Predictive Value of Coagulation Markers Concerning Clinical Outcome 90 Days after Anterior Myocardial Infarction

1999 ◽  
Vol 81 (05) ◽  
pp. 701-704 ◽  
Author(s):  
Frederic Kontny ◽  
Ulrich Abildgaard ◽  
Carl-Erik Dempfle

SummaryTo study the predictive value of coagulation markers concerning clinical outcome, prothrombin fragment F1.2 (F1.2), fibrin monomer antigen (FM), D-Dimer (DD), and fibrinogen were measured in plasma samples drawn 2 and 7 days after acute myocardial infarction (AMI) in 314 consecutive patients randomized in a clinical trial of low molecular weight heparin (Dalteparin) (the FRAMI trial). Placebo-treated patients suffering death or new AMI within 90 days had significantly higher levels at day 2 of FM (Enzymun-Test FM), and DD (TINAquant D-dimer) (p = 0.001 and 0.02, respectively), but not F1.2 (Enzygnost F1.2 micro), relative to those without serious clinical events. At day 7 all three coagulation activation markers were significantly higher in patients with subsequent adverse clinical outcome. The Dalteparin group had significantly lower levels of these markers as compared to the placebo group. Left ventricular (LV) thrombus formation was not associated with changes in coagulation activation. However, patients with thrombus had significantly higher fibrinogen levels than those without thrombus (p = 0.004 day 2), independent of treatment group. Thus, markers of coagulation activation may be useful in stratification of patients when estimating risk for adverse clinical outcome after AMI. Furthermore, elevated fibrinogen levels are associated with increased risk of LV thrombus formation.

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Shetelig ◽  
T Ueland ◽  
S Limalanathan ◽  
P Hoffmann ◽  
P Aukrust ◽  
...  

Abstract Background Soluble ST2, a member of the IL-1 receptor family, seems to be associated with adverse outcome in acute myocardial infarction and heart failure (HF), and is suggested to be involved in left ventricular (LV) remodelling. Purpose To elucidate a possible role of ST2 in LV injury, remodelling and prognosis in ST-elevation myocardial infarction (STEMI) patients. The main objectives of the study were to investigate whether circulating ST2 levels were associated with infarct size, LV function, adverse remodeling and clinical outcome in a cohort of patients with STEMI. Methods 270 patients with clinically stable first-time STEMI treated with primary percutaneous coronary intervention (PCI) were included. Blood samples were drawn before and immediately after the PCI procedure, at day 1 (median 18.3 hours after PCI) and after 4 months. Cardiac magnetic resonance (CMR) was performed in the acute phase and after 4 months. Clinical events and all-cause mortality were registered during 12 months' and 70 months' follow-up, respectively. A composite endpoint was defined as death, MI, unscheduled revascularisation >3 months after the index infarction, rehospitalisation for HF or stroke. Associations between ST2 and CMR parameters and clinical events were evaluated with linear regression and logistic regression, respectively. Results There was a significant increase in ST2 levels from the PCI procedure to day 1 with a subsequent decline from day 1 to 4 months in the POSTEMI cohort. Patients with high ST2 levels (>median) at all sampling points during hospitalisation had significantly larger infarct size, lower myocardial salvage, lower LVEF, larger increase in EDV and higher frequency of MVO. After adjustment for relevant clinical variables, peak CRP and peak troponin T, ST2 measured at day 1 remained associated with infarct size (β 2.0 per SD of ST2, p<0.001) and LVEF (β −1.8 per SD of ST2, p=0.02) at 4 months. High levels of ST2 measured at day 1 (>75th percentile) were associated with increased risk of having an adverse clinical event during the first year and with long-term all-cause mortality (Figure). High levels of ST2 measured in a stable phase 4 months after STEMI were also associated with an increased risk of all-cause mortality (Figure). Figure 1 Conclusions High levels of ST2 in STEMI patients were associated with large infarct size, impaired recovery of LV function, and adverse clinical outcome in patients with STEMI. ST2 measured 4 months after STEMI remained associated with all-cause mortality.


2020 ◽  
Vol 41 (Supplement_1) ◽  
Author(s):  
A S T Leow ◽  
C H Sia ◽  
B Y Q Tan ◽  
R Kaur ◽  
H W Sim ◽  
...  

Abstract Funding Acknowledgements None Background/Introduction Left ventricular (LV) thrombus is a widely recognized complication of acute myocardial infarction (AMI).  Limited data are available from South East Asian patients with this post-infarction complication nor on whether patients with non-ST segment elevation myocardial infarction (NSTEMI) or STEMI with associated LV thrombosis exhibit differing clinical characteristics and/or outcomes. Left Ventricular Ejection Fraction (LVEF) ≤ 40% is a recognized predictor of LV thrombus formation, but there is limited data on LV thrombus patients with EF &gt; 40% or in NSTEMI patients. Purpose This study aims to investigate and compare the clinical characteristics, treatment and outcomes of post-AMI patients with LV thrombus formation, with a particular emphasis on those with EF ≤ 40% and in NSTEMI patients.  Methods Among 5829 consecutive echocardiogram results containing the keyword "thrombus" from August 2006 to September 2017, we identified 289 post-AMI patients with acute LV thrombus formation. Demographics, treatment and outcome measures were analysed. Results Cardiovascular risk factors such as dyslipidaemia (54.0%) and hypertension (50.5%) were commonly present in post-AMI patients with LV thrombus. Mean LVEF was 33.0 ± 10.4%. The majority (68.0%) of patients received triple therapy and 59.5% achieved thrombus resolution. NSTEMI patients had greater number of co-morbidities including heart failure (p &lt; 0.01), documented history of  ischaemic heart disease preceding the AMI leading to thrombus formation (p &lt; 0.01) and lower LVEF (28.3 ± 9.3% vs. 34.8 ± 10.3% , p &lt; 0.01) compared with STEMI cases. On multivariate analysis, having a lower EF was a significant independent predictor of stroke (HR 0.96, 95% CI 0.93-1.00, p = 0.03) and all-cause mortality (HR 0.95, 95% CI 0.92-0.99, p &lt; 0.01). The categories of STEMI and NSTEMI did not predict thrombus resolution, stroke events or all-cause mortality after adjustment. Conclusion(s)   Post-AMI LV thrombus patients with NSTEMI and STEMI differed in terms of their co-morbidities in their demographics and co-morbidities but it was a lower EF that was associated with an increased risk of stroke and all-cause mortality. Further studies on this topic are required.


2020 ◽  
Vol 54 (8) ◽  
pp. 611-618
Author(s):  
Roland von Känel ◽  
Franziska Merz ◽  
Hildegard Pfister ◽  
Tanja Brückl ◽  
Petra Zimmermann ◽  
...  

Abstract Background Depressed patients have an increased risk of myocardial infarction, for which acute stress is a frequent trigger. Prothrombotic changes could be one involved mechanism that can be modulated by psychological coping. Purpose We examined the effects of remitted major depression and situation-specific coping strategies on stress-induced coagulation activation. Methods Forty patients with remitted depression and 23 healthy controls underwent the Trier Social Stress Test, rating applied coping strategies thereafter. Blood was sampled at baseline and 15 and 45 min poststress to measure fibrinogen, von Willebrand factor (VWF) and D-dimer. Coagulation activation over time was quantified as area under the curve (AUC) with respect to baseline activity. Standardized z-scores of individual coagulation AUC measures were added up to a prothrombotic index. Results Stress provoked significant VWF (p = .024) and D-dimer (p = .002) responses. Remitted depressed patients used positive distraction coping more frequently than controls did (p = .030). Coagulation AUC measures were similar in both groups. In all participants, higher positive coping total (p = 0.009), driven by devaluation/defense (p = .022) and distraction (p = .004) coping, was associated with a lower prothrombotic index. In controls, but not in remitted depressed patients, higher positive coping total (p = .008), driven by higher devaluation/defense (p = .010) and distraction (p = .023) coping, was associated with lower VWF AUC. Conclusions Despite the use of favorable coping strategies in a specific stress situation, remitted depressed patients may benefit less from a positive effect of positive situational coping on coagulation activation than controls. Such a mechanism could partially explain the increased risk of myocardial infarction in depressed individuals.


2018 ◽  
Vol 20 (1) ◽  
pp. 108-117 ◽  
Author(s):  
Pankaj Garg ◽  
Rob J van der Geest ◽  
Peter P Swoboda ◽  
Saul Crandon ◽  
Graham J Fent ◽  
...  

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi213-vi213
Author(s):  
Nadim Tawil ◽  
Rayhaan Bassawon ◽  
Brian Meehan ◽  
Laura Montermini ◽  
Ali Nehme ◽  
...  

Abstract BACKGROUND Vascular anomalies, including thrombosis, are a hallmark of glioblastoma (GBM) and an aftermath of dysregulated cancer cell genome and epigenome. Up-regulation of podoplanin (PDPN) by cancer cells has recently been linked to an increased risk of venous thromboembolism in glioblastoma patients. Thus, regulation of this platelet activating protein by transforming events and release from cancer cells is of considerable interest. AIMS I. Investigate the pattern of PDPN expression and characterize PDPN-expressing cellular populations in GBM. II. Evaluate the contribution of oncogenic drivers to PDPN expression in GBM models. III. Investigate the potential involvement of extracellular vesicles (EVs) as a mechanism for systemic dissemination of PDPN and tissue factor (TF). IV. Examine the role of PDPN in intratumoral and systemic thrombosis. METHODS Bioinformatics (single-cell and bulk transcriptome data mining), GBM cell lines and stem cell lines, xenograft models in mice, ELISA assays for PDPN and TF, platelet (PF4) and clotting activation markers (D-dimer), EV electron microscopy, density gradient fractionation, and nano-flow cytometry. RESULTS PDPN is expressed by distinct glioblastoma cell subpopulations (mesenchymal) and downregulated by oncogenic mutations of EGFR and IDH1 genes, via changes in chromatin modifications (EZH2) and DNA methylation, respectively. GBM cells exteriorize PDPN and/or TF as cargo of exosome-like EVs shed both in vitro and in vivo. Injection of glioma PDPN-EVs activates platelets. Increase of platelet activation (PF4) or coagulation markers (D-dimer) occurs in mice harboring the corresponding glioma xenografts expressing PDPN or TF, respectively. Co-expression of PDPN and TF by GBM cells cooperatively increases tumor microthrombosis. CONCLUSION Distinct cellular subsets drive multiple facets of GBM-associated thrombosis and may represent targets for diagnosis and intervention. We suggest that the preponderance of PDPN expression as a risk factor in glioblastoma and the involvement of platelets may merit investigating anti-platelets for potential inclusion in thrombosis management in GBM.


2006 ◽  
Vol 124 (4) ◽  
pp. 186-191 ◽  
Author(s):  
Afonso Celso Pereira ◽  
Roberto Alexandre Franken ◽  
Sandra Regina Schwarzwälder Sprovieri ◽  
Valdir Golin

CONTEXT AND OBJECTIVE: There is uncertainty regarding the risk of major complications in patients with left ventricular (LV) infarction complicated by right ventricular (RV) involvement. The aim of this study was to evaluate the impact on hospital mortality and morbidity of right ventricular involvement among patients with acute left ventricular myocardial infarction. DESIGN AND SETTING: Prospective cohort study, at Emergency Care Unit of Hospital Central da Irmandade da Santa Casa de Misericórdia de São Paulo. METHODS: 183 patients with acute myocardial infarction participated in this study: 145 with LV infarction alone and 38 with both LV and RV infarction. The presence of complications and hospital death were compared between groups. RESULTS: 21% of the patients studied had LV + RV infarction. In this group, involvement of the dorsal and/or inferior wall was predominant on electrocardiogram (p < 0.0001). The frequencies of Killip class IV upon admission and 24 hours later were greater in the LV + RV group, along with electrical and hemodynamic complications, among others, and death. The probability of complications among the LV + RV patients was 9.7 times greater (odds ratio, OR = 9.7468; 95% confidence interval, CI: 2.8673 to 33.1325; p < 0.0001) and probability of death was 5.1 times greater (OR = 5.13; 95% CI: 2.2795 to 11.5510; p = 0.0001), in relation to patients with LV infarction alone. CONCLUSIONS: Patients with LV infarction with RV involvement present increased risk of early morbidity and mortality.


Open Heart ◽  
2018 ◽  
Vol 5 (2) ◽  
pp. e000852 ◽  
Author(s):  
Artin Entezarjou ◽  
Moman Aladdin Mohammad ◽  
Pontus Andell ◽  
Sasha Koul

BackgroundST-elevation myocardial infarction (STEMI) occurs as a result of rupture of an atherosclerotic plaque in the coronary arteries. Limited data exist regarding the impact of culprit coronary vessel on hard clinical event rates. This study investigated the impact of culprit vessel on outcomes after primary percutaneous coronary intervention (PCI) of STEMI.MethodsA total of 29 832 previously cardiac healthy patients who underwent primary PCI between 2003 and 2014 were prospectively included from the Swedish Coronary Angiography and Angioplasty Registry and the Registry of Information and Knowledge about Swedish Heart Intensive care Admissions. Patients were stratified into three groups based on culprit vessel (right coronary artery (RCA), left anterior descending artery (LAD) and left circumflex artery (LCx)). The primary outcome was 1-year mortality. The secondary outcomes included 30-day and 5-year mortality, as well as heart failure, stroke, bleeding and myocardial reinfarction at 30 days, 1 year and 5 years. Univariable and multivariable analyses were done using Cox regression models.ResultsOne-year analyses revealed that LAD infarctions had the highest increased risk of death, heart failure and stroke compared with RCA infarctions, which had the lowest risk. Sensitivity analyses revealed that reduced left ventricular ejection fraction on discharge partially explained this increased relative risk in mortality. Furthermore, landmark analyses revealed that culprit vessel had no significant influence on 1-year mortality if a patient survived 30 days after myocardial infarction. Subgroup analyses revealed female sex and multivessel disease (MVD) as significant high-risk groups with respect to 1-year mortality.ConclusionsLAD and LCx infarctions had a relatively higher adjusted mortality rate compared with RCA infarctions, with LAD infarctions in particular being associated with an increased risk of heart failure, stroke and death. Culprit vessel had limited influence on mortality after 1 month. High-risk patient groups include LAD infarctions in women or with concomitant MVD.


Sign in / Sign up

Export Citation Format

Share Document