Predictor Of Left Ventricular Thrombus Research Articles

Clinical predictors of left ventricular thrombus after myocardial infarction as detected by magnetic resonance imaging.

The diagnosis of a left ventricular (LV) thrombus in patients with ST-segment elevation myocardial infarction (STEMI) remains challenging. The aim of the current study is to characterize clinical predictors for LV thrombus formation, as detected by cardiac magnetic resonance imaging (CMRI). We retrospectively evaluated 337 consecutive STEMI patients. All patients underwent transthoracic echocardiography (TTE) and CMRI during their index hospitalization. We developed a novel risk stratification model (ThrombScore) to identify patients at risk of developing an LV thrombus. CMRI revealed the presence of LV thrombus in 34 patients (10%), of whom 33 (97%) had experienced an anterior wall myocardial infarction (MI), and the majority (77%) had at least mildly reduced left ventricular ejection fraction (LVEF < 45%). The sensitivity for thrombus formation of the first and second TTE was 5.9% and 59%, respectively. Multivariate logistic regression model revealed that elevated C-reactive protein levels, lack of ST-segment elevation (STe) resolution, elevated creatine phosphokinase levels, and STe in anterior ECG leads are robust independent predictors for developing an LV thrombus. These variables were incorporated to construct the ThrombScore: a simple six-point risk model. The odds ratio for developing thrombus per one-point increase in the score was 3.2 (95% CI 2.1-5.01; p < 0.001). The discrimination analysis of the model revealed a c-statistic of 0.86 for thrombus development. The model identified three distinct categories (I, II, and III) with corresponding thrombus incidences of 0%, 1.6%, and 27.6%, respectively. ThrombScore is a simple and practical clinical model for risk stratification of thrombus formation in patients with STEMI.

Incidence and clinical predictors of left ventricular thrombus after ST elevation myocardial infarction as detected by magnetic resonance imaging

Abstract Funding Acknowledgements Type of funding sources: None. Background The aim of the current study was to characterize clinical predictors and to develop clinical risk score for left ventricular (LV) thrombus as detected by cardiac magnetic resonance imaging (CMR). Methods We evaluated 337 patients without known prior coronary disease, who underwent primary percutaneous coronary intervention for STEMI. All patients underwent transthoracic echocardiography (TTE) and CMR during their index hospitalization. We developed a novel prognostic risk model (ThrombScore) to identify patients at risk for LV thrombus development. Results Upon CMR, LV thrombus was present in 34 patients (10%), of whom 33 (97%) had an anterior wall MI and most (77%) had at least mildly reduced left ventricular ejection fraction (LVEF&amp;lt;45%) upon the first TTE. Sensitivity for thrombus formation of the first and second TTE was 5.9% and 59%, respectively. Multivariate logistic regression model revealed that elevated C reactive protein (CRP) levels, lack of ST-segment elevation (STe) resolution, elevated creatine phosphokinase (CPK) levels, and STe in anterior ECG leads are robust independent predictors of LV thrombus in STEMI patients. These variables were incorporated to construct the ThrombScore: a simple six-point risk model. The odds ratio for thrombus development per one-point increase in the score was 3.2 (95% Confidence Interval 2.1–5.01; p&amp;lt;0.001). Discrimination analysis of the model revealed c-statistics of 0.86 for thrombus development. The model identified three distinct risk categories (I, II and III) with thrombus incidence of 0%, 1.6% and 27.6%, respectively. Conclusions ThrombScore is a simple, practical, clinical risk model for risk stratification of thrombus formation in patients with STEMI.

Predictors of left ventricular thrombus after acute myocardial infarction: a systematic review and meta-analysis.

Left ventricular thrombus (LVT) is a recognized complication of acute myocardial infarction (AMI) which can cause significant morbidity and mortality from systemic embolism. We conducted a systematic review and meta-analysis of factors that have been shown in studies to be independently predictive of LVT post-AMI. A total of 23 studies met the inclusion criteria with 1 047 785 patients. The proportion of patients with LVT ranged from 0.2% in the nationwide study in the USA to 36.1% in the cohort of patients with LV aneurysm. Pooled results from nine studies suggest that greater values for left ventricular ejection fraction is associated with reduced odds of LVT formation [odds ratio (OR) 0.90; 95% confidence interval (CI), 0.86-0.93; I2 = 76%]. Left ventricular aneurysm was a significant predictor of LVT formation (OR 6.07; 95% CI, 2.27-16.19; I2 = 91%; seven studies) and anterior location of MI was also a significant predictor (OR 7.72; 95% CI, 2.41-24.74; I2 = 69%; four studies). Three studies suggest that there was an increase in odds of LVT formation with greater values of C-reactive protein (OR 2.06; 95% CI, 1.07-3.97; I2 = 89%; three studies). The use of glycoprotein IIb/IIIa inhibitors (OR 2.52; 95% CI, 1.55-4.10; I2 = 0%; two studies) and greater SYNTAX score (OR 1.21; 95% CI, 1.08-1.36; I2 = 46%; two studies) were associated with LVT. In conclusion, patients with reduced ejection fraction, AMI and with left ventricular aneurysm are at risk of LVT formation and careful imaging evaluation should be performed to identify LVT in these patients to prevent stroke or peripheral embolism.

Value of the platelet-to-lymphocyte ratio in the prediction of left ventricular thrombus in anterior ST-elevation myocardial infarction with left ventricular dysfunction

BackgroundThe predictors of left ventricular thrombus (LVT) formation are not well defined in the contemporary era, especially in those patients at high risk. We aimed to evaluate whether the platelet/lymphocyte ratio (PLR) is valuable in the determination of LVT formation in patients with anterior ST-elevation myocardial infarction (STEMI) and left ventricular (LV) dysfunction.MethodsThe LVT group (n = 46) was identified from anterior STEMI patients with LV dysfunction who were treated with primary percutaneous coronary intervention (PCI) from January 2017 to December 2019 at the China-Japan Union Hospital of Jilin University. The no-LVT group (n = 92) were also selected from the same batch of patients and were age- and sex-matched to the patients with LVT. The PLR was determined at admission and was calculated as the ratio of the platelet count to the lymphocyte count using the complete blood count. The presence of LVT was determined by echocardiography.ResultsThe PLR were significantly higher in patients with LVT than in no-LVT group (p = 0.001). In a receiver operator characteristic curve (ROC) analysis, using a cut-off value of 118.07 (AUC 0.673, 95% CI: 0.574–0.771, P = 0.001), the PLR could independently predict the occurrence of LVT. Multivariate analysis showed that an increased PLR (OR = 1.011, 95% CI: 1.004–1.018, P = 0.002), the presence of a left ventricular aneurysm (OR = 46.350, 95% CI: 5.659–379.615, P < 0.001) and increased DTBT (OR = 1.005, 95% CI: 1.001–1.009, P = 0.012) were independent predictors of LVT formation.ConclusionsIn acute anterior STEMI patients with LV dysfunction, an increased PLR and DTBT and the presence of an LV aneurysm were independent predictors of LVT formation. A larger prospective study is warranted to evaluate this result.Trial registrationThis study was registered (May 4, 2019) on Chinese Clinical Trial Registry (ChiCTR-DDD-17011214).

Incidence and Predictors of Left Ventricular Thrombus After Primary Percutaneous Coronary Intervention for Anterior ST-Segment Elevation Myocardial Infarction.

The role of warfarin in anterior ST-segment elevation myocardial infarction (STEMI) complicated by left ventricular (LV) dysfunction in patients treated with primary percutaneous coronary intervention (PCI) and dual antiplatelet therapy is unclear. Warfarin may prevent cardioembolic events but significantly increases bleeding in the setting of dual antiplatelet therapy. The incidence of LV thrombus in anterior STEMI patients treated with PCI is low, and clinical predictors might be valuable in determining patients at risk. We performed a retrospective, single-center study of 687 consecutive patients with anterior STEMI treated with PCI from 2006 to 2013. Baseline variables were evaluated in 310 patients at high risk for LV thrombus based on echocardiographic criteria. Patients with definite, probable, and no LV thrombus were compared by ANOVA, χ(2), or t test where appropriate. Logistic regression analysis was performed. The incidence of LV thrombus was 15% (n = 47 probable/definite thrombus). Cardiac arrest was the only independent characteristic associated with increased risk of LV thrombus (odds ratio [OR]: 4.06, 95% confidence interval [CI]: 1.3-12.7). Trends were observed for a lower risk in cardiogenic shock (OR: 0.33, 95% CI: 0.10-1.05) and aspirin use at baseline (OR: 0.43, 95% CI: 0.17-1.1). Treatment variables associated with LV thrombus included unfractionated heparin use post-PCI (OR: 2.43, 95% CI: 1.16-5.1) and use of balloon angioplasty without stent. In contemporary practice with primary PCI, definite LV thrombus following anterior STEMI with LV dysfunction is challenging to predict. Further investigation is needed to determine if there is a subset of patients that should be treated with prophylactic warfarin.

Clinical predictors and outcomes of patients with left ventricular thrombus following ST-segment elevation myocardial infarction.

We aimed to characterize the independent predictors of LVT following STEMI and the association with outcomes. The clinical predictors of left ventricular thrombus (LVT) formation after ST-segment elevation myocardial infarction (STEMI) are not well-defined in the contemporary era. We performed a retrospective analysis of STEMI patients at Duke from 2000 to 2011 who had a transthoracic echocardiogram within 90 days post-STEMI and compared patients with and without LVT (LVT+ vs. LVT-). Univariate Cox proportional hazards regression models of baseline characteristics were examined and significant variables were used in a multivariable model to assess adjusted relationships with LVT. A multivariable Cox PH survival model with covariate adjustments was used for assessment of LVT and long-term mortality. Of all eligible patients, 1734 patients met inclusion criteria and 4.3 % (N = 74) had a LVT. LVT+ patients tended to have a history of heart failure (HF) and higher initial troponin compared to LVT- patients. After adjustment, higher heart rate, non-white race, HF severity, and presence of left anterior descending artery (LAD) disease were independent predictors of LVT. There was a trend toward an association between LVT and increased all-cause mortality (HR 1.36; 95 % CI 0.84-2.21, P = 0.22), however this was not statistically significant. LVT was seen in over 4 % of this contemporary post-STEMI population. Several baseline characteristics were independently associated with LVT: Heart rate, HF severity, LAD disease, and non-white race. Prospective studies are warranted to determine whether anticoagulation in patients at increased risk for LVT improves outcomes.

Incidence and predictors of left ventricular thrombus following STEMI: A cardiac MRI study

Background: Left ventricular (LV) thrombus formation is a well-recognised complication following ST-elevation myocardial infarction (STEMI). Contrast-enhanced cardiac magnetic resonance imaging (CE-CMRI) outperforms transthoracic echocardiography in the detection of left ventricular thrombus following reperfused STEMI. This study aimed to examine the incidence and predictors of LV thrombus following STEMI.

Abstract 20119: Incidence and Predictors of Left Ventricular Thrombus in ST Elevation Myocardial Infarction

Introduction: Anticoagulation with coumadin is often employed after anterior ST-segment elevation myocardial infarction (STEMI) complicated by left ventricular (LV) dysfunction to prevent LV thrombus and cardioembolic events. However, the combination of dual antiplatelet therapy used for coronary stents and coumadin has been repeatedly shown to have a high incidence of bleeding. The current guidelines give coumadin a class II recommendation and support an individualized approach to treatment. Hypothesis: Determining the incidence and predictors of LV thrombus in a contemporary STEMI population at high risk for LV thrombus may assist in clinical decision making. Methods: Anterior STEMI patients at our institution between 2006 and 2013 treated with primary percutaneous intervention (PCI) that had an echocardiogram performed within 1 week and an ejection fraction of less than 40% or less than 50% with anterior apical akinesis were retrospectively identified. 687 patients with anterior STEMI were screened and 310 met inclusion. Demographic, clinical, and angiographic data was extracted from the medical record. Patients were categorized in 2 groups according to echocardiographic findings (no LV thrombus or probable/definite LV thrombus). The groups were compared by chi squared or T-test where appropriate. Logistic regression analysis was performed. Results: The mean age of the study population was 61.8% and 71.5% were male. The incidence of LV thrombus was 15% (n=263 no thrombus; n=47 probable/definite thrombus). Patients with LV thrombus were less likely to have hyperlipidemia, and more likely to have post procedure TIMI 0-1 flow and no stent use compared to patient with no LV thrombus. After adjustment, variables associated with LV thrombus risk were cardiac arrest (OR 4.06, 1.3-12.7), unfractionated heparin post PCI (2.43, 1.16-5.1), and stent use (DES 0.22, .06-.77, BMS 0.23 .07-.75, compared to balloon angioplasty). Conclusions: The incidence of LV thrombus in at risk STEMI patients remains high in contemporary practice. Development of a clinical risk score is limited by the lack of a sufficient number of predictive variables. Further investigation is needed to determine the optimal anticoagulation strategy in these patients.

Risk factors for development of left ventricular thrombus after first acute anterior myocardial infarction-association with anticardiolipin antibodies

BackgroundLeft ventricular thrombus(LVT] formation is a frequent complication in patients with acute anterior myocardial infarction(MI). LVT is associated with increased risk of embolism and higher mortality rates after acute MI. Anticardiolipin antibodies (ACA) are immunoglobulins that react with phospholipid-binding proteins interfering with the prothrombin activator complex. The effects of phospholipids on pathophysiology of cardiovascular thrombotic events are well known. In this study, we aimed to evaluate the importance of clinical and biochemical parameters including anticardiolipin antibodies on left ventricular thrombus formation after acute anterior MI.Methods and ResultsSeventy patients with a first anterior AMI were prospectively and consecutively enrolled. Patients with previous MI, autoimmune disease, collagen vascular disease and arterial or venous thrombosis history were excluded from this study. At the time of hospitalization, key demographic and clinical characteristics were collected including age, gender, ethanol intake and presence of traditional risk factors for atherosclerosis (hypertension, diabetes, smoking, hyperlipidemia, positive family history). Patients were evaluated for echocardiographic data, blood chemistry and ACA. Two-dimensional and Doppler echocardiographic examinations were performed in all patients within the first week and at 14 days after MI. LV thrombus was detected in 30 (42.8%) patients. ACA IgM levels were significantly higher in the patient group with LV thrombus than in the group without thrombus (12.44 ±4.12 vs. 7.69 ± 4.25 mpl, p = 0,01). ACA IgG levels were also found higher in the group with LV thrombus (24.2 ± 7.5 vs.17.98 ± 6.45 gpl, p = 0.02). Multivariate analyses revealed diabetes mellitus, higher WMSI, lower MDT and higher ACA IgM and higher ACA IgG levels as independent predictors of left ventricular thrombus formation.ConclusionsOur data demonstrate that beside the low ejection fraction, lower MDT and higher wall motion score index, modestly elevated ACA IgM and ACA IgG levels are associated with LV thrombus formation in patients with anterior MI.

Predictors of left ventricular thrombus formation in patients with dilated cardiomyopathy: role of activated protein C resistance.

The aim of this study was to investigate the association between left ventricular thrombus formation and natural anticoagulant systems including the protein C, protein S and antithrombin in patients with dilated cardiomyopathy. Sixty patients with dilated cardiomyopathy who met the inclusion criteria were included in the study. Patients were divided into two groups: group I consisted of 22 patients with left ventricular thrombus and group II consisted of 38 patients without left ventricular thrombus. Our main inclusion criteria were ejection fraction </= 35% and left ventricular end-diastolic diameter >/= 6.0 cm. These two groups were compared for clinical and hematologic parameters (activated protein C resistance, protein S and antithrombin). There were no statistically significant differences between patients with or without left ventricular thrombi with respect to left ventricular end-diastolic and end-systolic dimensions, ejection fraction, fractional shortening and left atrial diameter. There were no statistically significant differences between patients with and without left ventricular thrombus with respect to platelet count (252 +/- 64/mm3 x 10(3) compared with 260 +/- 74/mm3 x 10(3) respectively, P=0.68), prothrombin time (12.94 +/- 1.9 s compared with 12.86 +/- 1.3 s respectively, P=0.82), activated partial thromboplastin time (32 +/- 5 compared with 30 +/- 4 s respectively, P=0.32) and fibrinogen levels (36 +/- 9 mg/dl compared with 34 +/- 8 mg/dl respectively, P=0.41). None of the patients had protein S and antithrombin deficiency. Activated protein C resistance was found in 12 patients (12 out of 22, 54%) in group I and four patients (four out of 38, 9.5%) in group II (P < 0.01). It was also shown to be an independent predictor of left ventricular thrombus (P < 0.05). Activated protein C resistance is found to be an independent predictor of left ventricular thrombus in patients with dilated cardiomyopathy who have ejection fractions less then 35% and left ventricular end-diastolic dimensions > 6.0 cm.

Factor V Leiden and its relation to left ventricular thrombus in acute myocardial infarction

Objective — The genetic defect of coagulation factor V, known as factor V Leiden, produces a resistance to degradation by activated protein C (APC) and increases the risk of venous thrombosis. However, the role of factor V Leiden in the formation of left ventricular (LV) thrombus has not been studied.We investigated whether factor V Leiden is a risk factor for LV thrombus in patients with acute myocardial infarction (AMI).Methods and results — We have analyzed clinical, echocardiographic and biochemical data in 135 consecutive patients (aged 58 ± 13 years; 31 women) with first anterior AMI. Two-dimensional echocardiographic examination was performed on days I, 3, 7, 15 and 30; LV thrombus was detected in 33 (24.4%) of 135 patients with AMI. The study also included 95 control subjects. Healthy age and sex-matched subjects without a personal or family history of ischaemic heart disease, stroke or thromboembolic disease served as a control group. Blood samples from the patients and controls were analyzed for the factor V Leiden mutation by DNA analysis, using the polymerase chain reaction. In addition, concentrations of fibrinogen, von Willebrand factor (vWF), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-I (PAI-1) and D-dimer were measured in 135 patients. There was no significant difference in the prevalence of factor V Leiden between patients and control subjects. The prevalence of the factor V mutation was 9% (3/33) in patients with thrombus, and 7.7% (8/103) in patients without thrombus. The prevalence of factor V Leiden was 7.3% (7/95) in control subjects. No significant differences in plasma fibrinogen (480 ± 195 vs. 444 ± 179 mg/dl, p = 0.6), D-dimer (471 ± 256 vs. 497 ± 293 ng/dl, p = 0.7), vWF (112 ± 18 vs. 103 ± 15%, p = 0.5), PAI-I (26.7 ± 9.8 vs. 28.1 ± 10.2 ng/dl, p = 0.6), and t-PA (19.8 ± 8.7 vs. 17.2 ± 9.1 ng/dl, p = 0.7), levels are found in patients with LV thrombus when compared with those without LV thrombus. Multivariate analyses showed that peak creatine kinase level (p = 0.002) and LV wall motion score index (p = 0.003) were independent predictors of LV thrombus formation.Conclusion — Factor V Leiden mutation is not a risk factor for LV thrombus formation in patients with AMI. (Acta Cardiol 2001; 56(1 ): 1-6)

Doppler-derived mitral deceleration time as an early predictor of left ventricular thrombus after first anterior acute myocardial infarction

Background The relation between left ventricular (LV) diastolic function and LV thrombus has not yet been fully investigated. The aim of this study was to determine whether early assessment of Doppler-derived mitral deceleration time (DT), a measure of LV compliance and filling, may predict LV thrombus formation after acute myocardial infarction. Methods and Results Two-dimensional and Doppler echocardiographic examinations were performed in 98 consecutive patients (aged 57 ± 12 years; 8 women) with first acute myocardial infarction. The patients were studied within 24 hours and at days 3, 7, 15, and 30 after arrival to the coronary care unit. Mitral flow velocities were obtained from the apical 4-chamber view with pulsed Doppler. LV thrombus was detected in 20 of 98 patients. Patients were divided into 2 groups according to LV thrombus formation: group 1 (n = 20) with thrombus and group 2 (n = 78) without thrombus. Mitral E-wave DT was significantly shorter in group 1 than group 2 (134 ms vs 175 ms; P <.001). Patients in group 1 had significantly larger LV end-diastolic and end-systolic volumes and a higher wall motion score index than patients in group 2 (133 ± 39 mL vs 112 ± 41 mL, P =.03; 83 ± 34 mL vs 59 ± 30 mL, P =.003; and 1.8 ± 0.3 mL vs 1.5 ± 0.3 mL, P =.007, respectively). The LV ejection fraction was significantly lower in group 1 than in group 2 (39% ± 13% vs 48% ± 12%; P =.004). In a multivariate regression analysis, mitral E-wave DT was identified as an independent variable related to development of LV thrombus (P =.04). Conclusions Doppler-derived mitral DT is superior to conventional clinical and 2-dimensional echocardiographic assessment in estimating the risk of left ventricular thrombosis after myocardial infarction. (Am Heart J 2000;140:772-6.)