- Academic Editor
Background: To describe the
characteristics, treatment practices, and clinical outcomes of patients with
ventricular mural thrombus (VMT), with emphasis on the comparison of non-vitamin
K antagonist oral anticoagulants (NOACs) and vitamin K antagonists (VKAs).
Methods: We performed a retrospective cohort study between 2010 and 2019
in Fuwai Hospital, China. Patients with VMT newly treated with either NOACs or
VKAs were included. The primary outcome was the incidence rate of thrombus
resolution at 3 months. Results: We included 196 patients in total—68.9% (n = 135) were treated with VKAs while 31.1% (n = 61) were on NOACs.
Patients with a medical history of heart failure (HF) (odds ratio (OR) 2.10, 95%
confidence interval (CI) 1.17 to 3.77, p = 0.013) and a lower left
ventricular ejection fraction (OR 0.36, 95% CI 0.20 to 0.65, p = 0.001)
had a higher thrombus resolution. At 3 months, a significant difference was
observed in the thrombus resolution between the NOACs and VKAs group with or
without adjustment (OR 2.61, 95% CI 1.39 to 4.89, p = 0.003; adjusted
OR 2.93, 95% CI 1.51 to 5.66, p = 0.001). Further investigation
revealed that in the majority of the subgroups, individuals receiving NOAC
therapy had a superior thrombus resolution than those receiving VKA therapy.
Conclusions: Patients with a medical
history of HF or left ventricular ejection fraction
Patients with heart failure (HF) or myocardial infarction (MI) predispose to ventricular mural thrombus (VMT) formation, experiencing a combination of hypercoagulability, abnormal blood flow, and endothelial injury [1, 2]. The most severe VMT complication, which carries a substantial risk of mortality and morbidity, is the incidence of thromboembolism [3]. Whereas the typical use of Vitamin K antagonists (VKAs) for anticoagulation has been largely embraced in clinics, no particular guidelines are provided for the management of VMT [4, 5]. However, due to the drawbacks of warfarin’s late onset, multiple food or drug interactions, and restricted therapeutic window, treatment compliance among patients is relatively low, which increases the likelihood of bleeding or embolism events [6]. Therefore, non-vitamin K antagonist oral anticoagulants (NOACs) are increasingly used as off-label anticoagulant treatments in patients with VMT. From MI and stroke guidelines, the usage of NOACs for the treatment of left VMT was uncertain [7, 8]. Apixaban or rivaroxaban demonstrated a better or comparable thrombus resolution than warfarin in patients with left VMT, and the risks of major cardiovascular adverse events were comparable, according to two prospective multicenter randomized trials [9, 10]. In the No-LVT trial, for example, rivaroxaban was non-inferior to warfarin in terms of thrombus resolution (71.79% vs 47.50%) [10]. Several retrospective studies and meta-analyses also reported that NOACs were non-inferior even superior to warfarin in thrombus resolution while the risk of bleeding or stroke had not reached consensus [11, 12, 13, 14]. Therefore, we aimed to evaluate the characteristics and clinical outcomes of patients with VMT treated with various oral anticoagulants, as well as to explore potential factors related to thrombus resolution.
This retrospective cohort study was conducted from July 2010 through October 2019 using electronic medical records of Fuwai Hospital, National Center of Cardiovascular Diseases in China, which was registered in ClinicalTrials.gov: NCT 05006677. The inclusion criteria were: (1) Aged over eighteen years, regardless of sex or occupation; (2) Patients were given a new prescription for a NOAC or a VKA for less than 1 month; (3) VMT was identified newly within 3 months given that mechanized or calcified thrombus was less likely to resolve. Patients who switched medications or discontinued NOACs or VKAs over the course of treatment were excluded, as evidenced by objective data such as prescriptions from cardiologists and oral reports during the interviews. All medications according to the recommendation of guidelines for the treatment of underlying diseases were encouraged.
The diagnosis of VMT was confirmed by transthoracic echocardiography, computer tomography (CT), or cardiac magnetic resonance (CMR) imaging. X.Q. and other experts would analyze the image and make a determination. VMT was defined as an abnormal echo mass in the ventricular cavity whose margin was distinct from the ventricular endocardium [15]. Multiple sections confirmed the existence of the thrombus.
The primary outcome was the rate of thrombus resolution determined by repeat imaging within 3 months, and the secondary outcomes included thromboembolism events, bleeding, and all-cause death within 3-month follow-up. We confirmed the resolved thrombus by screening the image data in the electronic system and conducted a survey by phone or media contact with patients to obtain long-term outcomes. Thromboembolism events were defined as the combination of an acute embolism in a coronary or peripheral artery, ischemic stroke, and transient ischemic attack. Bleeding events were classified as major bleeding as defined by the International Society on Thrombosis and Haemostasis [16], clinically relevant non-major bleeding [17], and minor bleeding that failed to comply with the criteria for the abovementioned two categories of bleeding.
Data regarding patient demographics (age, gender), clinical characteristics (presenting diagnosis, medical history, and laboratory testing), imaging parameters (left ventricular ejection fraction (LVEF), thrombi features), treatment (type of anticoagulation and combined medications), and clinical outcomes (thrombus resolution, thromboembolism events, bleeding, and all-cause death) were collected. To assure coherence, two colleagues (Q.Y. and X.Q.) separately extracted the data and compared the results. A third researcher then addressed any inconsistencies. Data were obtained from electronic medical records and oral consent was acquired at the time of the telephone interview.
Normally distributed continuous data were presented as mean and standard
deviation (SD) while non-normally distributed continuous data by the median and
interquartile range (IQR), and the dichotomous data were computed using frequency
and percentage [18]. Analysis of variance was used to compare normally continuous
variables and the Kruskal-Wallis H test was to compare non-normally distributed
continuous variables. When comparing categorical data, the Fisher’s exact test
and Pearson chi-squared test (when more than 20% of cells have expected
frequencies
We identified 610 patients with VMT on the whole between July 2010 and October
2019 throughout this center. There were 78 patients that received thrombectomy
therapy or ventricular aneurysm resection while 32 patients with heart
transplantation within a 6-week follow-up. Additionally, we disqualified 14
patients with a long history of VMT (more than 3 months) and 9 patients who were
not adolescents. Furthermore, 116 patients without oral anticoagulants and 165
patients lost to imaging follow-up were excluded (Fig. 1). Consequently, we
enrolled 196 eligible patients: of them, 68.9% (n = 135) received VKAs while
31.1% (n = 61) received NOACs (Table 1). Both groups were predominately made up
of men. In patients with NOACs, most of them were given rivaroxaban (n = 58,
95.1%) and two patients were administered dabigatran while one patient was given
apixaban. Patients receiving NOACs were generally younger than those receiving
VKAs. More than half of enrolled patients were diagnosed with ‘others’ diseases—hypertrophic cardiomyopathy, peripartum cardiomyopathy, myocarditis,
arrhythmogenic right ventricular cardiomyopathy, hypertensive heart disease,
noncompaction of ventricular myocardium, and other cardiovascular diseases, and
approximately 20% of patients had ischemic cardiomyopathy (ICM) and dilated
cardiomyopathy (DCM) respectively, while 55.8% of the patients with ICM
experienced an acute MI with or without ventricular aneurysm. The majority of
patients in our study were first diagnosed with VMT using routine
echocardiography (n = 178, 90.8%), whereas the remaining patients with minor
thrombus or apex thrombus were found by contrast echocardiography (n = 2, 1.0%),
CT with a delayed phase scan (n = 10, 6.1%), and late gadolinium enhancement CMR
imaging (n = 6, 3.1%). The median baseline LVEF was 31.5% and 83 out of 196
patients (42.3%) had LVEF
Flow diagram to show the inclusion and exclusion criteria. 610 patients were found with ventricular mural thrombus and 196 were included in our analysis—61 received NOACs and 135 received VKAs. NOACs, non-vitamin K antagonist oral anticoagulants; VKAs, vitamin K antagonists.
Total | NOACs | VKAs | p value | ||
---|---|---|---|---|---|
(N = 196) | (N = 61) | (N = 135) | |||
Age, y [Median (IQR)] | 49.0 (34.0, 58.0) | 41.0 (27.0, 56.0) | 50.0 (37.0, 59.0) | 0.040 | |
Male | 151 (77.0) | 43 (70.5) | 108 (80.0) | 0.200 | |
BMI, kg/m |
24.4 |
24.6 |
24.3 |
0.539 | |
Presenting diagnosis | 0.150 | ||||
ICM | 43 (21.9) | 10 (16.4) | 33 (24.4) | - | |
DCM | 39 (19.9) | 9 (14.8) | 30 (22.2) | - | |
Others |
114 (58.2) | 42 (68.9) | 72 (53.3) | - | |
Prior medical history | |||||
Coronary artery diseases | 87 (44.4) | 21 (34.4) | 66 (48.9) | 0.083 | |
Atrial fibrillation | 20 (10.2) | 4 (6.6) | 16 (11.9) | 0.316 | |
Heart failure | 118 (60.2) | 37 (60.7) | 81 (60.0) | 1.000 | |
Hypertension | 56 (28.6) | 17 (27.9) | 39 (28.9) | 1.000 | |
Diabetes | 31 (15.8) | 7 (11.5) | 24 (17.8) | 0.298 | |
Hyperlipidemia | 81 (41.3) | 20 (32.8) | 61 (45.2) | 0.140 | |
Embolism | 48 (24.5) | 17 (27.9) | 31 (23.0) | 0.575 | |
Chronic kidney diseases | 9 (4.6) | 1 (1.6) | 8 (5.9) | 0.278 | |
Gastrointestinal bleeding | 5 (2.6) | 1 (1.6) | 4 (3.0) | 1.000 | |
Current smoker | 102 (52.0) | 30 (49.2) | 72 (53.3) | 0.701 | |
Excessive alcohol consumption |
45 (23.0) | 17 (27.9) | 28 (20.7) | 0.360 | |
Location of ventricular thrombi | 0.002 | ||||
Left ventricular | 169 (86.2) | 45 (73.8) | 124 (91.9) | - | |
Right ventricular | 19 (9.7) | 10 (16.4) | 9 (6.7) | - | |
Biventricular | 8 (4.1) | 6 (9.8) | 2 (1.5) | - | |
Number of ventricular thrombi | 0.445 | ||||
1 | 176 (89.8) | 53 (86.9) | 123 (91.1) | - | |
20 (10.2) | 8 (13.1) | 12 (8.9) | - | ||
Size of ventricular thrombi, mm [Median (IQR)] | |||||
Diameter | 22.0(14.5, 30.0) | 22.0 (16.0, 29.5) | 22.0 (14.0, 30.2) | 0.776 | |
Thickness | 15.0 (11.0, 21.0) | 16.0 (13.0, 22.0) | 15.0 (10.0, 21.0) | 0.305 | |
Width | 26.0 (11.5, 44.5) | 17.5 (13.2, 21.7) | 42.0 (13.0, 47.0) | 0.245 | |
LVEF, % [Median (IQR)] | 31.5 (25.0, 42.2) | 31.0 (25.0, 45.0) | 32.0 (24.0, 41.5) | 0.410 | |
D-Dimer, ug/mL [Median (IQR)] | 1.35 (0.46, 2.62) | 1.39 (0.47, 2.74) | 1.29 (0.47, 2.61) | 0.793 | |
Combined medications | |||||
Parenteral anticoagulants | 123 (62.8) | 25 (41.0) | 98 (72.6) | 0.001 | |
Antiplatelet therapy | 66 (33.7) | 16 (26.2) | 50 (37.0) | 0.187 |
A total of 40 patients (65.5%) in NOACs use were successful in resolving their thrombi at 3 months as opposed to 57 patients (42.2%) in the VKAs group (p = 0.004). The median time of thrombus resolved or unresolved was non-significant between the two anticoagulants (p = 0.921, p = 0.985, respectively; Table 2). When assessing the relation between thrombus resolution rates and the baseline features of patients, we conducted a Logistic regression. In the univariable analysis, patients who received NOACs had a greater risk to have the thrombus resolved than those who were in the VKAs group (OR 2.61, 95% CI 1.39 to 4.89, p = 0.003). The medical history of HF in patients with VMT was associated with a close to two-fold increased resolution rate compared to VMT patients without prior HF (OR 2.10, 95% CI 1.17 to 3.77, p = 0.013). Likewise, patients with a lower LVEF had a higher likelihood of achieving thrombus resolution (OR 0.36, 95% CI 0.20 to 0.65, p = 0.001) (Table 3).
Total | NOACs | VKAs | p value* | ||
---|---|---|---|---|---|
(N = 196) | (N = 61) | (N = 135) | |||
Primary outcome | |||||
Thrombus resolution | 97 (49.5) | 40 (65.6) | 57 (42.2) | 0.004 | |
Time of thrombus resolved, d [Median (IQR)] | 41 (30, 60) | 40 (33, 51) | 43 (29, 67) | 0.921 | |
Time of thrombus unresolved, d [Median (IQR)] | 48 (32, 58) | 41 (30, 60) | 48 (33, 57) | 0.985 | |
Secondary outcome | |||||
Bleeding | 10 (5.1) | 1 (1.6) | 9 (6.7) | 0.258 | |
Thromboembolism | 1 (0.5) | 0 (0.0) | 1 (0.7) | 1.000 | |
All-cause death | 3 (1.5) | 0 (0.0) | 3 (2.2) | 0.586 |
*Calculated by Fisher’s exact test.
Abbreviations: VMT, ventricular mural thrombus; IQR, interquartile range; NOACs, non-vitamin K antagonist oral anticoagulants; VKAs, vitamin K antagonists.
Variable | OR (95% CI) | p value | |
---|---|---|---|
Treatments | |||
NOACs vs VKAs | 2.61 (1.39, 4.89) | 0.003 | |
Demography | |||
Age | 0.66 (0.38, 1.16) | 0.152 | |
Male (vs Female) | 1.03 (0.53, 2.01) | 0.628 | |
BMI | 1.28 (0.73, 2.24) | 0.392 | |
Presenting diagnosis | 0.206 | ||
DCM (vs ICM) | 0.72 (0.30, 1.73) | 0.462 | |
Others |
1.37 (0.68, 2.77) | 0.379 | |
Medical history | |||
Coronary artery diseases | 0.66 (0.37, 1.16) | 0.147 | |
Atrial fibrillation | 1.02 (0.41, 2.58) | 0.962 | |
Heart failure | 2.10 (1.17, 3.77) | 0.013 | |
Hypertension | 0.84 (0.45, 1.57) | 0.588 | |
Diabetes | 0.95 (0.44, 2.04) | 0.894 | |
Hyperlipidemia | 0.84 (0.47, 1.48) | 0.545 | |
Embolism | 1.03 (0.54, 1.97) | 0.935 | |
Chronic kidney diseases | 0.81 (0.21, 3.11) | 0.757 | |
Gastrointestinal bleeding | 0.25 (0.03, 2.25) | 0.215 | |
Current smoker | 0.82 (0.47, 1.43) | 0.478 | |
Excessive alcohol consumption |
0.77 (0.39, 1.50) | 0.441 | |
Location of ventricular thrombus | 0.617 | ||
Right ventricular (vs left ventricular) | 0.74 (0.28, 1.92) | 0.531 | |
Biventricular (vs left ventricular) | 1.69 (0.39, 7.28) | 0.484 | |
Number of ventricular thrombus | |||
1.28 (0.51, 3.24) | 0.604 | ||
LVEF | 0.36 (0.20, 0.65) | 0.001 | |
D-Dimer | 0.83 (0.42, 1.65) | 0.601 | |
Combined medications | |||
Parenteral anticoagulants | 0.71 (0.40, 1.27) | 0.253 | |
Antiplatelet therapy | 0.65 (0.36, 1.18) | 0.160 |
Abbreviations: NOACs, non-vitamin K antagonist oral anticoagulants; VKAs, vitamin K antagonists; BMI, body mass index; ICM, ischemic cardiomyopathy; DCM, dilated cardiomyopathy; LVEF, left ventricular ejection fraction; OR, odds ratio, CI, confidence interval.
And adjusting variables that were identified in the univariate analysis to be statistically significant, NOACs remained a favorable resolution of thrombus versus VKAs (OR 2.93, 95% CI 1.51 to 5.66, p = 0.001). In multivariable Logistic regression, patients with LVEF under 30% experienced a greater thrombus resolution than those with LVEF over 30% (OR 0.37, 95% CI 0.18 to 0.76, p = 0.006) (Fig. 2).
Forest plot of multivariable analysis based on the statistically significant predictors in the univariable analysis. Error bars represent 95% CI. NOACs, non-vitamin K antagonist oral anticoagulants; VKAs, vitamin K antagonists; OR, odds ratio; CI, confidence interval; LVEF, left ventricular ejection fraction.
Within a 3-month follow-up, a total of ten (5.1%) patients had minor bleeding events—one patient (1.6%) was in the NOACs group while nine (6.7%) patients were in the VKAs group (Table 2). No significant difference was observed in the bleeding rate among NOACs and VKAs group (p = 0.258). In the VKAs group, there was one patient (0.7%) who experienced lower extremity deep vein thrombosis. As a consequence of serious multiple organ dysfunction, progressive HF decompensation, or catastrophic infection illnesses, three patients (2.2%) died during their initial hospitalization while no patients died in the NOACs group.
To determine how confounding factors influenced thrombus resolution, two models were taken into account. In the crude model, the result echoed that of univariable analysis (OR 2.61 95% CI 1.39 to 4.89, p = 0.003). The statistical significance was maintained in model 2 when the medical history of HF and LVEF levels were included (OR 2.93, 95% CI 1.51 to 5.66, p = 0.001) (Fig. 3).
Forest plot of subgroup analysis. The following adjustments were performed in regression models: model 1, crude model; model 2: model 1 + history of heart failure and LVEF. Error bars represent 95% CI. NOACs, non-vitamin K antagonist oral anticoagulants; VKAs, vitamin K antagonists; OR, odds ratio; CI, confidence interval; BMI, body mass index; ICM, ischemic cardiomyopathy; DCM, dilated cardiomyopathy; Others, included hypertrophic cardiomyopathy, peripartum cardiomyopathy, myocarditis, arrhythmogenic right ventricular cardiomyopathy, hypertensive heart disease, and noncompaction of ventricular myocardium; LVEF, left ventricular ejection fraction.
According to the subgroup study, patients over 50 years old benefit more from
NOAC anticoagulation than those using VKAs (OR 3.01, 95% CI 1.16 to 7.78,
p = 0.023), and the interaction was not significant not only across age
groups (p = 0.171) but also between age and anticoagulation treatment
(p = 0.627). Compared with VKAs, males using NOACs might have superior
resolution compared to VKAs (OR 2.42, 95% CI 1.16 to 5.04, p = 0.018),
whereas no significance was observed in females (OR 3.40, 95% CI 0.97 to 11.91,
p = 0.056). Patients who had a medical history of HF experienced a
greater efficacy in NOACs use than VKAs (OR 4.10, 95% CI 1.67 to 10.05,
p = 0.002), while those without a history of coronary artery diseases
(CAD) had a similar outcome (OR 2.86, 95% CI 1.25 to 6.53, p = 0.013).
Moreover, we conducted an additional subgroup analysis of patients with left VMT
alone and there was no difference in the baseline characteristics between the
NOACs group and the VKAs group. And the outcome in univariate and multivariate
logistic regression remained consistent with that of all VMT patients (Supplementary Table 3).
Patients with left VMT alone in the NOACs group experienced a higher resolution
of thrombus than those in the VKAs group (OR
3.41, 95% CI 1.63 to 7.12, p = 0.001; adjusted OR 3.79, 95% CI 1.76 to
8.19, p
In addition, using cumulative event probability curves obtained from
Kaplan-Meier estimates at one-year follow-up, we evaluated the rate of thrombus
resolution between the NOACs group and the VKAs group, and the results indicated
that patients receiving NOACs had higher rates of resolution than those receiving
VKAs (Log-rank test, p = 0.0041; Fig. 4). The same analysis was
conducted for patients with different levels of LVEF at baseline, which showed
that patients in the group with lower LVEF had a higher rate of thrombus
resolution than those with LVEF over 30% during the follow-up period (Log-rank
test, p = 0.0015; Supplementary Fig. 1). And considering the
LVEF as a continuous variable, we performed a restricted cubic spline curve which
showed a linear relationship between the LVEF level and the thrombus resolution
(p for linearity
Cumulative event probability curve for ventricular mural thrombus resolution of NOACs and VKAs within one-year follow-up. Kaplan-Meier method was used to calculate the cumulative event probability of two oral anticoagulants. Log-rank test was used to compare the cumulative event among groups (p = 0.0041). NOACs, non-vitamin K antagonist oral anticoagulants; VKAs, vitamin K antagonists.
In this retrospective observational study, NOACs were shown to be significantly
associated with greater resolution of VMT than VKAs in the early period of
observation, with or without adjustment, and patients with a medical history of
HF or LVEF
In aspects of our key findings, patients diagnosed with VMT might benefit better from NOACs as a therapy option than of VKAs, which were in line with multiple additional studies [19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35] (Supplementary Table 4). Albabtain et al. 2021 [22] found that in the warfarin group 68.6% of patients, and in the rivaroxaban group 71.4 % of patients, respectively, obtained thrombus resolution. The median time to resolution was shorter in the rivaroxaban group of patients, which was comparable to our study [22]. Several studies found that NOACs and VKAs had comparable efficacy and safety in the treatment of patients with left VMT [21, 22, 23, 24, 25, 26]. Willeford et al. [21] analyzed that in either the unadjusted or the adjusted analysis, there was no noticeable difference between the NOACs and VKAs groups for the effectiveness or safety outcome. Herald et al. 2022 [36] supported that the NOACs treatment for left VMT could be as safe and effective as the warfarin treatment in the diverse population-based cohort of patients. The study especially focused on the safety outcome and it indicated that NOACs use was associated with a lower risk of bleeding without adding risks of embolism events [36]. Another meta-analysis also reported that patients with NOACs were less likely to experience major bleeding [37]. Chen et al. [38] included a total of thirteen retrospective studies with 2467 patients (NOACs = 489 vs warfarin = 1539), in terms of stroke events or clinically related bleeding events, NOACs had a lower risk than warfarin though no significant difference was observed in the resolution rate or bleeding events. And whether NOACs brought benefits or hazards in stroke or systemic embolism events was unknown. One study in 2021 included eighty-seven patients with left VMT, in the univariate logistic regression analysis, the NOACs group had a lower incidence of 66% in stroke or systemic embolism than the VKAs groups when antiplatelets were controlled [39]. Otherwise, a meta-analysis provided conflicting results that the incidence of systemic embolism in the NOACs group was 1.86 times higher than that in the VKAs group [40]. Also, Robinson et al. [41] discovered that the rate of systemic embolism was 2.71 times higher in the NOACs group than in the VKAs group.
Anticoagulants including NOACs and VKAs, which are extensively prescribed for
the prevention and treatment of venous thromboembolism or stroke events,
primarily act on clotting factors to prevent blood coagulation and block
thrombosis [42, 43]. From the study, most of the baseline characteristics,
including demographics, presenting diagnosis, medical history, thrombi features,
and agent combinations, showed no correlation with the thrombus resolution.
Interestingly, the rate of VMT resolution was found to be correlated with both
the history of HF and lower baseline LVEF values (either being the continuous
variable or the binary variable according to a cutoff of
Considering the influence of these factors related to thrombus resolution, we
performed subgroup analyses of different models and other potential factors.
Patients treated with NOACs had a resolution rate that was over twice as high as
those who administered VKAs in these models which created potential confounders.
And in patients with a medical history of HF, NOACs showed a better rate of
resolution than VKAs. Furthermore, our study indicated that patients
First, given the observational study’s intrinsic limits and the small sample size, the externality of the result is further constrained. Additionally, it is difficult to determine the adherence of patients prescribed warfarin due to restrictions to INR measurements, and the net outcome of warfarin is still unclear in the current study. Second, we mostly relied on transthoracic echocardiography, which may have missed minor thrombi during the follow-up period since CMR or contrast echocardiography is the gold standard for detecting VMT.
More randomized controlled trials are required to assess the efficacy and hard outcomes in the comparison of NOACs versus VKAs and we hope those upcoming results from large trials will provide cheerful and reliable evidence on this topic (NCT03764241 [50], NCT 03415386, NCT03232398, NCT02982590, NCT04970576, ChiCTR2100048098). The evidence-based VMT guideline is critical for regulating clinician practice and guaranteeing consistency of treatment across specific doctors.
In this single-center retrospective cohort study, patients with a medical
history of HF or LVEF
VMT, ventricular mural thrombus; NOACs, non-vitamin K antagonist oral anticoagulants; VKAs, vitamin K antagonists; BMI, body mass index; SD, standard deviation; IQR, interquartile range; OR, odds ratio; CT, computer tomography; CMR, cardiac magnetic resonance; HF, heart failure; MI, myocardial infarction; CAD, coronary artery diseases; ICM, ischemic cardiomyopathy; DCM, dilated cardiomyopathy; LVEF, left ventricular ejection fraction; INR, international normalized ratio; ISTH, International Society on Thrombosis and Haemostasis.
The data used to support the findings of this study are available from the corresponding author upon request.
QY and XQ extracted the data, and XL contributed to data analysis. QY and DG drafted the manuscript, XL performed the statistical analysis. YL reviewed and corrected the manuscript. QY, XQ and YL discussed the results and contributed to the final manuscript. All authors read and approved the manuscript.
The study protocol was approved by the local ethics committee (Ethics Committee of Fuwai Hospital, Approval No.: 20221757, Trial No.: 2022-ZX025) and oral consent was obtained at the time of the telephone interview.
We are indebted to all authors of the study we have included in our paper.
This research received no external funding.
The authors declare no conflict of interest.
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