scholarly journals 0335: Reduced scar maturation and contractility lead to exaggerated left ventricular dilation after myocardial infarction in mice lacking AMPKα1

2014 ◽  
Vol 6 ◽  
pp. 58
Author(s):  
Cécile Dufeys ◽  
Gauthier Noppe ◽  
Patricia Buchlin ◽  
Nicolas Marquet ◽  
Diego Castanares-Zapatero ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricular ◽  
Ventricular Dilation ◽  
Left Ventricular Dilation ◽  
Scar Maturation

Reduced scar maturation and contractility lead to exaggerated left ventricular dilation after myocardial infarction in mice lacking AMPKα1

2014 ◽  
Vol 74 ◽  
pp. 32-43 ◽  
Author(s):  
Gauthier Noppe ◽  
Cécile Dufeys ◽  
Patricia Buchlin ◽  
Nicolas Marquet ◽  
Diego Castanares-Zapatero ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricular ◽  
Ventricular Dilation ◽  
Left Ventricular Dilation ◽  
Scar Maturation

scholarly journals Exaggerated Left Ventricular Dilation and Reduced Collagen Deposition After Myocardial Infarction in Mice Lacking Osteopontin

2001 ◽  
Vol 88 (10) ◽  
pp. 1080-1087 ◽  
Author(s):  
Nathan A. Trueblood ◽  
Zhonglin Xie ◽  
Catherine Communal ◽  
Flora Sam ◽  
Soeun Ngoy ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricular ◽  
Collagen Deposition ◽  
Ventricular Dilation ◽  
Left Ventricular Dilation

scholarly journals Collateral channels that develop after an acute myocardial infarction prevent subsequent left ventricular dilation

1996 ◽  
Vol 27 (5) ◽  
pp. 1133-1139 ◽  
Author(s):  
Kazuhisa Kodama ◽  
Hideo Kusuoka ◽  
Akihiko Sakai ◽  
Takayoshi Adachi ◽  
Shinji Hasegawa ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Left Ventricular ◽  
Ventricular Dilation ◽  
Left Ventricular Dilation

Reduction of Left Ventricular Dilation Beyond the First Year After Anterior Myocardial Infarction

2019 ◽  
Vol 25 (8) ◽  
pp. 645-653
Author(s):  
Jaume Figueras ◽  
Jordi BaÑeras ◽  
Santiago AguadÉ ◽  
Antonia Sambola ◽  
JosÉ A. BarrabÉs ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricular ◽  
First Year ◽  
Anterior Myocardial Infarction ◽  
Ventricular Dilation ◽  
Left Ventricular Dilation

scholarly journals Interaction of Obesity and Hypertension on Cardiac Metabolic Remodeling and Survival Following Myocardial Infarction

2021 ◽  
Vol 10 (6) ◽  
Author(s):  
Alan J. Mouton ◽  
Elizabeth R. Flynn ◽  
Sydney P. Moak ◽  
Xuan Li ◽  
Alexandre A. da Silva ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Left Ventricular ◽  
Metabolic Changes ◽  
Pulmonary Congestion ◽  
High Fat ◽  
Ventricular Dilation ◽  
Left Ventricular Dilation ◽  
Metabolic Remodeling ◽  
Phosphorylated Akt

Background Obesity and hypertension are risk factors for myocardial infarction (MI); however, their potential interactions on post‐MI outcomes are unclear. We examined interactions of obesity and hypertensionon post‐MI function, remodeling, metabolic changes, and recovery. Methods and Results Male and female C57BL/6J mice were provided standard chow or high‐fat/fructose diet for 8 weeks and then infused with angiotensin II for 2 weeks to induce hypertension. MI was then induced by surgical ligation of the left coronary artery for 7 days. Obesity alone did not cause cardiac injury or exacerbate hypertension‐induced cardiac dysfunction. After MI, however, obese‐normotensive mice had lower survival rates compared with chow‐fed mice (56% versus 89% males; 54% versus 75% females), which were further decreased by hypertension (29% males; and 35% females). Surviving obese‐normotensive males displayed less left ventricular dilation and pulmonary congestion compared with chow‐fed males after MI; hypertension reversed left ventricular dilation because of high‐fat/fructose diet and promoted significant pulmonary congestion compared with chow‐fed controls. Obese‐normotensive males displayed higher left ventricular α‐MHC (alpha‐myosin heavy chain) protein, phosphorylated Akt (protein kinase B) and AMPK (adenosine‐monophosphate activated kinase), PPAR‐γ (peroxisome proliferator activated receptor gamma), and plasma adiponectin levels after MI, indicating favorable contractile and metabolic changes. However, these favorable contractile and metabolic changes were attenuated by hypertension. Obese‐hypertensive males also had lower levels of collagen in the infarcted region, indicating decreased ability to promote an adaptive wound healing response to MI. Conclusions Obesity reduces post‐MI survival but is associated with improved post‐MI cardiac function and metabolism in surviving normotensive mice. When hypertension accompanies obesity, favorable metabolic pathways associated with obesity are attenuated and post‐MI cardiac function and remodeling are adversely impacted.

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