR
NR
2 years
2003
Niessner
Admission
CAD
56/52
103/38
NR
All-cause mortality and MI, revascularization procedures including PTCA with/without coronary stenting and ACBG.
ELISA
NR
13 years
2002
Eikelboom
Admission
ACS
NR
78/407
Anticoagulant, Antiplatelet
CV death, MI, stroke or refractory ischaemia
NR
NR
30 days
2000
Redondo
Admission
CAD
59/57
37/157
NR
Fatal MI, non-fatal MI, percutaneous transluminal coronary angioplasty or CABG.
ELISA
NR
2 years
1999
Moss
Admission
MI
59/47
81/964
NR
Death due to coronary heart disease or recurrent nonfatal MI
ELISA
NR
26 months
1998
Montalescot
Admission, 48 h
CAD
70/70
48/20
Antiplatelet
Death, MI, recurrent angina, or revascularization
ELISA
NR
30 days
Abbreviations: ACBG aorto coronary bypass graft, ACS acute coronary syndromes, AMI acute myocardial infarction, CABG coronary artery bypass grafting, C/CTL case/control group, CV cardiovascular, ELISA enzyme-linked immunosorbent assay, HF heart failure, NR unreported, LV left ventricular, MI myocardial infarction, non-STEMI non-ST-elevated myocardial infarction, PCI percutaneous coronary intervention, PTCA percutaneous transluminal coronary angioplasty, STMI ST-elevated myocardial infarction

Plasma vWF and MACEs

The meta-analyses were conducted according to the time points of vWF examination (on admission, 24 h and 48 h after admission). Consistent with previous reports, we found that the plasma level of vWF is elevated in CAD patients. The result of meta-analyses further to reveal that plasma level of vWF is significantly higher in CAD patients with MACEs than those without MACEs (Fig. 2). The pooled SMD for vWF examined at 24 h and 48 h after admission was 0.55 (95% CI = 0.30–0.80, P < 0.0001) and 0.70 (95% CI = 0.27–1.13, P = 0.001), respectively. However, there was no significant difference in plasma level of vWF examined on admission between the two groups. The pooled SMD was − 0.25 (95% CI = − 0.75-0.06, P = 0.12). In addition, heterogeneity across studies was present.

Quality evaluation

Four studies [3, 4, 14, 15] with 8 NOS scores and eight studies [10, 1622] with 7 NOS scores were considered as good quality. Other studies [13, 23, 24] achieved 6 scores indicating moderate quality. The results of the quality assessment of the included studies were shown in Table 2.
Table 2
Quality assessment of the included studies based on the Newcastle–Ottawa Scale
Author
Study design
Selection
Comparability
Outcome
Total scores
HAMID
Cohort study
3
2
2
7
Liu
Cohort study
3
2
3
8
Leu
Cohort study
3
2
3
8
Hyseni
Cohort study
3
1
2
6
yu
Cohort study
3
2
2
7
BOOS
Cohort study
3
2
3
8
Fuchs
Cohort study
2
2
2
6
An
Cohort study
2
2
2
6
Lee
Cohort study
3
2
3
8
Warlo
Cohort study
2
2
3
7
Niessner
Cohort study
3
2
2
7
Eikelboom
Cohort study
3
2
2
7
Redondo
Cohort study
3
2
2
7
Montalescot
Cohort study
2
2
3
7
Moss
Cohort study
2
2
3
7

Heterogeneity

Subgroup analyses were conducted to evaluate potential sources of heterogeneity. Include studies were subgrouped according to the duration of follow-up. As shown in Table 3, the pooled effects of the meta-analyses were not reversed by the duration of follow-up. However, when subgrouped by the severity of CAD, a significant difference in SMD in vWF plasma levels examined at 24 h after admission was found between the subgroups. The pooled SMD was 0.67 (95% CI = 0.47–0.86, P < 0.00001) for acute coronary syndrome (ACS) and myocardial infarction (MI) patients and was 0.21 (95% CI = − 0.03-0.45, P = 0.09) for stable CAD patients. No significant difference in SMD in vWF plasma levels examined at 24 h after admission was found between patients treated with PCI (SMD = 0.63, 95% CI = 0.42–0.84, P < 0.00001) and those without PCI (SMD = 0.33, 95% CI = 0.11–0.54, P = 0.003). To validate the results from subgroup analyses, we performed meta-regression to determine the source of heterogeneity. The associations between types of coronary disease, high range of follow up sample size, patients treated with PCI and the utilization of antiplatelet or anticoagulation were evaluated. As shown in Table 4, types of coronary disease, high range of follow up sample size, patients treated with PCI, and the utilization of antiplatelet or anticoagulation were not the source of heterogeneity in vWF plasma levels examined on admission (types of coronary disease: P = 0.489; high range of follow up sample size: P = 0.364; patients treated with PCI: P = 0.725; the utilization of antiplatelet: P = 0.527; the utilization of anticoagulation drugs: P = 0.509). However, both high range of follow up sample size and the utilization of antiplatelet or anticoagulation contribute to heterogeneity in vWF plasma levels examined at 24 h after admission (high range of follow up sample size: P = 0.033; the utilization of antiplatelet or anticoagulation: P = 0.007).
Table 3
Subgroup analyses on MACEs
Subgroup
No. of studies
No. of subjects
Meta-analysis
Heterogeneity
MACEs
Non MACEs
SMD
95% CI
P
I2 (%)
P
Follow-up duration
 On admission
< 1 year
4
172
509
−0.57
−1.44-0.3
0.2
93
< 0.00001
≥1 year
6
577
1349
−0.10
−0.39-0.19
0.5
76
0.0007
 24 h
< 1 year
2
38
120
0.76
0.38–1.13
< 0.0001
0
0.47
≥1 year
3
173
1246
0.48
0.17–0.78
0.002
69
0.04
Type of CAD
 On admission
CAD
4
221
257
−0.20
−0.42-0.01
0.06
93
< 0.00001
ACS、MI
6
528
1601
−0.09
−0.22-0.04
0.16
76
0.04
 24 h
CAD
1
73
927
0.21
−0.03-0.45
0.09
  
ACS、MI
4
138
439
0.67
0.47–0.86
< 0.00001
0
0.86
PCI
 On admission
Yes
2
323
148
−0.46
−0.99-0.07
0.09
76
0.04
No
8
426
1710
−0.20
−0.55-0.15
0.27
86
0.00001
 24 h
Yes
3
117
380
0.63
0.42–0.84
< 0.00001
0
1
No
2
94
986
0.33
0.11–0.54
0.003
82
0.02
Abbreviations No number, MI myocardial infarction, SMD standardized mean difference, NR unreported, CI confidence interval, ACS acute coronary syndromes, CAD coronary artery disease, MACEs major adverse cardiac events
Table 4
Source of heterogeneity by meta-regression analysis
Factors
Coefficient
Standard error
P
Follow-up duration
 On admission
0.4594606
0.4769995
0.364
 24 h
0.7399235
0.1979834
0.033
Type of CAD
 On admission
−0.3537444
0.4880535
0.489
 24 h
0.4633034
0.1574912
0.06
PCI
 On admission
−0.2209772
0.6057707
0.725
 24 h
0.3064662
0.2227691
0.263
Regular anticoagulant drugs
 On admission
0.3608304
0.5222992
0.509
 24 h
0.6721909
0.1000211
0.007
Antiplatelet
 On admission
−0.3252659
0.4913701
0.527
 24 h
0.6721909
0.1000211
0.007

Sensitivity analyses

Each study was excluded sequentially to evaluate the influence of an individual study on the results. No study fundamentally changed the combined effects at any time points. Furthermore, the study by Warlo [10] was found to be the source of heterogeneity. When the study was eliminated from analysis, heterogeneity become minimal (examined on 24 h: SMD = 0.67, 95% CI = 0.47–0.86, P < 0.00001, I2 = 0%).

Publication bias

Funnel plot was performed to evaluate the publication bias of literatures. As shown in Fig. 3.

Discussion

This meta-analysis summarizes evidence for association between high-circulation vWF levels and clinically adverse outcomes in patients with CAD. The data on plasma vWF at three time points was included. Results indicated that the plasma vWF was significantly increased in the adverse event group on 24 h and 48 h after primary CAD. However, the level of vWF on admission showed no significant difference between the two groups. Subgroup analyses revealed that the association of increased vWF level with short-term MACEs is stronger. In addition, increased vWF level displays a positive association on MACEs in ACS and MI other than stable CAD. Together, our results suggested that plasma level of vWF is an indicator for the risk of MACEs among patients with CAD.
vWF is mainly synthesized in endothelial cells [25, 26]. Upon endothelial cell injury, vWF is released into the blood circulation. In blood plasma, vWF binds to platelet receptors GPIb-IX-V, GPIIb/IIIa and GPIb to promote thrombosis [27, 28]. The combination of vWF and collagen causes a conformational change in the site of vWF binding to factor VIII, which promotes fibrin agglutination [29, 30]. VWF also mediates platelet adhesion on activated endothelial cells, enhancing thrombus formation even in the absence of endothelial denudation [31]. Several studies have reported that high plasma vWF levels are associated with endothelial dysfunction and inflammation [32, 33], which contribute to the cardiovascular risks. In addition, vWF involves in the pathogenesis of atherosclerosis [34].
MACEs, such as nonfatal myocardial infarction, nonfatal stroke, or target vessel revascularization, are more likely to occur in patients with severe CAD [3]. The increased risk of vWF for MACEs in CAD may be caused by prothrombotic or hypercoagulable conditions, which promote the formation of occlusive thrombus [35]. Both acute myocardial infarction (AMI) and stroke are precipitated by an occlusive thrombus on a preexisting atherosclerotic plaque [36]. VWF promotes thrombus formation by mediating platelet adhesion and aggregation [36]. The inflammatory response involved in the progression of atherosclerotic plaques may also promote an increased secretion of vWF [37]. Therefore, vWF may be considered as a potential clinical biomarker. Previous studies reported that PCI leads to a significant increase of vWF levels compared with the pre-procedural levels [38]. PCI itself causes endothelial cell damage due to mechanical injury by catheter manipulations [39]. In addition, hemodynamic effects of transient myocardial injury during PCI contributes to the increased vWF levels [40].
The prognostic role of vWF in patients with CAD is even more convinced than other acute phase-reactive proteins such as his-CRP and fibrinogen [41]. Studies have shown that elevated early vWF levels in patients with CAD are an independent predictor of adverse events over the next 2 weeks to 1 month, whereas other acute phase response proteins are not [42]. Compared with reactive proteins, vWF is released locally during vascular injury without new synthesis of proteins. Recent case-control studies also demonstrated that the higher plasma vWF or lower ADAMTS13 levels were closely associated with the risk of MI [33, 4345], ischaemic stroke [46]. However, the present study is the first meta analysis that highlights the long-term prognostic value of plasma vWF levels in patients with CAD.
Our study has several advantages. First, vWF is a promised indicator of the clinical outcome in patients with coronary artery disease. The dramatic increase of plasma vWF implies its potential roles in the diagnosis of CAD. Second, all the studies included in this meta-analysis were medium-to-high quality as assessed by Newcastle-Ottawa Quality Assessment Scale. Third, publication bias assessment confirmed the robustness and reliability of our results. Moreover, circulating vWF level was collected on admission, 24 h and 48 h after primary CAD respectively, which provides a variation of vWF with the progression of disease. Our study has several limitations. First, the number of studies of duration on 24 h or 48 h available for meta analyzes was relatively small. Second, the articles included many types of coronary artery disease including acute coronary syndrome, myocardial infarction, angina, which may contributes to clinical heterogeneity. Third, detailed information regarding symptom duration was not available in several studies.

Conclusion

Plasma vWF levels of CAD patients examined at 24 h and 48 h after admission might be an independent prognostic factor for MACE. However, many studies had incomplete information, and more studies with more detailed data and sufficient sample size are necessary to confirm our findings.

Acknowledgements

None.
Not applicable.
Not applicable.

Competing interests

The authors declare that they have no competing interests.
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Metadaten
Titel
Prognostic value of plasma von Willebrand factor levels in major adverse cardiovascular events: a systematic review and meta-analysis
verfasst von
Mengge Fan
Xia Wang
Xun Peng
Shuo Feng
Junyu Zhao
Lin Liao
Yong Zhang
Yinglong Hou
Ju Liu
Publikationsdatum
01.12.2020
Verlag
BioMed Central
Erschienen in
BMC Cardiovascular Disorders / Ausgabe 1/2020
Elektronische ISSN: 1471-2261
DOI
https://doi.org/10.1186/s12872-020-01375-7

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