P3095Left ventricular thrombus formation after ST-elevation myocardial infarction: a prospective observational CMR study

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Holzknecht ◽  
S J Reinstadler ◽  
M Reindl ◽  
C Tiller ◽  
A Mayr ◽  
...  

Abstract Background Left ventricular (LV) thrombus formation is a severe complication after acute ST-segment elevation myocardial infarction (STEMI). The incidence and determinants of LV thrombus formation are still a matter of controversy. Purpose We aimed to assess the incidence as detected by cardiac magnetic resonance (CMR) imaging as well as the determinants of LV thrombus formation in contemporary reperfused STEMI patients. Methods This prospective observational study included 530 consecutive STEMI patients treated with primary percutaneous coronary intervention (PCI). Comprehensive CMR was performed at a median of 3 days (interquartile range 2–4 days) after symptom onset for the evaluation of LV thrombus formation as well as LV function and infarct severity. Results LV thrombi were detected in 17 patients (3.2% of the overall cohort). The incidence of LV thrombi in anterior STEMI patients (n=247) was 6.9%. In all patients presenting with LV thrombus left anterior descending artery (LAD) was identified as culprit lesion. The occurrence of thrombi was significantly associated with reduced LV ejection fraction (LVEF) (p<0.001), larger LV end-diastolic volume (p<0.001) and LV end-systolic volume (p<0.001), larger areas of microvascular obstruction (MVO) (p=0.003) and larger infarct size (IS) (p<0.001). Furthermore, increased levels of peak high sensitivity cardiac Troponin T (p<0.001) and hyperlipidaemia (p=0.038) were significantly related to LV thrombi. In multivariable analysis including IS, LVEF and MVO, only LVEF (odds ratio: 0.91 (95% confidence interval: 0.87–0.96); p=0.001) emerged as independent predictor of LV thrombus formation. Conclusion The risk of LV thrombus formation remains considerable in contemporary treated STEMI patients, especially in those with LAD as culprit lesion. Among CMR parameters of LV dysfunction and infarct severity, only baseline LVEF, but not IS or MVO, independently predicted LV thrombus formation after STEMI.

Cardiology ◽  
2016 ◽  
Vol 134 (4) ◽  
pp. 398-405 ◽  
Author(s):  
Erlend G. Singsaas ◽  
Cord A. Manhenke ◽  
Kenneth Dickstein ◽  
Stein Orn

Objectives: Galectin-3 (Gal-3) is involved in cardiac inflammation and fibrosis, and is in use as a biomarker that indicates increased risk in heart failure. This study examined the relationship between Gal-3 levels and acute and old myocardial infarction (MI) in patients assessed by cardiac magnetic resonance (CMR) imaging. Methods: Group 1 consisted of 38 patients with ST-elevation MI and single-vessel disease treated with primary percutaneous coronary intervention (PCI). Group 2 consisted of 52 patients with prior complicated MI. Twenty-two controls were included. CMR was performed in group 1 at 2 days, 1 week, 2 months and 1 year following PCI and in group 2 at >4 years after MI. Results: Median Gal-3 was elevated in patients compared with controls, group 1: 11.93 ng/ml (IQR 6.34-17.52, p = 0.03), group 2: 12.96 (IQR 6.33-19.29, p = 0.03) and controls: 10.16 (IQR 5.59-14.73). Gal-3 levels did not change during acute MI, and there was no relationship between Gal-3 and infarct size, troponin-T, high-sensitivity C-reactive protein, left-ventricular (LV) volumes or LV ejection fraction (LVEF) in group 1. In group 2, Gal-3 correlated modestly with MI size (r = 0.28, p < 0.05), LV end-diastolic volume index (r = 0.40, p < 0.01), LV end-systolic volume index (r = 0.43, p < 0.01) and LVEF (r = -0.39, p < 0.01). Conclusion: There was no relationship between Gal-3 levels and acute ischemic myocardial injury. A significant, modest relationship between Gal-3 levels, MI size and LV remodeling was only found in patients with old MI.


2021 ◽  
Vol 0 (Ahead of Print) ◽  
Author(s):  
Ferhat Eyyupkoca ◽  
Mehmet Ali Felekoglu ◽  
Gultekin Karakus ◽  
Ajar Kocak ◽  
Onur Yildirim ◽  
...  

Objective: Cardiac enzymes that are released during acute myocardial infarction (AMI) are of prognostic importance. This study aimed to investigate the relationship between cardiac troponin T (cTnT) and creatine kinase myocardial band (CK-MB) release during AMI and 6-month post-AMI left ventricular (LV) function, as assessed by magnetic resonance imaging. Methods: This prospective cohort observational study included 131 adult patients (113 males, 18 females, mean age 53.8 (8.6) years) who had been diagnosed with a new ST-segment elevation AMI (STEMI) in the emergency department. Cardiac enzymes were assessed by serial measurements. Blood samples obtained at 12 h post-AMI were included in the analysis. The reference value for CK-MB was 2–25 U/L, while for troponin it was - 0.1 ng/mL. Values above the reference limit were accepted as positive. Patients underwent cardiovascular magnetic resonance at 2 weeks and 6 months post-AMI. LV stroke volume was quantified as LV EDV – LV ESV, and ejection fraction (EF) was determined with the following equation: EF = [(LV EDV – LV ESV)/LV EDV] × 100. Adverse remodeling was defined based on the threshold values that are commonly accepted for changes in the LV end-diastolic volume (∆LV-EDV, &qt;10%) and LV end-systolic volume (∆LV-ESV, &qt;12%). Results: All of the patients were cTnT- and CK-MB-positive at 12 h. There was no found significant difference between both groups regarding the risk factors of coronary artery disease (including diabetes mellitus, hypertension, hyperlipidemia and smoking).  Adverse cardiac remodeling was observed in 32.1% (n = 42) of the patients. cTnT/CK-MB was determined to be an independent predictor of the ΔLV-EDV (β ( SE = 0.55 ( 0.08, p&lt;0.001), ΔLV-ESV (β ( SE = 1.12 ( 0.28, p&lt;0.001), and adverse remodeling (OR = 1.13, p&lt;0.001). The cTnT/CK-MB ratio was able to predict adverse remodeling with 85.7% sensitivity and 74.2% specificity (area under the ROC curve (AUC) = 0.856, p&lt;0.001). The cTnT levels were able to predict adverse remodeling with 73.8% sensitivity and 78.7% specificity (AUC = 0.796, p&lt;0.001). CK-MB did not significantly predict adverse remodeling (AUC = 0.516, (p=0.758). Conclusion: The cTnT/CK-MB ratio was superior to its components in predicting changes in LV function after STEMI. The cTnT/CK-MB ratio can be used in clinical practice for risk stratification and treatment optimization.


2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
E Tzolos ◽  
R Bing ◽  
J Andrews ◽  
M Macaskill ◽  
A Tavares ◽  
...  

Abstract Background Coronary artery thrombus is typically present in type 1 myocardial infarction, but small volumes in the setting of an uncertain culprit lesion may be beyond the detection limit of current imaging modalities. Purpose Using a novel glycoprotein IIb/IIIa-receptor radiotracer, 18F-GP1, we investigated whether positron emission tomography-computed tomography (PET-CT) could detect thrombus formation in coronary arteries. Methods In a single centre cross-sectional study, patients over 40 years of age with myocardial infarction were recruited after myocardial infarction and underwent underwent CT angiography and 18F-GP1 PET-CT. Stable patients with and without coronary artery disease formed a control cohort. Coronary artery 18F-GP1 uptake was visually assessed and quantified using maximum target-to-background ratios (TBRmax). Results Ninety-four (44 post-myocardial infarction and 50 control patients) were included in the cross-sectional analysis. The mean age of the post-myocardial infarction group was 61±9 years, three-quarters were male and two thirds had presented with ST elevation on electrocardiography. 34 (80%) patients post-myocardial infarction, but none of the control patients, demonstrated focal 18F-GP1 uptake in the coronary arteries. Of 42 vessels with an angiographic culprit lesion, 35 (83%) had 18F-GP1 uptake which was significantly higher than non-culprit vessels (p&lt;0.0001) as well as control vessels (p&lt;0.0001), while non-culprit vessel uptake was similar to control vessel uptake (p=0.567): culprit vessel median TBRmax 1.2 [interquartile range 0.96–1.44], non-culprit vessel TBRmax 0.96 [0.84–1.03] and control vessel TBRmax 0.9 [0.76 to 0.94]. Linear regression models demonstrated univariable associations between coronary 18F-GP1 TBRmax and time from myocardial infarction, male sex and presence of culprit vessel. On multivariable analysis, only culprit vessel status was associated with TBRmax (adjusted R2= 0.22, P&lt;0.001). Based on the Youden's index of the ROC curves, the optimal cut-off of predicting the presence of a culprit vessel was 1.20 with a specificity of 97%, accuracy of 83%, sensitivity (60%) and c-statictic of 0.74. A patient with ectatic vessel and visual thrombus demonstrated the most intense 18F-GP1 uptake (TBRmax 2.0, highest in the cohort) in the region of heaviest thrombus burden (Figure 2). Extra-coronary uptake was seen in regions of left ventricular thrombus, left atrial appendage thrombus, pulmonary thromboembolism and intramyocardial microvascular obstruction. Conclusions 18F-GP1 PET-CT is able to detect coronary artery thrombus in culprit lesions following myocardial infarction, as well as extra-coronary thrombotic pathologies that may be important in guiding patient management. 18F-GP1 is highly specific in recognising a culprit lesion from a non-culprit lesion both visually as well as quantitatively. FUNDunding Acknowledgement Type of funding sources: Foundation. Main funding source(s): British Heart Foundation Figure 1 Figure 2


2020 ◽  
Vol 21 (3) ◽  
pp. 807 ◽  
Author(s):  
Iwona Świątkiewicz ◽  
Przemysław Magielski ◽  
Jacek Kubica ◽  
Adena Zadourian ◽  
Anthony N. DeMaria ◽  
...  

Acute ST-segment elevation myocardial infarction (STEMI) activates inflammation that can contribute to left ventricular systolic dysfunction (LVSD) and heart failure (HF). The objective of this study was to examine whether high-sensitivity C-reactive protein (CRP) concentration is predictive of long-term post-infarct LVSD and HF. In 204 patients with a first STEMI, CRP was measured at hospital admission, 24 h (CRP24), discharge (CRPDC), and 1 month after discharge (CRP1M). LVSD at 6 months after discharge (LVSD6M) and hospitalization for HF in long-term multi-year follow-up were prospectively evaluated. LVSD6M occurred in 17.6% of patients. HF hospitalization within a median follow-up of 5.6 years occurred in 45.7% of patients with LVSD6M vs. 4.9% without LVSD6M (p < 0.0001). Compared to patients without LVSD6M, the patients with LVSD6M had higher CRP24 and CRPDC and persistent CRP1M ≥ 2 mg/L. CRP levels were also higher in patients in whom LVSD persisted at 6 months (51% of all patients who had LVSD at discharge upon index STEMI) vs. patients in whom LVSD resolved. In multivariable analysis, CRP24 ≥ 19.67 mg/L improved the prediction of LVSD6M with an increased odds ratio of 1.47 (p < 0.01). Patients with LVSD6M who developed HF had the highest CRP during index STEMI. Elevated CRP concentration during STEMI can serve as a synergistic marker for risk of long-term LVSD and HF.


Sign in / Sign up

Export Citation Format

Share Document