Left Ventricular Thrombus Formation In Patients Research Articles

Prophylactic Rivaroxaban Therapy forLeft Ventricular Thrombus After Anterior ST-Segment Elevation Myocardial Infarction.

The aim of this study was to investigate the effects of rivaroxaban on left ventricle thromboprophylaxis in patients with anterior ST-segment elevation myocardial infarction (STEMI). Anterior STEMI is associated with an increased risk of left ventricular thrombus (LVT) formation. The contemporary role of prophylactic rivaroxaban therapy remains unclear. We randomly assigned 279 patients with anterior STEMI who had undergone primary percutaneous coronary intervention to receive, in a 1:1 ratio, low-dose rivaroxaban (2.5mg twice daily for 30days) and dual antiplatelet therapy (DAPT) or only DAPT. The primary efficacy outcome was the LVT formation within 30days. Net clinical adverse events were assessed at 30days and 180days, including all-cause mortality, LVT, systemic embolism, rehospitalization for cardiovascular events, and bleeding. The addition of low-dose rivaroxaban to DAPT reduced LVT formation within 30days compared with only DAPT (0.7% vs 8.6%; HR: 0.08; 95%CI: 0.01-0.62; P=0.015; P< 0.001 for superiority). Net clinical adverse events were lower within 30days in the rivaroxaban group versus those in the only DAPT group and remained relatively low throughout the follow-up period. There were no significant differences in bleeding events between the 2 groups in 30days and 180days. However, 1 case of intracranial hemorrhage (major bleeding) occurred in the rivaroxaban group within 30days. Our results supported that the short-duration addition of low-dose rivaroxaban to DAPT could prevent LVT formation in patients with anterior STEMI following primary percutaneous coronary intervention. A larger multiple-institution study is necessary to determine the generalizability.

Abstract 13758: Right Ventricular Dysfunction Contributes to Left Ventricular Thrombus Formation After Myocardial Infarction

Introduction: Thromboembolic events such as stroke due to left ventricular thrombus (LVT) formation accompany acute myocardial infarction (MI). Risk factors for the development of LVT after MI have been identified based on limited data, including MI location, severe ventricular wall motion abnormalities or aneurysm, and reduced left ventricular ejection fraction (LVEF). Hypothesis: The purpose of this study was to define additional determinants of LVT formation following acute anterior MI through comparing clinical and echocardiographic characteristics between patients with and without LVT formation during the first 3 months after MI. Methods: This case-control-study comprised acute anterior MI patients with and without LVT, who were selected from a cohort of 1327 consecutive patients with ischemic heart failure in our hospital. The cases and controls were matched for age, sex, and LVEF. LVT was detected by routine/contrast echocardiography or cardiac magnetic resonance imaging during the first 3 months following MI. Results: Formation of apical aneurysm after MI was independently associated with LVT formation (72.0% vs. 43.5%, odds ratio [OR]=5.06, P=0.005). Echocardiographic risk factors associated with LVT formation included reduced mitral annular plane systolic excursion (MAPSE&lt;7mm, OR=4.69), moderate-severe diastolic dysfunction (OR=2.71), and right ventricular (RV) dysfunction [reduced tricuspid annular plane systolic excursion (TAPSE)&lt;17mm (OR=5.48), reduced RV factional area change (RV_FAC)&lt;0.35 (OR=3.32), and enlarged RV diameters (OR=1.62)]. Subgroup analysis showed reduced TAPSE (OR=5.12, P=0.010) associated with increased risk of LVT formation in anterior MI patients without apical aneurysm, independent of clinical and other echocardiographic covariates. Conclusions: RV dysfunction as determined by reduced TAPSE and RV_FAC is independently associated with LVT formation in acute anterior MI patients, especially in the setting of MI patients without the formation of an apical aneurysm. This suggests that besides assessment of left ventricular abnormalities, assessment of concomitant RV dysfunction is of importance in risk stratification of LVT formation in patients with acute anterior MI.

Echocardiographic risk factors of left ventricular thrombus in patients with acute anterior myocardial infarction.

AimsThis study aimed to identify echocardiographic determinants of left ventricular thrombus (LVT) formation after acute anterior myocardial infarction (MI).Methods and resultsThis case–control study comprised 55 acute anterior MI patients with LVT as cases and 55 acute anterior MI patients without LVT as controls, who were selected from a cohort of consecutive patients with ischemic heart failure in our hospital. The cases and controls were matched for age, sex, and left ventricular ejection fraction. LVT was detected by routine/contrast echocardiography or cardiac magnetic resonance imaging during the first 3 months following MI. Formation of apical aneurysm after MI was independently associated with LVT formation [72.0% vs. 43.5%, odds ratio (OR) = 5.06, 95% confidence interval (CI) 1.65–15.48, P = 0.005]. Echocardiographic risk factors associated with LVT formation included reduced mitral annular plane systolic excursion (<7 mm, OR = 4.69, 95% CI 1.84–11.95, P = 0.001), moderate–severe diastolic dysfunction (OR = 2.71, 95% CI 1.11–6.57, P = 0.028), and right ventricular (RV) dysfunction [reduced tricuspid annular plane systolic excursion < 17 mm (OR = 5.48, 95% CI 2.12–14.13, P < 0.001), reduced RV fractional area change < 0.35 (OR = 3.32, 95% CI 1.20–9.18, P = 0.021), and enlarged RV mid diameter (per 5 mm increase OR = 1.62, 95% CI 1.12–2.34, P = 0.010)]. Reduced tricuspid annular plane systolic excursion (<17 mm) significantly associated with increased risk of LVT in anterior MI patients (OR = 3.84, 95% CI 1.37–10.75, P = 0.010), especially in those patients without apical aneurysm (OR = 5.12, 95% CI 1.45–18.08, P = 0.011), independent of body mass index, hypertension, anaemia, mitral annular plane systolic excursion, and moderate–severe diastolic dysfunction.ConclusionsRight ventricular dysfunction as determined by reduced TAPSE or RV fractional area change is independently associated with LVT formation in acute anterior MI patients, especially in the setting of MI patients without the formation of an apical aneurysm. This study suggests that besides assessment of left ventricular abnormalities, assessment of concomitant RV dysfunction is of importance on risk stratification of LVT formation in patients with acute anterior MI.

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).

Relationship of Mitral Annular Plane Systolic Excursion (MAPSE) to Left Ventricular Thrombus Formation

Background: Dilated cardiomyopathy is associated by radial and longitudinal contractile cardiac dysfunction. Left ventricular (LV) thrombus is a frequent finding in patients with dilated cardiomyopathy. Themain purpose of our study was to evaluate the role of mitral annular plane systolic excursion (MAPSE) in LV thrombus formation in patients with dilated cardiomyopathy by assessing their correlation. Our additional objective was to compare the relationshipof average MAPSE to relations of other LV features [LV size, LV ejection fraction (EF), wall motion score index (WMSI), sphericity index -width to length ratio (w/l) of the LV] and LV thrombus development. OriginalResearch Article

Frequency and Correlates of Early Left Ventricular Thrombus Formation Following Anterior Wall Acute Myocardial Infarction Treated With Primary Percutaneous Coronary Intervention

The introduction of primary percutaneous coronary intervention (PPCI) for the treatment of patients with acute ST-segment elevation myocardial infarctions has resulted in a significant decrease in the prevalence of diagnosed left ventricular (LV) thrombus. However, reported rates are still as high as 10% to 20% in patients when followed up to 30 days. The aim of this study was to assess the frequency and predictors of early (<7 days after admission) LV thrombus formation in patients with acute anterior ST-segment elevation myocardial infarctions treated with PPCI. The cohort included 429 consecutive patients with documented acute anterior ST-segment elevation myocardial infarctions, who were treated with PPCI from January 2006 to July 2012. All patients underwent cardiac echocardiography on the first or second day of admission and repeat echocardiography 5 to 7 days after admission. Correlates of LV thrombus were estimated using a logistic multivariate regression model. LV thrombus formations were found in 18 of 429 patients (4%) during hospitalization. The first echocardiographic study diagnosed 11 of 18 LV thrombus formations. Patients with identified LV thrombus had significantly lower LV ejection fractions than those without LV thrombus at admission (p = 0.005) and at discharge (p <0.001). Lower admission LV ejection fractions, Thrombolysis In Myocardial Infarction (TIMI) flow grade ≤1 before angioplasty, and a longer time from symptom onset to PPCI were independent predictors of early LV thrombus formation. In conclusion, late reperfusion, a lower LV ejection fraction, and a lower TIMI score significantly increased the risk for early LV thrombus formations, even in the era of PPCI. Early echocardiographic assessment is warranted when admission test results identify at-risk patients.

Abnormal Left Ventricular Vortex Flow Patterns in Association With Left Ventricular Apical Thrombus Formation in Patients With Anterior Myocardial Infarction

The current study was designed to investigate the correlation between the left ventricular (LV) vortex flow pattern and LV apical thrombus formation in patients with acute anterior wall myocardial infarction (MI). Fifty-seven patients with acute anterior wall MI were enrolled in this study. Eighteen patients with apical thrombus (thrombus group) and 39 patients without apical thrombus (non-thrombus group) underwent 2-dimensional contrast echocardiography (CE). Morphology and pulsatility parameters of the LV vortex were measured using Omega flow(®) and compared between the 2 groups. In the thrombus group, the vortex was located more centrally and did not extend to the apex. In the thrombus group, quantitative vortex parameters of vortex depth (0.409±0.101 vs. 0.505±0.092, respectively; P=0.002) and relative strength (1.574±0.310 vs. 1.808±0.376, respectively, P=0.034) were significantly lower than the non-thrombus group. Following multivariate analysis, the vortex depth below 0.45 remained a significant independent parameter for formation of the LV apical thrombus (odds ratio 9.714, 95% confidence interval 1.674-56.381, P=0.011). These findings suggest that the location and pulsatility power of the LV vortex are strongly associated with the LV thrombus formation in patients with anterior MI. Therefore, LV vortex flow analysis using CE can be clinically useful for characterizing and quantifying the risk of LV apical thrombus in patients with anterior MI.

P1086 The association between anticardiolipin antibodies and left-ventricular thrombus formation in patients with first acute anterior myocardial infarction

P1086 The association between anticardiolipin antibodies and left-ventricular thrombus formation in patients with first acute anterior myocardial infarction

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)

Influence of thrombolytic therapy on the incidence of left ventricular thrombi after acute anterior myocardial infarction: role of successful reperfusion.

Previous studies have reported controversial results regarding the effectiveness of systemic thrombolysis in preventing left ventricular (LV) thrombus after acute myocardial infarction (MI). This study was performed to evaluate the influences of thrombolysis, and particularly successful reperfusion, on the incidence of LV thrombus formation after acute anterior MI. In all, 191 patients suffering from a first attack of acute anterior MI were prospectively evaluated by two-dimensional echocardiography and coronary angiography, performed at the end of the first week and within the first two weeks of MI, respectively. Of these, 98 who presented within 12 h of onset of symptoms received intravenous streptokinase (1.5 million IU), while the remaining 93 patients who, either because of contraindications or late admission, did not receive thrombolytic treatment served as control group. All patients received aspirin and full-dose anticoagulation with intravenous heparin. Successful reperfusion in the streptokinase group was assessed by enzymatic and electrocardiographic evidence. The overall incidence of LV thrombi was 24.6% (47/191). When all patients were evaluated, no statistically significant difference was found between the frequency of LV thrombi in the patients who had thrombolysis (22.4%) and those who did not (26.8%), despite a trend toward the formation of fewer thrombi in the initial group (p > 0.05). However, the patients who had successful reperfusion with streptokinase (n = 64) had significantly reduced incidence of LV thrombi compared with those who did not receive thrombolytic therapy (20 vs. 26.8%, p < 0.05). Stepwise multivariate analysis suggested that LV abnormal wall motion score (p = 0.01) and presence of LV aneurysm were independent predictors of LV thrombus formation in patients with acute anterior MI. Not all patients who received streptokinase for acute anterior MI, but only those with successful reperfusion had reduced incidence of LV thrombi. The favorable effects of thrombolysis on LV thrombus formation are probably due to the preservation of global LV systolic function.