Rheolityc thrombectomy in acute myocardial infarction: Effect on microvascular obstruction, infarct size, and left ventricular remodeling

2015 ◽  
Vol 87 (1) ◽  
pp. E1-E8 ◽  
Author(s):  
Nazario Carrabba ◽  
Guido Parodi ◽  
Akiko Maehara ◽  
Silvia Pradella ◽  
Angela Migliorini ◽  
...  
2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Zequan Yang ◽  
Yikui Tian ◽  
Stuart S. Berr ◽  
Brent A. French

Background. We hypothesized that daily administration of a potent antioxidant (α-lipoic acid: ALA) would protect the heart against both acute myocardial infarction (AMI) and left ventricular remodeling (LVR) post-AMI. Methods and Results. Two separate studies were conducted. In the AMI study, C57Bl/6 mice were fed ALA daily for 7 d prior to a 45-minute occlusion of the left coronary artery (LCA). Mean infarct size in control mice (fed water) was 60 ± 2%. Mean infarct size in ALA-treated mice was 42 ± 3% in the 15 mg/kg·d group and 39 ± 3% in the 75 mg/kg·d group (both P<0.05 vs. control). In the LVR study, AMI increased LV end-systolic volume (LVESV) and reduced LV ejection fraction (LVEF) to a similar extent in both groups when assessed by cardiac MRI 1 day after a 2-hour LCA occlusion. Treatment with ALA (75 mg/kg·d) or H2O was initiated 1 day post-AMI and continued until study’s end. Both LVESV and LVEF in ALA-treated mice were significantly improved over control when assessed 28 or 56 days post-AMI. Furthermore, the survival rate in ALA-treated mice was 63% better than in control mice by 56 days post-AMI. Conclusions. Daily oral ingestion of ALA not only protects mice against AMI but also attenuates LVR and preserves contractile function in the months that follow.


2009 ◽  
Vol 104 (9) ◽  
pp. 1179-1183 ◽  
Author(s):  
Stein Ørn ◽  
Unni M. Breland ◽  
Tom Eirik Mollnes ◽  
Cord Manhenke ◽  
Kenneth Dickstein ◽  
...  

1995 ◽  
Vol 25 (3) ◽  
pp. 567-573 ◽  
Author(s):  
Panithaya Chareonthaitawee ◽  
Timothy F. Christian ◽  
Ken Hirose ◽  
Raymond J. Gibbons ◽  
John A. Rumberger

Circulation ◽  
2000 ◽  
Vol 101 (23) ◽  
pp. 2734-2741 ◽  
Author(s):  
Bernhard L. Gerber ◽  
Carlos E. Rochitte ◽  
Jacques A. Melin ◽  
Elliot R. McVeigh ◽  
David A. Bluemke ◽  
...  

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.


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