A Mixed Component Supramolecular Hydrogel to Improve Mice Cardiac Function and Alleviate Ventricular Remodeling after Acute Myocardial Infarction

2017 ◽  
Vol 27 (34) ◽  
pp. 1701798 ◽  
Author(s):  
Guoqin Chen ◽  
Jinliang Li ◽  
Mingcai Song ◽  
Zhiye Wu ◽  
Wenzhu Zhang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Function ◽  
Ventricular Remodeling ◽  
Supramolecular Hydrogel ◽  
Mixed Component

scholarly journals Colchicine Improves Survival, Left Ventricular Remodeling, and Chronic Cardiac Function After Acute Myocardial Infarction

2017 ◽  
Vol 81 (8) ◽  
pp. 1174-1182 ◽  
Author(s):  
Koichiro Fujisue ◽  
Koichi Sugamura ◽  
Hirofumi Kurokawa ◽  
Junichi Matsubara ◽  
Masanobu Ishii ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Function ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular

scholarly journals Endothelial Cell Indoleamine 2, 3-Dioxygenase 1 Alters Cardiac Function Following Myocardial Infarction Through Kynurenine

Circulation ◽  
2020 ◽  
Author(s):  
Nada Joe Melhem ◽  
Mouna Chajadine ◽  
Ingrid Gomez ◽  
Kiave-Yune Howangyin ◽  
Marion Bouvet ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Smooth Muscle ◽  
Endothelial Cell ◽  
Cardiac Function ◽  
Smooth Muscle Cells ◽  
Ventricular Remodeling ◽  
Muscle Cells ◽  
Protective Effects ◽  
Indoleamine 2

Background: Ischemic cardiovascular diseases, particularly acute myocardial infarction (MI) is one of the leading cause of mortality worldwide. Indoleamine 2, 3-dioxygenase 1 (IDO) catalyzes one rate-limiting step of L-Tryptophan (Trp) metabolism, and emerges as an important regulator of many pathological conditions. We hypothesized that IDO could play a key role to locally regulate cardiac homeostasis after MI. Methods: Cardiac repair was analyzed in mice harboring specific endothelial or smooth muscle cells or cardiomyocyte or myeloid cell deficiency of IDO and challenged with acute myocardial infarction. Results: We show that Kynurenine (Kyn) generation through IDO is markedly induced after MI in mice. Total genetic deletion or pharmacological inhibition of IDO limits cardiac injury and cardiac dysfunction after MI. Distinct loss of function of IDO in smooth muscle cells, inflammatory cells, or cardiomyocytes does not impact cardiac function and remodeling in infarcted mice. In sharp contrast, mice harboring endothelial cell-specific deletion of IDO show an improvement of cardiac function, as well as cardiomyocyte contractility and reduction in adverse ventricular remodeling. In vivo Kyn supplementation in IDO-deficient mice abrogates the protective effects of IDO deletion. Notably, Kyn precipitates cardiomyocyte apoptosis through reactive oxygen species production in an aryl hydrocarbon receptor-dependent mechanism. Conclusions: These data suggest that IDO could constitute a new therapeutic target during acute MI.

scholarly journals Association of ADAMTS-7 Levels with Cardiac Function in a Rat Model of Acute Myocardial Infarction

2016 ◽  
Vol 38 (3) ◽  
pp. 950-958 ◽  
Author(s):  
Wenjing Wu ◽  
Hui Wang ◽  
Changan Yu ◽  
Jiahui Li ◽  
Yanxiang Gao ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Function ◽  
Matrix Protein ◽  
Ventricular Remodeling ◽  
Structural Parameters ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Post Surgery

Background/Aims: High ADAMTS-7 levels are associated with acute myocardial infarction (AMI), although its involvement in ventricular remodeling is unclear. In this study, we investigated the association between ADAMTS-7 expression and cardiac function in a rat AMI model. Methods: Sprague-Dawley rats were randomized into AMI (n = 40) and sham (n = 20) groups. The left anterior descending artery was sutured to model AMI. Before surgery and 7, 14, 28, and 42 days post-surgery, ADAMTS-7 and brain natriuretic peptide (BNP), and cartilage oligomeric matrix protein (COMP) were assessed by ELISA, western blot, real-time RT-PCR, and/or immunohistochemistry. Cardiac functional and structural parameters were assessed by M-mode echocardiography. Results: After AMI, plasma ADAMTS-7 levels increased, peaking on day 28 (AMI: 13.2 ± 6.3 vs. sham: 3.4 ± 1.3 ng/ml, P < 0.05). Compared with the sham group, ADAMTS-7 expression was higher in the infarct zone at day 28. COMP present in normal myocardium was degraded by day 28 post-AMI. Plasma ADAMTS-7 correlated positively with BNP (r = 0.642, P = 0.025), left ventricular end-diastolic diameter (r = 0.695, P = 0.041), left ventricular end-systolic diameter (r = 0.710, P = 0.039), left ventricular ejection fraction (r = 0.695, P = 0.036), and left ventricular short-axis fractional shortening (r = 0.721, P = 0.024). Conclusions: ADAMTS-7 levels may reflect the degree of ventricular remodeling after AMI.

Predictors of Left Ventricular Remodeling Post Acute Myocardial Infarction. Protocol for a Clinical Study

2019 ◽  
Vol 4 (3) ◽  
pp. 120-123
Author(s):  
Ioana Cîrneală ◽  
Diana Opincariu ◽  
István Kovács ◽  
Monica Chițu ◽  
Imre Benedek
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Speckle Tracking ◽  
Ventricular Remodeling ◽  
Speckle Tracking Echocardiography ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Serum Biomarkers ◽  
Remodeling Index

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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