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Factors predicting resolution of left ventricular thrombus in different time windows after myocardial infarction

BMC Cardiovascular Disorders volume 24, Article number: 278 (2024) Cite this article

Abstract

Background

Left ventricular thrombus (LVT) is a serious complication after myocardial infarction. However, due to its asymptomatic nature, early detection is challenging. We aimed to explore the differences in clinical correlates of LVT found in acute to subacute and chronic phases of myocardial infarction.

Methods

We collected data from 153 patients who were diagnosed with LVT after myocardial infarction at the Affiliated Hospital of Qingdao University from January 2013 to December 2022. Baseline information, inflammatory markers, transthoracic echocardiograph (TTE) data and other clinical correlates were collected. Patients were categorized into acute to subacute phase group (< 30 days) and chronic phase group (30 days and after) according to the time at which echocardiograph was performed. The resolution of thrombus within 90 days is regarded as the primary endpoint event. We fitted logistic regression models to relating clinical correlates with phase-specific thrombus resolution.

Results

For acute to subacute phase thrombus patients: C-reactive protein levels (OR: 0.95, 95% CI: 0.918–0.983, p = 0.003) were significantly associated with thrombus resolution. For chronic phase thrombus patients: anticoagulant treatment was associated with 5.717-fold odds of thrombus resolution (OR: 5.717, 95% CI: 1.543–21.18, p = 0.009).

Conclusions

Higher levels of CRP were associated with lower likelihood of LVT resolution in acute phase myocardial infarction; Anticoagulant therapy is still needed for thrombus in the chronic stage of myocardial infarction.

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Introduction

Left ventricular thrombus (LVT) refers to the presence of blood clots in the left ventricle. The formation of LVT after myocardial infarction is related to Virchow’s triad as the formation of other thrombus, including vascular intima injury [1], slow blood flow [2] and a hypercoagulable state [3]. Although the incidence of LVT decreased annually [4], it is still a nonnegligible complication after acute myocardial infarction (AMI) due to the serious consequences such as stroke and deformation of heart valves. Many previous studies have confirmed that anterior myocardial infarction, lower left ventricular ejection fraction (LVEF) [5, 6], and more severe inflammatory reaction [7] are related to the formation of LVT after AMI. Previous studies have shown that the most LVTs after AMI do not appear immediately after AMI, but occur after one week [8, 9]. The current timeframe available for diagnosis is often insufficient compared to the hospitalization time required for most patients after experiencing an AMI. This limitation hinders our ability to promptly detect and treat LVT cases, leading to an increase in embolic events and the formation of older, more challenging-to-resolve thrombus. The treatment of LVT after AMI is not fully clear, with previous studies yielding inconsistent conclusions regarding the use of anticoagulant drugs [10,11,12,13,14]. Given this, our aim is to investigate the differences in clinical correlates of phase-specific resolution of LVT after AMI.

Methods

Study design and population

This is a single-center retrospective study, authorized by the local institutional review board (Approval No.: QYFY WZLL 27,959). Diagnosis of AMI is made in patients who manifest a minimum of two of the following criteria: symptoms indicative of chest pain, elevated troponin (Tn) levels, and distinctive electrocardiogram (ECG) findings [15].

LVT detected through non-contrast transthoracic echocardiography (TTE) within the initial 30 days following AMI are assigned to the acute to subacute phase group (ALVT), whereas those detected beyond the 30 days after AMI are assigned to the chronic phase group (CLVT). A total of 1510 patients with documented occurrences of “thrombus” in their echocardiography reports were retrospectively assembled for this study from January 2013 to December 2022, drawing data from the Electronic Health Records (EHR) of the Qingdao University Affiliated Hospital. The following patients were excluded: (1) Poor image quality (n = 16); (2) Atrial and right ventricular thrombus (n = 1134); (3) Patients with non-acute myocardial infarction (n = 23); (4) Inability to accurately determine time to resolution(n = 118); (5) Patients with missing variables required for the study (n = 66). Ultimately, a cohort of 153 eligible patients presenting LVT was constituted, comprising 63 ALVT and 90 CLVT. They were dichotomized based on whether the thrombus resolved within 90 days post-detection, categorized into the early resolution group and the late resolution (including non-resolution) group. (Fig. 1) Their relevant baseline characteristics, biochemical and examination data, treatment, and outcomes were collected.

Fig. 1
figure 1

Sampling strategy

Full size image

Baseline and data collection

The resolution time of LVT was obtained through follow-up using echocardiography. LVEF, ventricular aneurysm, LVEDd, LVEDs and Fractional shortening was obtained by the initial echocardiographic data at the time of first LVT detection. Routine laboratory examinations when upon admission, including blood routine, renal function, coagulation function, and blood lipid analysis, were collected. Neutrophil-to-Lymphocyte Ratio (NLR) and Platelet-to-Lymphocyte Ratio (PLR) are obtained by dividing neutrophil count and platelet count by absolute lymphocyte count respectively, and lymphocyte-to- monocyte Ratio (LMR) is obtained by dividing lymphocyte count by Monocyte count. The use of beta-blockers, Angiotensin-converting enzyme inhibitor (ACEI), angiotensin receptor blockers (ARB), Angiotensin receptor-neprilysin inhibitors (ARNI), dual antiplatelet therapy, and anticoagulants was defined as the medication usage after the detection of LVT. Age, medical history, and other data are obtained from EHR. Patients with diagnosed LVT underwent regular echocardiograms every 3–6 months to monitor the resolution of the thrombus.

Study outcomes

The end point events included early resolution, late resolution (including non-resolution) of LVT. Early resolution was defined as the disappearance of LVT detected in TTE within 90 days after the initial detection. If LVT persisted in TTE 90 days later, it was defined as late resolution.

Statistical analysis

Continuous variables following a normal distribution were presented as mean ± standard deviation, while non-normally distributed continuous variables were represented by median and interquartile range. Analysis of variance (ANOVA) was used for continuously distributed variables that followed a normal distribution, the Mann-Whitney U test was used for those with non-normal distributions, and the chi-square test was used for categorical variables. We constructed a univariate logistic regression to detect impact of variables on thrombus resolution, including thrombus period, gender, age, smoking, diabetes, anticoagulation, LVEF, ventricular aneurysm, neutrophil count, lymphocyte ratio, CRP, triglycerides, low-density lipoprotein, and high-density lipoprotein. The above variables were then incorporated into the multivariate logistic regression model. Univariate logistic regression models and multivariate regression models were fitted separately for ALVT and CLVT. All analyses were performed using SPSS version 26.0 (SPSS Inc., Chicago, IL, USA). A two-sided significance level of 0.05 was used for all hypothesis tests.

Results

Comparison of LVT resolution and non-resolution at different stages

In this study, 153 patients with LVT were enrolled, with 63 (41.2%) having ALVT. Patients with ALVT have a higher probability of regression (p = 0.001), more use of PCI (p = 0.011) and anticoagulation (p = 0.001), Higher CRP (p = 0.001), higher fibrinogen (p = 0.003) and higher NT-proBNP (p = 0.012) than when CLVT patients were identified (Table 1). Among these patients, patients who had LVT resolution within 90 days compared with after 90 days had more anticoagulant medication (p = 0.047), triglyceride levels (p = 0.030), total bilirubin (p = 0.007), and indirect bilirubin (p = 0.022). Conversely, there were no statistically significant differences observed with respect to age, gender, medical history, medication history, or other laboratory indicators. (Table S1)

Table 1 AMI patients complicated by ALVT vs. CLVT
Full size table

However, when patients are stratified according to the time of thrombus discovery, the statistical results differ from not discriminating time. Among the 63 cases of ALVT, 44 patients (69.8%) demonstrated thrombus resolution within 90 days. Variance analysis indicated no significant associations with age, gender, or medical history, while a significant relationship was observed with lower levels of inflammation (neutrophil count: 7.94 ± 3.94 vs. 10.12 ± 3.41, p = 0.049; lymphocyte ratio: 20.71 ± 11.92 vs. 13.37 ± 6.35, p = 0.020; C-reactive protein: 45.78 ± 43.6 vs. 107.54 ± 98.28, p = 0.015) (Table S2). Among the 90 cases of CLVT, only 33 cases (36.7%) exhibited thrombus resolution within 90 days. In the analysis of variance, male (p = 0.049), use of anticoagulant drugs (p = 0.001), and elevated creatinine levels (106.09 ± 52.1 vs. 88.56 ± 26.59, p = 0.045) were beneficial for thrombus regression. Additionally, younger age (64.58 ± 12.69 vs. 68.6 ± 9.23, p = 0.087) and lower triglyceride levels (1.43 ± 0.66 vs. 1.18 ± 0.57, p = 0.071) appeared to have some relevance to earlier thrombus resolution (Table S3).

Predictors of LVT resolution in different discovery stage

In logistic regression that does not distinguish between thrombotic periods, we found that CRP and triglycerides are important factors affecting thrombus regression, and ALVT resolves more easily than CLVT (Table 2). Univariate logistic regression analyses were conducted separately for the ALVT and CLVT groups. In patients with ALVT, it was observed that neutrophil count (OR:0.86, 95% CI:0.75–1.003, P = 0.054), lymphocyte ratio (OR:1.081, 95%CI: 1.01–1.058, p = 0.026), and CRP (OR:0.986, 95%CI: 0.974–0.999, p = 0.035) were associated with thrombus resolution. (Table 3) Among CLVT patients, gender (OR:0.28, 95%CI: 0.074–1.054, p = 0.06), age (OR: 0.96, 95%CI: 0.92–1.006, p = 0.09), and the use of anticoagulants (OR: 5.76, 95%CI: 2.06–16.10, p = 0.001) were associated with thrombus resolution. However, after adjusting for covariates, only C-reactive protein remained as an independent predictor of thrombus resolution in ALVT (OR = 0.95; 95% CI 0.918–0.983; p = 0.003). In the multivariate logistic regression analysis, no statistically significant predictors for the resolution of CLVT were identified (Table 4).

Table 2 Univariate and multivariate Logistic regression of predictors of thrombus resolution in AMI patients with LVT
Full size table
Table 3 Univariate and multivariate Logistic regression of predictors of thrombus resolution in AMI patients with ALVT
Full size table
Table 4 Univariate and multivariate logistic regression of predictors of thrombus resolution in AMI patients with CLVT
Full size table

Regarding treatment, the majority of ALVT patients (62/63) received dual antiplatelet therapy with anticoagulation following AMI. Among CLVT patients, 60% (54/90) underwent anticoagulant treatment, while 36 out of 90 did not receive any anticoagulant medication, and 54 out of 90 were treated with low molecular weight heparin, vitamin K antagonists (VKA), or direct oral anticoagulants (DOACs). A total of 44 (69.8%) ALVT patients achieved thrombus resolution, in contrast to 33 (36.7%) CLVT patients. However, it’s noteworthy that 50% of CLVT cases achieved thrombus resolution through anticoagulant therapy (27/54) (Table 1). After adjusting for covariates, logistic regression revealed that CLVT patients receiving anticoagulant therapy had a 5.71-fold higher incidence of early resolution compared to those without anticoagulant therapy (95% CI: 1.543–21.18; p = 0.009) (Table 4). There was no significant difference between Warfarin and DOAC in the resolution of acute and old LVT (ALVT: OR = 1.143, 95% CI 0.22–5.928, p = 0.874; CLVT: OR = 1.707, 95% CI 0.53–5.496, p = 0.37).

Discussion

As a retrospective cohort study comparing LVT at different discovery times following AMI, this study explored the clinical correlates associated with thrombus resolution in both acute-to-subacute and chronic AMI phases. We observed that ALVT is more likely to achieve thrombus resolution compared to CLVT. Moreover, the correlates related to the resolution of left ventricular thrombus differed by AMI phases.Prior research has mainly focused on identifying the risk factors associated with thrombus formation following AMI. These studies have uncovered associations between thrombus formation and factors such as cardiac function, the severity of the inflammatory response, the presence of ventricular aneurysms [6, 7, 16, 17]. Furthermore, some studies have suggested that a heightened inflammatory response can hinder the resolution of LVT in non-PCI patients [18]. However, as the thrombotic and fibrinolytic propensity may varied by AMI phase [19, 20], few studies so far have focused on phase-specific thrombus resolution. Due to the fact that over 70% of LVT occurring 1 week after AMI [8, 9], this time window is shorter than the hospitalization time for most AMI patients, leading to less likelihood to promptly perform TTE to discover thrombus. Therefore, in this study, we addressed this point by considering the phase at which thrombus detection was performed.

The occurrence mechanism of LVT after AMI is similar to most thrombus formations and is associated with Virchow’s triad, which includes continuous activation of coagulation mechanisms [21], persistent inflammatory state [22], impaired ventricular wall motion [23], and endocardial injury [24]. In our study, we found varied results between ALVT and CLVT. ALVT resolves more easily than CLVT, and resolution of ALVT is associated with inflammation but is absent in CLVT, which may be related to the several reasons. First, ALVT is more prone to resolution compared to CLVT, possibly due to delayed detection and prolonged existence of CLVT. Second, it may also be related to partial organization of the thrombus and strong adherence of the thrombus to the ventricular wall. Finally, more aggressive use of antiplatelet and anticoagulant medications in the acute-to-subacute phase may also provide insights into our observations.

In recent years, research has found that inflammation is not limited to classic defensive pathophysiological processes, but also forms a complex regulatory network with coagulation, anticoagulation, and fibrinolysis systems [25]. The mutual promotion between the activation of the coagulation system and inflammatory response is an important cause of local thrombosis. Sia et al. showed in their study that NLR and PLR can predict the resolution of Left ventricular thrombus after non-PCI [18]. In our study, the lymphocyte ratio and neutrophil count seem to indicate similar results. In addition, Lechner’s study suggests a correlation between CRP and the prediction of LVT after AMI [7], and our study also found that CRP has significance in the resolution of thrombus.

At present, there are no clear guidelines for the treatment of old arterial thrombosis, but the use of anticoagulant therapy has become a consensus [26]. There is meta-analysis indicating that DOAC treatment for LVT is superior to warfarin [27]. Our study did not find a difference between the two, but this could also be due to the limited sample size. Our study once again confirms that anticoagulant therapy may be still effective for chronic phase ventricular thrombus. This suggests that for high-risk patients with thrombus, more frequent TTE examinations might be considered for the screening of thrombus earlier and initiate anticoagulant therapy. For patients with a significant elevation CRP after myocardial infarction, it is important to take echocardiographic examinations more frequently to prevent cannot resolve of the thrombus once it is formed. For patients with chronic stage thrombus, active anticoagulation therapy may be considered.

Limitation

As a single center, retrospective study, this study has the following limitations. Firstly, the number of research subjects is relatively small, and the interval and frequency of echocardiography are different, making it difficult to accurately understand the specific time of thrombus resolution or occurrence. It is possible that the detection of LVT through TTE but not cardiac magnetic resonance (CMR) imaging for assessing LVT could result in the omission of certain cases. The lack of statistical data on anticoagulant medication dosage, time in therapeutic range (TTR), and duration of administration indicates the need for large-scale studies. Such studies would provide a more robust evaluation of the efficacy and optimal dosing strategies of anticoagulant drugs for the treatment of LVT.

Conclusion

In general, ALVT is more likely to resolve compared to CLVT. Higher level of CRP is indicative of a lower likelihood of LVT resolution following AMI in ALVT but not CLVT. Additionally, anticoagulant therapy is still necessary for the management of LVT in chronic phase AMI.

Data availability

The datasets used and analysed during the current study available from the corresponding author on reasonable request.

Abbreviations

LVT:

Left Ventricular thrombus

TTE:

Transthoracic echocardiograph

AMI:

Acute myocardial infarction

ALVT:

Acute phase of Left ventricular thrombus

CLVT:

Chronic phase of Left ventricular thrombus

NLR:

Neutrophil-to-Lymphocyte Ratio

PLR:

Platelet-to-Lymphocyte Ratio

LMR:

lymphocyte-to- monocyte Ratio

ACEI:

Angiotensin-converting enzyme inhibitor

ARB:

angiotensin receptor blockers

ARNI:

Angiotensin receptor-neprilysin inhibitors

HER:

Electronic Health Records

VKA:

vitamin K antagonists

DOACs:

direct oral anticoagulants

TTR:

time in therapeutic range

References

  1. Nihoyannopoulos P, Smith GC, Maseri A, Foale RA. The natural history of left ventricular thrombus in myocardial infarction: a rationale in support of masterly inactivity. J Am Coll Cardiol. 1989;14(4):903–11.

    Article  CAS  PubMed  Google Scholar 

  2. Gianstefani S, Douiri A, Delithanasis I, Rogers T, Sen A, Kalra S, Charangwa L, Reiken J, Monaghan M, MacCarthy P. Incidence and predictors of early left ventricular thrombus after ST-elevation myocardial infarction in the contemporary era of primary percutaneous coronary intervention. Am J Cardiol. 2014;113(7):1111–6.

    Article  PubMed  Google Scholar 

  3. Stein B, Fuster V. Antithrombotic therapy in acute myocardial infarction: prevention of venous, left ventricular and coronary artery thromboembolism. Am J Cardiol. 1989;64(4):b33–40.

    Article  Google Scholar 

  4. McCarthy CP, Vaduganathan M, McCarthy KJ, Januzzi JL Jr., Bhatt DL, McEvoy JW. Left ventricular Thrombus after Acute myocardial infarction: screening, Prevention, and treatment. JAMA Cardiol. 2018;3(7):642–9.

    Article  PubMed  Google Scholar 

  5. Gökdeniz T, Boyacı F, Hatem E, Aslan AO, Aykan A, Gül I, Turan T, Kalaycıoğlu E, Celik Ş. SYNTAX score predicts the left ventricle thrombus development in patients undergoing primary percutaneous coronary intervention for first anterior myocardial infarction. Clin Appl Thromb Hemost. 2014;20(7):698–705.

    Article  PubMed  Google Scholar 

  6. Jiang YX, Jing LD, Jia YH. Clinical characteristics and risk factors of left ventricular Thrombus after Acute myocardial infarction: a matched case-control study. Chin Med J (Engl). 2015;128(18):2415–9.

    Article  PubMed  Google Scholar 

  7. Lechner I, Reindl M, Tiller C, Holzknecht M, Fink P, Plangger J, Mayr A, Klug G, Bauer A, Reinstadler SJ, Metzler B. Association between inflammation and left ventricular thrombus formation following ST-elevation myocardial infarction. Int J Cardiol. 2022;361:1–6.

    Article  PubMed  Google Scholar 

  8. Meurin P, Brandao Carreira V, Dumaine R, Shqueir A, Milleron O, Safar B, Perna S, Smadja C, Genest M, Garot J, Carette B, Payot L, Tabet JY. Incidence, diagnostic methods, and evolution of left ventricular thrombus in patients with anterior myocardial infarction and low left ventricular ejection fraction: a prospective multicenter study. Am Heart J. 2015;170(2):256–62.

    Article  PubMed  Google Scholar 

  9. Gellen B, Biere L, Logeart D, Lairez O, Vicaut E, Furber A, Mercadier JJ, Sirol M. Timing of Cardiac magnetic resonance imaging impacts on the detection rate of Left ventricular Thrombus after myocardial infarction. JACC Cardiovasc Imaging. 2017;10(11):1404–5.

    Article  PubMed  Google Scholar 

  10. Yang Q, Lang X, Quan X, Gong Z, Liang Y. Different Oral Antithrombotic Therapy for the Treatment of Ventricular Thrombus: An Observational Study from 2010 to 2019. Int J Clin Pract 2022, 2022, 7400860.

  11. Bass ME, Kiser TH, Page RL 2nd;, McIlvennan CK, Allen LA, Wright G, Shakowski C. Comparative effectiveness of direct oral anticoagulants and warfarin for the treatment of left ventricular thrombus. J Thromb Thrombolysis. 2021;52(2):517–22.

  12. Robinson AA, Trankle CR, Eubanks G, Schumann C, Thompson P, Wallace RL, Gottiparthi S, Ruth B, Kramer CM, Salerno M, Bilchick KC, Deen C, Kontos MC, Dent J. Off-label use of direct oral anticoagulants compared with Warfarin for Left Ventricular Thrombi. JAMA Cardiol. 2020;5(6):685–92.

    Article  PubMed  PubMed Central  Google Scholar 

  13. Abdelnabi M, Saleh Y, Fareed A, Nossikof A, Wang L, Morsi M, Eshak N, Abdelkarim O, Badran H, Almaghraby A. Comparative study of oral anticoagulation in Left Ventricular Thrombi (No-LVT trial). J Am Coll Cardiol. 2021;77(12):1590–2.

    Article  PubMed  Google Scholar 

  14. Guddeti RR, Anwar M, Walters RW, Apala D, Pajjuru V, Kousa O, Gujjula NR, Alla VM. Treatment of left ventricular Thrombus with direct oral anticoagulants: a retrospective observational study. Am J Med. 2020;133(12):1488–91.

    Article  CAS  PubMed  Google Scholar 

  15. Byrne RA, Rossello X, Coughlan JJ, Barbato E, Berry C, Chieffo A, Claeys MJ, Dan GA, Dweck MR, Galbraith M, Gilard M, Hinterbuchner L, Jankowska EA, Jüni P, Kimura T, Kunadian V, Leosdottir M, Lorusso R, Pedretti RFE, Rigopoulos AG, Rubini Gimenez M, Thiele H, Vranckx P, Wassmann S, Wenger NK, Ibanez B. 2023 ESC guidelines for the management of acute coronary syndromes. Eur Heart J 2023.

  16. Chen M, Liu D, Weidemann F, Lengenfelder BD, Ertl G, Hu K, Frantz S, Nordbeck P. Echocardiographic risk factors of left ventricular thrombus in patients with acute anterior myocardial infarction. ESC Heart Fail. 2021;8(6):5248–58.

    Article  PubMed  PubMed Central  Google Scholar 

  17. Duus LS, Pedersen S, Ravnkilde K, Galatius S, Fritz-Hansen T, Biering-Sørensen T, Olsen FJ. Association between the E-wave propagation index and left ventricular thrombus formation after ST-elevation myocardial infarction. Int J Cardiol. 2021;326:213–9.

    Article  PubMed  Google Scholar 

  18. Sia CH, Leow AS, Tan BY, Low CJ, Kaur R, Yeo TC, Chan MY, Tay EL, Yeo LL, Yap ES, Loh JP. The neutrophil-lymphocyte ratio and platelet-lymphocyte ratio predict left ventricular thrombus resolution in acute myocardial infarction without percutaneous coronary intervention. Thromb Res. 2020;194:16–20.

    Article  CAS  PubMed  Google Scholar 

  19. Lee SH, Kim HK, Ahn JH, Kang MG, Kim KH, Bae JS, Cho SY, Koh JS, Park Y, Hwang SJ, Gorog DA, Tantry US, Bliden KP, Gurbel PA, Hwang JY, Jeong YH. Prognostic impact of hypercoagulability and impaired fibrinolysis in acute myocardial infarction. Eur Heart J. 2023;44:1718–28.

    Article  CAS  PubMed  Google Scholar 

  20. Watanabe R, Wada H, Sakakura M, Mori Y, Nakasaki T, Okugawa Y, Gabazza EC, Hayashi T, Nishioka J, Suzuki K, Shiku H, Nobori T. Plasma levels of activated protein C-protein C inhibitor complex in patients with hypercoagulable states. Am J Hematol. 2000;65(1):35–40.

    Article  CAS  PubMed  Google Scholar 

  21. Merlini PA, Bauer KA, Oltrona L, Ardissino D, Cattaneo M, Belli C, Mannucci PM, Rosenberg RD. Persistent activation of coagulation mechanism in unstable angina and myocardial infarction. Circulation. 1994;90(1):61–8.

    Article  CAS  PubMed  Google Scholar 

  22. Ross R. Atherosclerosis–an inflammatory disease. N Engl J Med. 1999;340(2):115–26.

    Article  CAS  PubMed  Google Scholar 

  23. Delemarre BJ, Visser CA, Bot H, Dunning AJ. Prediction of apical thrombus formation in acute myocardial infarction based on left ventricular spatial flow pattern. J Am Coll Cardiol. 1990;15(2):355–60.

    Article  CAS  PubMed  Google Scholar 

  24. Johnson RC, Crissman RS, DiDio LJ. Endocardial alterations in myocardial infarction. Lab Invest. 1979;40(2):183–93.

    CAS  PubMed  Google Scholar 

  25. Colling ME, Tourdot BE, Kanthi Y. Inflammation, infection and venous thromboembolism. Circ Res. 2021;128(12):2017–36.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  26. Levine GN, McEvoy JW, Fang JC, Ibeh C, McCarthy CP, Misra A, Shah ZI, Shenoy C, Spinler SA, Vallurupalli S, Lip GYH. Management of patients at risk for and with left ventricular Thrombus: a Scientific Statement from the American Heart Association. Circulation. 2022;146(15):e205–23.

    Article  PubMed  Google Scholar 

  27. Condello F, Maurina M, Chiarito M, Sturla M, Terzi R, Fazzari F, Sanz-Sanchez J, Cannata F, Condorelli G, Stefanini GG. Direct oral anticoagulants versus vitamin K antagonists in the treatment of left ventricular thrombosis: a systematic review and meta-analysis. Minerva Cardiol Angiol. 2022;70(6):666–76.

    PubMed  Google Scholar 

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Acknowledgements

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Funding

This study was funded in part by the National Natural Science Foundation of China (Grant No. 82370272) and Shandong Provincial Natural Science Foundation (ZR2023MH337) and Qingdao Outstanding Health Professional Development Fund. The funding sources had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.

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Authors and Affiliations

  1. Department of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China

    Zhen Lu, Bingxue Song, Xin Liu, Ning Zhang, Fuhai Li, Fengqiang Xu, Zhexun Lian & Junjie Guo

  2. Qingdao University, Qingdao Medical College, Qingdao, China

    Zhen Lu

  3. Qingdao Municipal Key Laboratory of Hypertension (Key Laboratory of Cardiovascular Medicine), Qingdao, Shandong, China

    Bingxue Song, Xin Liu, Ning Zhang, Fuhai Li, Fengqiang Xu, Zhexun Lian & Junjie Guo

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Contributions

ZL and JG had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analyses. ZL, BS, JG, and NZ contributed to the concept and design. XL, FL and JG contributed to the acquisition, analysis, and interpretation of data. ZL and JG contributed to the drafting of the manuscript. ZL and JG contributed to the administrative, technical, and material support. ZL contributed to the supervision. All authors contributed to the critical revision of the manuscript for important intellectual content. All authors contributed to the article and approved the submitted version.

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Correspondence to Zhexun Lian or Junjie Guo.

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We solemnly make a statement that written informed consent were obtained from all subjects, and all participants were aware of the study purpose, risks and benefits. All participants provided written consent before participating in the study. The study was approved by the Ethics Committee of Affiliated Hospital of Qingdao University, with the ethical Approval Number: QYFY WZLL 27959.

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Lu, Z., Song, B., Liu, X. et al. Factors predicting resolution of left ventricular thrombus in different time windows after myocardial infarction. BMC Cardiovasc Disord 24, 278 (2024). https://doi.org/10.1186/s12872-024-03898-9

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BMC Cardiovascular Disorders

ISSN: 1471-2261

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