scholarly journals Left ventricular blood flow energetics after acute ST-segment elevation myocardial infarction associate with left ventricular remodeling

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
A Demirkiran ◽  
P Garg ◽  
R J Geest ◽  
H J Berkhof ◽  
R Nijveldt ◽  
...  

Abstract Background Myocardial infarction (MI) leads to complex changes in left ventricular (LV) haemodynamics. It remains unknown how four-dimensional (4D) acute changes in LV blood flow kinetic energy (KE) affect LV remodeling. We hypothesized that LV blood flow energetics are independently associated with adverse LV-remodeling. Methods In total, 69 revascularised ST-segment elevation MI patients were enrolled. All patients underwent cardiovascular magnetic resonance (CMR) examination within 2 days of the index event and at 3-month. CMR examination included cine, late gadolinium enhancement, and whole-heart 4D flow acquisitions. CMR analysis included: LV volumes, function, infarct size (indexed to body surface area), microvascular obstruction (MVO), two-dimensional, retrospective valve tracking derived mitral inflow metrics, and 4D blood flow KE components (Fig. 1). Adverse LV-remodeling was defined and categorized according to increase in LV end-diastolic volume: 10% (mild), 15% (moderate), and 20% (severe). Results Twenty-four patients (35%) developed mild, 17 patients (25%) moderate, 11 patients (16%) severe LV remodeling. Demographics and clinical history were comparable between patients with/without LV remodeling. In univariable logistic regression analysis, A-wave KE was associated with mild, moderate, and severe LV remodeling (p=0.03, p=0.02, p=0.02, respectively), whereas infarct size was associated with only mild LV remodeling (p=0.02). In multivariable logistic regression analysis, whilst the infarct size and A-wave KE were identified as independent markers for mild LV remodeling (p=0.03, p=0.09, respectively), A-wave KE was the only independent marker regarding moderate and severe LV remodeling (both, p<0.01). In ROC analysis for A-wave KE to be associated with the presence of adverse LV remodeling, the area under the curve was 0.67 for mild (p=0.02), 0.70 for moderate (p=0.01), 0.71 for severe (p=0.03) LV remodeling. Conclusion In patients with STEMI, LV hemodynamics assessment by LV blood flow KE demonstrated an incremental value to predict adverse LV-remodeling. A-wave KE early after acute MI had an independent effect on adverse LV remodeling. FUNDunding Acknowledgement Type of funding sources: Foundation. Main funding source(s): This work was supported by the British Heart Foundation [FS/10/62/28409 to S.P.] and Dutch Technology Foundation (STW), project number 11626 (JW, ME).

2016 ◽  
Vol 10 ◽  
pp. CMC.S35734 ◽  
Author(s):  
Mohamed Loutfi ◽  
Sanaa Ashour ◽  
Eman El-Sharkawy ◽  
Sara El-Fawal ◽  
Karim El-Touny

Assessment of left ventricular (LV) function is important for decision-making and risk stratification in patients with acute coronary syndrome. Many patients with non-ST segment elevation myocardial infarction (NSTEMI) have substantial infarction, but these patients often do not reveal clinical signs of instability, and they rarely fulfill criteria for acute revascularization therapy. Aim This study evaluated the potential of strain Doppler echocardiography analysis for the assessment of LV infarct size when compared with standard two-dimensional echo and cardiac magnetic resonance (CMR) data. Methods Thirty patients with NSTEMI were examined using echocardiography after hospitalization for 1.8 ± 1.1 days for the assessment of left ventricular ejection fraction, wall motion score index (WMSI), and LV global longitudinal strain (GLS). Infarct size was assessed using delayed enhancement CMR 6.97 ± 3.2 days after admission as a percentage of total myocardial volume. Results GLS was performed in 30 patients, and 82.9% of the LV segments were accepted for GLS analysis. Comparisons between patients with a complete set of GLS and standard echo, GLS and CMR were performed. The linear relationship demonstrated moderately strong and significant associations between GLS and ejection fraction (EF) as determined using standard echo ( r = 0.452, P = 0.012), WMSI ( r = 0.462, P = 0.010), and the gold standard CMR-determined EF ( r = 0.57, P < 0.001). Receiver operating characteristic curves were used to analyze the ability of GLS to evaluate infarct size. GLS was the best predictor of infarct size in a multivariate linear regression analysis (β = 1.51, P = 0.027). WMSI >1.125 and a GLS cutoff value of −11.29% identified patients with substantial infarction (≥12% of total myocardial volume measured using CMR) with accuracies of 76.7% and 80%, respectively. However, GLS remained the only independent predictor in a multivariate logistic regression analysis to identify an infarct size ≥12%. Conclusion GLS is a good predictor of infarct size in NSTEMI, and it may serve as a tool in conjunction with risk stratification scores for the selection of high-risk NSTEMI patients.


2018 ◽  
Vol 15 (1) ◽  
pp. 15-21
Author(s):  
Đỗ Hữu Chí ◽  
Nguyễn Thị Minh Phương ◽  
Bùi Thị Huyền ◽  
Nguyễn Tiến Dũng ◽  
Phạm Đình Minh ◽  
...  

Acute Coronary Syndrome (ACS) is one of the foremost causes of mortality and morbidity worldwide as well as Vietnam. ACS was evoked by rupture or erosion of atherosclerotic plaques that was divided into Non–ST-segment elevation Acute Coronary Syndrome (NSTEACS) and ST-segment elevation myocardial infarction groups (STEMI). The matrix metalloproteinase (MMPs) is an enzyme family with fucntioning in the degradation of extracellular matrix and disruption of basement membranes. Of the MMPs, MMP-9 is expressed in the atherosclerotic plaques and plays a key role in the rupture of vulnerable atherosclerotic plaques. In this work, we measured the serum MMP-9 level in 205 patients with acute coronary syndrome (including 103 of NSTE-ACS and 102 of STEMI patients) and 101 healthy participants by sandwich Elisa method. The results showed that the MMP-9 level was significantly higher in NSTE-ACS and STEMI compared to the control group (208.59 ± 100.47 ng/mL, 189.98 ± 112.81 ng/mL vs 168.50 ± 79.52 ng/mL, respectively, P=0.014). However, a logistic regression analysis indicated that the MMP-9 level was only significantly higher in patients with NSTE ACS (OR= 1.0048, CI 95%= 1.000-1.009; P= 0.018). The serum MMP-9 level is correlated with traditional risk factors such as glucose, Cholesterol and Triglyceride by multiple logistic regression analysis. Conclusion: Our study suggests that the serum MMP-9 level is significantly associated with the NSTEACS and is a potential marker for dianogsis of ACS in the Vietnamese patients


2021 ◽  
Vol 10 (22) ◽  
pp. 5445
Author(s):  
Tomasz Fabiszak ◽  
Michał Kasprzak ◽  
Marek Koziński ◽  
Jacek Kubica

Objective: To assess the performance of ten electrocardiographic (ECG) parameters regarding the prediction of left ventricular systolic dysfunction (LVSD) after a first ST-segment-elevation myocardial infarction (STEMI). Methods: We analyzed 249 patients (74.7% males) treated with primary percutaneous coronary intervention (PCI) included into a single-center cohort study. We sought associations between baseline and post-PCI ECG parameters and the presence of LVSD (defined as left ventricular ejection fraction [LVEF] ≤ 40% on echocardiography) 6 months after STEMI. Results: Patients presenting with LVSD (n = 52) had significantly higher values of heart rate, number of leads with ST-segment elevation and pathological Q-waves, as well as total and maximal ST-segment elevation at baseline and directly after PCI compared with patients without LVSD. They also showed a significantly higher prevalence of anterior STEMI and considerably wider QRS complex after PCI, while QRS duration measurement at baseline showed no significant difference. Additionally, patients presenting with LVSD after 6 months showed markedly more severe ischemia on admission, as assessed with the Sclarovsky-Birnbaum ischemia score, smaller reciprocal ST-segment depression at baseline and less profound ST-segment resolution post PCI. In multivariate regression analysis adjusted for demographic, clinical, biochemical and angiographic variables, anterior location of STEMI (OR 17.78; 95% CI 6.45–48.96; p < 0.001), post-PCI QRS duration (OR 1.56; 95% CI 1.22–2.00; p < 0.001) expressed per increments of 10 ms and impaired post-PCI flow in the infarct-related artery (IRA; TIMI 3 vs. <3; OR 0.14; 95% CI 0.04–0.46; p = 0.001) were identified as independent predictors of LVSD (Nagelkerke’s pseudo R2 for the logistic regression model = 0.462). Similarly, in multiple regression analysis, anterior location of STEMI, wider post-PCI QRS, higher baseline number of pathological Q-waves and a higher baseline Sclarovsky-Birnbaum ischemia score, together with impaired post-PCI flow in the IRA, higher values of body mass index and glucose concentration on admission were independently associated with lower values of LVEF at 6 months (corrected R2 = 0.448; p < 0.00001). Conclusions: According to our study, baseline and post-PCI ECG parameters are of modest value for the prediction of LVSD occurrence 6 months after a first STEMI.


2017 ◽  
Vol 22 (6) ◽  
pp. 538-545 ◽  
Author(s):  
Daniel Medeiros Moreira ◽  
Maria Emilia Lueneberg ◽  
Roberto Leo da Silva ◽  
Tammuz Fattah ◽  
Carlos Antonio Mascia Gottschall

Purpose: Methotrexate is an anti-inflammatory drug that has been shown to have anti-ischemic effects. Our aim was to evaluate if methotrexate could reduce infarct size in patients with ST-segment elevation myocardial infarction (STEMI). Methods: We randomly assigned patients with STEMI to receive either methotrexate or placebo. Primary outcome was infarct size determined by calculating the area under the curve (AUC) for creatine kinase (CK) release. Secondary outcomes were AUC of CK MB (CK-MB) and AUC of troponin I; peak CK, peak CK-MB, and troponin I; B-type natriuretic peptide (BNP) level, high-sensitivity C-reactive protein (hsCRP) result, and erythrocyte sedimentation rate (ESR); left ventricular ejection fraction (LVEF); thrombolysis in myocardial infarction (TIMI) frame count; Killip score; mortality and reinfarction incidence; and incidence of adverse reactions. Results: We included 84 patients. Median AUC of CK was 78 861.0 in the methotrexate group and 68 088.0 in the placebo group ( P = .10). Patients given methotrexate and placebo exhibited, respectively, median AUC for CK-MB of 9803.4 and 8037.0 ( P = .42); median AUC for troponin of 3691.1 and 2132.6 ( P = .09); peak CK of 2806.0 and 2147.0 ( P = .05); peak CK-MB of 516.0 and 462.3 ( P = .25); and peak troponin of 121.0 and 85.1 ( P = .06). At 3 months, LVEF was lower in patients who received methotrexate (49.0% ± 14.1%) than in patients given placebo (56.4% ± 10.0%; P = .01). There were no differences in hsCRP, ESR, BNP, Killip scores, TIMI frame count, reinfarction, and mortality rates. There was a higher median serum glutamic–pyruvic transaminase levels in the methotrexate group. Conclusion: Methotrexate did not reduce infarction size and worsened LVEF at 3 months ( Clinicaltrials.gov identifier NCT01741558).


2019 ◽  
Vol 125 (2) ◽  
pp. 245-258 ◽  
Author(s):  
Giampaolo Niccoli ◽  
Rocco A. Montone ◽  
Borja Ibanez ◽  
Holger Thiele ◽  
Filippo Crea ◽  
...  

Primary percutaneous coronary intervention is nowadays the preferred reperfusion strategy for patients with acute ST-segment–elevation myocardial infarction, aiming at restoring epicardial infarct-related artery patency and achieving microvascular reperfusion as early as possible, thus limiting the extent of irreversibly injured myocardium. Yet, in a sizeable proportion of patients, primary percutaneous coronary intervention does not achieve effective myocardial reperfusion due to the occurrence of coronary microvascular obstruction (MVO). The amount of infarcted myocardium, the so-called infarct size, has long been known to be an independent predictor for major adverse cardiovascular events and adverse left ventricular remodeling after myocardial infarction. Previous cardioprotection studies were mainly aimed at protecting cardiomyocytes and reducing infarct size. However, several clinical and preclinical studies have reported that the presence and extent of MVO represent another important independent predictor of adverse left ventricular remodeling, and recent evidences support the notion that MVO may be more predictive of major adverse cardiovascular events than infarct size itself. Although timely and complete reperfusion is the most effective way of limiting myocardial injury and subsequent ventricular remodeling, the translation of effective therapeutic strategies into improved clinical outcomes has been largely disappointing. Of importance, despite the presence of a large number of studies focused on infarct size, only few cardioprotection studies addressed MVO as a therapeutic target. In this review, we provide a detailed summary of MVO including underlying causes, diagnostic techniques, and current therapeutic approaches. Furthermore, we discuss the hypothesis that simultaneously addressing infarct size and MVO may help to translate cardioprotective strategies into improved clinical outcome following ST-segment–elevation myocardial infarction.


Author(s):  
I.А. Mezhiievska

Coronary heart disease remains one of the leading causes of temporary and persistent disability, invalidization and mortality in economically developed countries and is one of the most pressing problems in cardiology. Myocardial infarction is the most common manifestation of coronary heart disease and one of the main causes of the disability and mortality of the working population. The aim is to evaluate the structural and functional status of the myocardium in patients with acute myocardial infarction without ST segment elevation, depending on the plasma level of growth factor-stimulating factor expressed by gene 2 (ST2). 90 patients with acute myocardial infarction without ST segment elevation from 38 to 79 years old were examined. Among them, 60 (66.7%) male patients. Echocardiography assessed the structural and functional status of the myocardium. By enzyme-linked immunosorbent assay determined ST2 levels in blood plasma. It has been determined that myocardial infarction without ST segment elevation is associated with more severe structural left ventricular remodeling, left atrial overload, and decreased left ventricular contractility. In patients, myocardial infarction without ST segment elevation is associated with an increase in cases of left ventricular concentric hypertrophy. Analysis of the nature of diastolic transmitral blood flow showed a significant increase in cases of blood flow by type of pseudonormalization (43.5% versus 8.7%). Therefore, the data obtained showed that in patients with myocardial infarction without ST segment elevation, ST2 elevation was associated with a more frequent manifestation of diastolic transmitral blood flow by type of pseudonormalization. Patients with myocardial infarction without ST segment elevation showed a predominance of systolic dysfunction in the group with relatively high levels of ST2 in the blood plasma, and no significant differences in remodeling types were found in all study groups.


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