STEMI
|
F. G. Biccirè 2021[42]
|
STEMI
|
132
|
64
|
19.1
|
R
|
In-hospital
|
Adverse events (cardiogenic shock, resuscitated cardiac arrest and death).
|
Events vs control group: log-transformed D-dimer 6.8±1.1 vs 6.3±0.8, p=0.019
|
Patients experiencing in-hospital adverse events had higher values of D-dimer compared to those free from events.
|
Huang
2020 [43]
|
STEMI
|
1165
|
63.5
|
17
|
R
|
In-hospital
|
CVEs including cardiac death, non-fatal AMI, revascularization, and stroke.
|
≥ 800 vs <800 ng/mL
|
Increased D-dimer level predicted CVEs (OR 8.408, 95% CI 4.065–17.392, P=0.001). D-dimer AUC was 0.840 (95% CI 0.769–0.911). The best cut-off value was 640 ng/mL.
In the subgroup with no-reflow phenomenon, increased D-dimer predicted CVEs (OR 8.114, 95%CI 1.598–41.196, p=0.012)
|
Luo
2020 [44]
|
STEMI
|
400
|
62.5
|
21
|
R
|
12
|
CVEs (all-cause death, TVR, MI, UA, HF, stroke or TIA)
|
Groups (µg/L)
1: 74.0;
2: 146.0;
3: 256.5;
4: 576.0.
|
The incidence of CVEs and all-cause mortality within 30 days (p<0.001), 6 months (p=0.001), and 1 year (p=0.001) after PCI in the highest quartile of the D-dimer groups were higher than those in the other 3 groups.
|
Qi Zhou 2020 [45]
|
STEMI
|
872
|
63.7
|
19.8
|
R
|
29
|
All-cause mortality
|
Groups (µg/mL)
1: ≤0.33;
2: 0.33-0.64;
3: 0.64-1.33;
4: ≥1.33.
|
Higher in-hospital HF (40.2 vs 10.2%, p<0.0001), malignant arrhythmia (14.2 vs 2.3%, p<0.0001), and all-cause mortality (5.9 vs 0%, p<0.0001) rates were observed in Group 4.
84 patients died. Group 4 was a predictor of all-cause mortality (HR: 2.53, 95%CI 1.02–6.26, p=0.045).
|
Lin
2020 [46]
|
STEMI
|
550
|
63.5
|
12.2
|
P
|
16
|
CI-AKI, in-hospital outcomes and long-term mortality and CVEs §
|
D-dimer quartiles (µg/ml):
1: < 0.38;
2: 0.38-0.67;
3: 0.68-1.03;
4: >1.03 .
|
D-dimer > 0.69 µg/ml was an independent risk factor for long-term mortality (HR: 3.41 [95% CI, 1.4–8.03], p=0.005) and CVEs
|
Zhang
2018 [21]
|
STEMI
|
926
|
52.6
|
54.7
|
P
|
In-hospital
|
Mortality
|
383.1 ng/ml ± 264.2
|
Patients without pre-infarction angina with high D-dimer level on admission had significantly increased in-hospital mortality compared to the other patients (p=0.041).
|
Gao
2018 [22]
|
STEMI with T2DM
|
822
|
62.5
|
46.1
|
P
|
100
|
Mortality
|
D-dimer 430.0 ng/ml ± 256.8
|
Patients with high plasma D-dimer level on admission showed a significantly shorter survival time (p<0.001 in the log-rank test).
|
C. H. Hansen 2018 [47]
|
STEMI
|
971
|
61
|
20
|
cross-sectional cohort study
|
55
|
Composite of all-cause mortality, reinfarction, stroke, unscheduled revascularization, or rehospitalization for HF
Secondary outcome was total mortality
|
Median D-dimer
456 ng/mL (IQR 286- 801)
|
Adjusted OR for composite endpoints for D-dimer above 456 ng/mL: 1.179 (95% CI, 0.814-1.706 p=0.384)
Adjusted OR for total mortality for D-dimer above 456 ng/mL: 2.01 (95% CI, 1.06- 3.83; p=0.034)
|
B. Sarli 2015 [25]
|
STEMI
|
266
|
64
|
38
|
P
|
in-hospital
|
CVEs: nonfatal MI, in-stent thrombosis, and in-hospital mortality during hospitalization.
|
D-dimer 686 µg/l±236 vs
418 µg/l±164
p<0.001
|
D-dimer level predicted CVEs (OR: 1.002; 95% CI: 1.000–1.004; p=0.029).
Optimal cut-off value was 544 µg/ml for CVEs.
|
Ayhan Erkol 2014 [15]
|
STEMI
|
569
|
56
|
16
|
A
|
38
|
Mortality and CVEs (death, non-fatal MI, stroke, revascularization, and advanced HF at long-term follow-up)
|
D-dimer overall 0.40 mg/L (0.20–0.87).
|
Univariable HR for long-term mortality 1.56 (95%CI, 1.24–1.95, p<0.001) and CVEs 1.60 (95%CI, 1.37–1.83, p<0.001); not significant association at multivariable analysis.
|
HORIZONS-AMI substudy 2014 [48]
|
STEMI
|
461
|
1st : 55.8
2nd : 61.0
3rd : 70.2
|
20.61
|
R
|
36
|
CVEs (composite of all-cause death, recurrent MI, stroke, or TVR for ischemia.)
|
Tertiles (µg/mL):
1: <0.30 (n=215)
2: 0.30–0.71
(n=161)
3: ≥0.71 (n=85)
|
D-dimer levels ≥0.71 µg/mL on admission predicted CVEs (HR 2.58 [95% CI, 1.44–4.63], p=0.0014), compared to the lowest group.
|
Ozgur Akgul
2013 [49]
|
STEMI
|
453
|
55.6
|
19.65
|
P
|
6
|
Mortality
|
High D-dimer group: >0.72 ug/ml;
Low D-dimer group: lowest two tertiles
(≤0.72 ug/ml).
|
Highest tertile of D-dimer associated with in-hospital CV mortality and 6-month all-cause mortality (7.2 vs. 0.6%, P<0.001 and 13.9 vs. 2%, p<0.001, respectively).
Fatal reinfarction, advanced HF, and CVEs
were more frequent in high D-dimer group (p<0.001).
|
Javier Pineda 2010 [50]
|
AMI
STEMI (85.9%)
|
142
|
41
|
8.45
|
P
|
36
|
Adverse CV events included stroke, ACS, CABG/PCI, hospitalisation due to congestive HF, CV and global mortality.
|
Event 360.0 ng/ml vs no event 297.5 ng/ml, p=0.314
|
No significant differences in D-Dimer levels in the event group.
|
NSTEMI
|
Lu
2021 [28]
|
NSTEMI
|
1357
|
65
|
31.4
|
P
|
12
|
Mortality and CVEs including all-cause death, hospital admission for UA and/or HF, nonfatal recurrent MI and stroke)
|
0.380 µg/mL (0.27-0.65)
Event group (mortality at 1 year): 0.95 (0.50, 2.00)
Control group: 0.37 (0.26, 0.60)
|
HR for D-dimer for 1-year death and CVEs : 2.12 (95%CI, 1.50-2.99, p<0.0001).
|
Hulusi Satilmisoglu 2017 [51]
|
NSTEMI
|
234
|
57.2
|
24.8
|
R
|
14
|
Mortality
|
Non-survivors: 1568±1489 ng/ml
Survivors: 632±995 ng/ml
|
D-dimer correlated with GRACE (r=0.215, p=0.01) and TIMI scores (r=0.253, p<0.001). Higher levels recorded for D-dimer assay (p=0.003) in non-survivors. At multivariate analysis, D-dimer assay no significant predictor of increased mortality risk.
|
A. Tello-Montoliu 2007 [52]
|
NSTEMI
|
358
|
67.4
|
35.8
|
R
|
6
|
Death, new ACS, revascularization, and HF
|
Overall D-dimer level: 340 (211–615) ng/mL
|
Admission D-dimer levels did not predict events [HR: 1.26 (0.79–2.02), p=0.337).
|
AMI
|
Fu 2020 [27]
|
AMI with ESRD
|
113
|
69.2
|
33.6
|
R
|
In-hospital
|
Mortality
|
Mortality: 3.2 mg/L
Survival: 1.1 mg/L
p=0.023
|
D-dimer ≥2.4 mg/L predicted in-hospital mortality (OR 2.771[95% CI, 1.017–8.947], p<0.001).
|
P. Wang 2020 [53]
|
AMI
|
197
|
Male 61.8
Female 74.2
|
20
|
P
|
6
|
All-cause mortality (in- and out-of-hospital deaths) or readmission.
|
Male D-dimer (mg/L) 0.4 vs 1.0 P<0.001
Female D-dimer (mg/L) 0.4 vs 0.6
p=0.015.
|
HR for continuous D-dimer in women 2.029 (95%CI, 1.403-2.933; p<0.001). D-dimer ≥ 0.43 mg/L as an independent predictor of poor prognosis in female AMI patients.
|
Zhang
2020 [54]
|
AMI
|
4495
|
62
|
31.03
|
P
|
24
|
All-cause mortality
|
<145 ng/mL
≥145 ng/mL
|
Elevated D-dimer was associated with mortality (univariable HR 1.20, 95%CI, 1.04-1.37, p=0.01) and in the patients in different groups (HFpEF, HFrEF, non-HF).
|
Yu
2019 [29]
|
AMI
|
5923
|
62.2
|
30.5
|
P
|
In-hospital
|
Mortality
|
D-dimer tertiles (ng/mL):
Low: ≤88; Intermediate: 89–179; High: >179.
|
After multivariable adjustment, D-dimer significantly predicted in-hospital mortality (OR 1.060 [95% CI, 1.026–1.094], p<0.001).
D-dimer levels significantly improved the prognostic performance of GRACE score (C-statistic: p=2.269, p=0.023; IDI: 0.016, p=0.032; NRI: 0.291, p=0.035).
|
REBUS study
2017 [55]
|
AMI
|
412
|
67
|
22.3
|
P
|
24
|
Composite endpoint (all-cause death, MI, congestive HF, or all-cause stroke)
|
Median D-dimer was 677 µg/L at inclusion
|
D-dimer was not associated with the composite endpoint (HR 1.22 [95% CI 0.99–1.51], p=0.06, for one SD increase).
|
M. SMID 2011 [56]
|
AMI
|
135
|
61
|
26
|
P
|
12
|
CV death, recurrent MI, a second PCI or CABG and ischemic stroke.
|
On admission D-dimer: 370 (260–718) ng/mL
|
D-dimer on admission was higher in patients with recurrent thrombotic CV event (medians 550 vs. 365 ng/mL, p=0.06)
OR for D-Dimer against endpoints: 2.9 (95%CI 0.9–8.8)
|
THROMBO study
2000 [57]
|
AMI
|
1045
|
Male 58
Female
62
|
24.3
|
P
|
26
|
Recurrent cardiac events (nonfatal
reinfarction or cardiac death)
|
D-dimer mean in men 508 ±690 ng/ml vs women 564 ± 430 ng/ml
|
D-dimer had prognostic value in men (HR 2.35, 95%CI 1.27-4.35], p=0.006) but not in women (HR 1.58, 95%CI 0.59-4.22, p=0.360).
|
ACS/CAD
|
Chen, 2018 [58]
|
CAD (76.9% AMI)
|
238
|
64.4
|
21.1
|
P
|
24
|
All-cause mortality and CVEs (cardiac death and nonfatal outcomes: recurrent MI, TVR or re-admission due to advanced HF).
|
Mean D-dimer: 0.7±1.1 mg/L.
|
OR for long-term CVEs: 1.526 (95% CI, 1.174-1.983), p=0.002.
D-dimer in multivariate Cox regression of CVEs: 1.420 (1.069-3.014), p=0.046
|
Kosaki 2018 [59]
|
ACS (76.3% AMI)
|
400
|
71.1
|
27.2
|
P
|
27
|
CVEs (all-cause mortality, recurrent MI, unplanned repeat revascularization, surgical revascularization, fatal arrhythmia, admission for HF, and stroke.
|
Patients without CVEs: 1.67 mg/ml ±2.49
Patients with CVEs: 2.11 mg/ml ±2.72
p=0.0003
|
Univariate analysis for D-dimer ≥0.84 mg/ml predicting CVEs: OR 2.49 (95%CI 1.54–4.11), p=0.0001
|
ATLAS ACS-TIMI46 Trial Substudy 2018 [34]
|
ACS (73.9% AMI)
|
1834
|
Placebo 57.9
Rivaroxaban
57.2
|
23.2
|
Post-hoc RCT
|
6
|
Composite endpoint of CV death, myocardial infarction, or stroke
|
Baseline D-dimer (ug/ml) Placebo 0.39(0.24-0.73) vs Rivaroxaban 0.42(0.24-0.78) p=0.370
|
Continuous D-dimer prognostic factor for composite outcome: univariate OR 1.15 (1.03-1.29) p=0.015, multivariate OR 1.13 (1.0-1.28) p=0.048
|
O. R. Mjelva, 2016 [60]
|
CAD (44.3% AMI)
|
871
|
69.5
|
38.7
|
P
|
84
|
All-cause mortality; a combined endpoint consisting of death or recurrent non-fatal MI; recurrent non-fatal MI alone.
|
194 (106–437) µg/L
Median D-dimer in survivors vs non-survivors
were for 153 vs 346 µg/L (p<0.001)
|
D-dimer above 436 µg/L independently predicted mortality (4th vs 1st quartile HR 1.83 [95% CI 1.20–2.78], p=0.005)
Death or MI (4th vs 1st quartile HR 1.38 [95% CI 0.96-1.98], p=0.08)
Recurrent MI (4th vs 1st quartile HR 0.70 [95% CI 0.43-1.15], p=0.16)
|
P. Gong 2016 [61]
|
CAD (29.2% AMI)
|
2209
|
58.58
|
25.9
|
P
|
18
|
Cardiac death, nonfatal MI, recurrence of MI, and stroke
|
Tertiles (µg/mL)
1: <0.23, n=816;
2: 0.23-0.36, n=629;
3: > 0.36, n=764.
|
D-dimer was linked to the severity of CAD (95% CI: 1.20-6.84, p=0.005)
Continuous D-dimer predictor of total outcome (HR= 1.22, 95% CI: 1.09-1.37, p=0.001).
|
Charoensri 2011 [62]
|
ACS (61% AMI)
|
74
|
66
|
54.1
|
R
|
In-hospital
|
CHF, arrhythmias and death
|
D-dimer levels (µg/L)
CHF: 1475 vs No CHF 385; Arrhythmia 5422 vs No arrhythmia 550; Death 5118 vs No death 2550
|
D-dimer levels correlated with complication of ACS (CHF; p<0.001, arrhythmia; p=0.007 and death; p=0.009). D-Dimer was significantly increased with the number of coronary arteries affected (p=0.03).
|
Trygve Brugger-Andersen 2008 [17]
|
STEMI (15%), NSTEMI (29,3%), UA (9,4%), No ACS (46,3%)
|
871
|
69.6
|
39
|
P
|
24
|
All-cause mortality, CVEs (cardiac death or recurrent positive troponin T)
|
Quartiles of D-Dimer (ug/l):
Q1 <106,
Q2 ≥106–191,
Q3 ≥191–438,
Q4 ≥438.
|
In the univariate analysis highest D-dimer quartile predicted all-cause mortality compared with the lowest quartile (Q1) (OR 7.78 [95%IC, 3.95–15.33], p<0.001), but not confirmed at multivariable logistic regression analysis (OR 1.80 [95%IC, 0.81 to 3.97]; p=0.148).
|
D. Prisco 2001 [63]
|
CAD (52,9% AMI)
|
54
|
60
(44–75)
65
(38–81)
|
11.1
|
P
|
18
|
Restenosis
|
D-Dimer before PCI: AMI (group 1) 55 ng/ml vs elective PCI (group 2) 29.0 ng/ml, p<0.001
|
In group 1, D-dimer levels at the end of the procedure were higher in patients with restenosis than in those without (p<0.005). Increased D-Dimer in patients with restenosis (61%) than those without (25%, p<0.05).
|
J. Oldgren 2001 [12]
|
ACS
|
320
|
66
|
--
|
P
|
29
|
Death, MI, and refractory angina during and after anticoagulant treatment in unstable CAD
|
<82 µg/L (N = 105); 82–149 µg/L (N = 106);
> 149 µg/L (N = 103)
|
No difference in clinical outcome at 72h, 7 days and 30 days. During long-term follow-up, there was a relation between higher baseline levels of D-dimer and increased mortality (p=0.003).
|