scholarly journals Usefulness of serial post-systolic shortening by speckle tracking echocardiography to predict major adverse cardiovascular events and segmental function improvement after acute myocardial infarction

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0244589
Author(s):  
Ju-Feng Hsiao ◽  
Kuo-Li Pan ◽  
Chi-Ming Chu ◽  
Shih-Tai Chang ◽  
Chang-Min Chung ◽  
...  

Purpose The aim is to determine whether serial post-systolic shortening (PSS) using speckle tracking echocardiography (STE) could predict major adverse cardiovascular events (MACE), especially symptom-driven infarct-related artery (IRA) revascularization and improvement in segmental function in post-myocardial infarction patients. Methods/Results Ninety-four patients (average age 61.1 ± 12.5 y, 84 [84.9%] male) with new-onset acute myocardial infarction were enrolled. Serial echocardiography was performed during the initial presentation, and at 3, 6 and 12 months after admission. PSS, strain and systolic strain rate were calculated using STE. Improvement in segmental function was defined as a decrease of ≧1 grade in wall motion score. During the follow-up (29.4 ± 12.7months), 22 patients (23.4%) had MACE and 17 patients had symptom-driven IRA revascularization. In multivariate model, PSS at 3 months was independently predictive for symptom-driven IRA revascularization (Hazard ratio (HR) = 0.5, 95% CI = 0.26–0.97) and for MACE (HR = 0.4, 95% CI = 0.24–0.67) (p < 0.05). Segmental function improvements were found in 255 segments (66.1%) and ROC curve analyses showed that AUC (95% CI) of the initial PSS was 0.7(0.65–0.77) (cut-off values = -1.08, sensitivity = 58%, specificity = 73% specificity). Conclusions Post-systolic shortening at 3 months is an independent predictor for symptom-driven IRA revascularization and MACE. Regional wall motion recovery also could be predicted by initial PSS. Serial assessment of two-dimensional STE should be investigated in post-myocardial infarction patients in the future.

2019 ◽  
Vol 4 (3) ◽  
pp. 120-123
Author(s):  
Ioana Cîrneală ◽  
Diana Opincariu ◽  
István Kovács ◽  
Monica Chițu ◽  
Imre Benedek

Abstract Heart failure is a clinical syndrome that appears as a consequence of a structural disease, and the most common cause of left ventricular systolic dysfunction results from myocardial ischemia. Cardiac remodeling and neuroendocrine activation are the major compensatory mechanisms in heart failure. The main objective of the study is to identify the association between serum biomarkers illustrating the extent of myocardial necrosis (highly sensitive troponin as-says), left ventricular dysfunction (NT-proBNP), and systemic inflammatory response (illustrated via serum levels of hsCRP and interleukins) during the acute phase of a myocardial infarction, and the left ventricular remodeling process at 6 months following the acute event, quantified via speckle tracking echocardiography. The study will include 400 patients diagnosed with acute myocardial infarction without signs and symptoms of heart failure at the time of enrollment that will undergo a complex clinical examination and speckle tracking echocardiography. Serum samples from the peripheral blood will be collected in order to determine the inflammatory serum biomarkers. After 6 months, patients will be divided into 2 groups according to the development of ventricular remodeling, quantified by speckle tracking echocardiography: group 1 will consist of patients with a remodeling index lower than 15%, and group 2 will consist of patients with a remodeling index higher than 15%. All clinical and imaging data obtained at the baseline will be compared between these two groups in order to determine the features associated with a higher risk of deleterious ventricular remodeling and heart failure.


1986 ◽  
Vol 58 (6) ◽  
pp. 406-410 ◽  
Author(s):  
Nagara Tamaki ◽  
Tsunehiro Yasuda ◽  
Robert C. Leinbach ◽  
Herman K. Gold ◽  
Kenneth A. McKusick ◽  
...  

2014 ◽  
Vol 32 (3) ◽  
pp. 454-460 ◽  
Author(s):  
Maciej Haberka ◽  
Jerzy Liszka ◽  
Andrzej Kozyra ◽  
Maciej Finik ◽  
Zbigniew Gąsior

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C X Song ◽  
R Fu ◽  
J G Yang ◽  
K F Dou ◽  
Y J Yang

Abstract Background Controversy exists regarding the use of beta-blockers (BBs) among patients with acute myocardial infarction (AMI) in contemporary reperfusion era. Previous studies predominantly focused on beta-blockers prescribed at discharge, and the effect of long-term adherence to beta-blocker on major adverse cardiovascular events (MACE) remains unclear. Objective To explore the association between long-term beta-blocker use patterns and MACE among contemporary AMI patients. Methods We enrolled 7860 patients with AMI, who were discharged alive and prescribed with BBs based on CAMI registry from January 2013 to September 2014. Patients were divided into two groups according to BBs use pattern: Always users group (n=4476) were defined as patients reporting BBs use at both 6- and 12-month follow-up; Inconsistent users group were defined as patients reporting at least once not using BBs at 6- or 12-month follow-up. Primary outcome was defined as MACE at 24-month follow-up, including all-cause death, non-fatal MI and repeat-revascularization. Multivariable cox proportional hazards regression model was used to assess the association between BBs and MACE. Results Baseline characteristics are shown in table 1. At 2-year follow-up, 518 patients in inconsistent users group (15.6%) and 548 patients in always users group (12.3%) had MACE. After multivariable adjustment, inconsistent use of BBs was associated with higher risk of MACE (HR: 1.323, 95% CI: 1.171–1.493, p<0.001). Table 1 Baseline characteristics Variable Always user (N=4476) Inconsistent user (N=3384) P value Age (years) 60.6±12.0 61.2±12.2 <0.001 Male 3381 (75.7%) 2461 (74.3%) 0.084 Diabetes 892 (20.0%) 610 (18.4%) 0.003 Hypertension 2372 (53.2%) 1543 (46.6%) <0.001 Dyslipidemia 244 (5.5%) 126 (3.8%) <0.001 Prior myocardial infarction 351 (7.9%) 232 (7.0%) <0.001 Heart failure 88 (2.0%) 63 (1.9%) <0.001 Chronic obstructive pulmonary disease 66 (1.5%) 60 (1.8%) <0.001 Current smoker 2054 (46.1%) 1579 (47.8%) 0.179 Left ventricular ejection fraction (%) 53.7±11.48 54.0±10.9 <0.001 Major Adverse Cardiovascular Events 548 (12.3%) 518 (15.6%) <0.001 Conclusions Our results showed consistent BBs use was associated with reduced risk of MACE among patients with AMI managed by contemporary treatment. Acknowledgement/Funding CAMS Innovation Fund for Medical Sciences (CIFMS) (2016-I2M-1-009)


2017 ◽  
Vol 4 (4) ◽  
pp. 926
Author(s):  
Anjali V. Shivpuje ◽  
Shrikant Page

Background:2D Echo can evaluate LV anatomy, function and diagnose post AMI complications in early stages, thus help in management and determining the prognosis. The present study was undertaken to evaluate LV function in patient following AMI and also to find out the incidence of various echocardiographically detectable complications of following AMI.Methods: The present study was conducted on patients visiting our tertiary health centre during study duration. 50 patients were included in the study. Patients with prior history of acute myocardial infarction, pericarditis and early repolarisation syndrome, and primary myocardial disease diagnosed by serum enzyme levels were not included in the study. Patients were classified as per Killip classification and 2D echo study was performed in all patients.Results: Maximum incidence of AMI was found in 51-60 years of age, with male predominance (64%). Anterior wall AMI (58%) was more common. 94% of patients had wall motion abnormalities. Incidence of LV thrombus was found to be 24%. In present study, as the extent and severity of wall motion abnormalities increased, the incidence of LV thrombus also increased. Thus, 2DE study of LV regional wall motion can predict the incidence of LV thrombus.Conclusions: The echocardiographic assessment of LV function in patients of AMI is important as, it detects the regional wall motion abnormality, LVEF and also the complications like LV thrombus, pericardial effusion and LV aneurysm. These observations are of great value in the management of AMI.  


Circulation ◽  
2019 ◽  
Vol 140 (9) ◽  
pp. 751-764 ◽  
Author(s):  
Yulin Li ◽  
Boya Chen ◽  
Xinying Yang ◽  
Congcong Zhang ◽  
Yao Jiao ◽  
...  

Background: Myocardial ischemia-reperfusion (MI/R) injury is a significant clinical problem without effective therapy. Unbiased omics approaches may reveal key MI/R mediators to initiate MI/R injury. Methods: We used a dynamic transcriptome analysis of mouse heart exposed to various MI/R periods to identify S100a8/a9 as an early mediator. Using loss/gain-of-function approaches to understand the role of S100a8/a9 in MI/R injury, we explored the mechanisms through transcriptome and functional experiment. Dynamic serum S100a8/a9 levels were measured in patients with acute myocardial infarction before and after percutaneous coronary intervention. Patients were prospectively followed for the occurrence of major adverse cardiovascular events. Results: S100a8/a9 was identified as the most significantly upregulated gene during the early reperfusion stage. Knockout of S100a9 markedly decreased cardiomyocyte death and improved heart function, whereas hematopoietic overexpression of S100a9 exacerbated MI/R injury. Transcriptome/functional studies revealed that S100a8/a9 caused mitochondrial respiratory dysfunction in cardiomyocytes. Mechanistically, S100a8/a9 downregulated NDUF gene expression with subsequent mitochondrial complex I inhibition via Toll-like receptor 4/Erk–mediated Pparg coactivator 1 alpha/nuclear respiratory factor 1 signaling suppression. Administration of S100a9 neutralizing antibody significantly reduced MI/R injury and improved cardiac function. Finally, we demonstrated that serum S100a8/a9 levels were significantly increased 1 day after percutaneous coronary intervention in patients with acute myocardial infarction, and elevated S100a8/a9 levels were associated with the incidence of major adverse cardiovascular events. Conclusions: Our study identified S100a8/a9 as a master regulator causing cardiomyocyte death in the early stage of MI/R injury via the suppression of mitochondrial function. Targeting S100a8/a9-intiated signaling may represent a novel therapeutic intervention against MI/R injury. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT03752515


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