scholarly journals Development of a Closed Chest Model of Chronic Myocardial Infarction in Swine: Magnetic Resonance Imaging and Pathological Evaluation

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Verónica Crisóstomo ◽  
Juan Maestre ◽  
Manuel Maynar ◽  
Fei Sun ◽  
Claudia Báez-Díaz ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Function ◽  
Ethanol Administration ◽  
Chronic Myocardial Infarction ◽  
Therapeutic Approaches ◽  
Closed Chest ◽  
Postoperative Mri ◽  
Pathological Evaluation ◽  
And Training ◽  
Over Time

Our aim was to develop an easy-to-induce, reproducible, and low mortality clinically relevant closed-chest model of chronic myocardial infarction in swine using intracoronary ethanol and characterize its evolution using MRI and pathology. We injected 3-4 mL of 100% ethanol into the mid-LAD of anesthetized swine. Heart function and infarct size were assessed serially using MRI. Pigs were euthanized on days 7, 30, and 90 (n=5 at each timepoint). Postoperative MRI revealed compromised contractility and decreased ejection fraction, from 53.8% ± 6.32% to 43.79% ± 7.72% (P=0.001). These values remained lower than baseline thorough the followup (46.54% ± 11.12%, 44.48% ± 7.77%, and 40.48% ± 6.40%, resp., P<0.05). Progressive remodeling was seen in all animals. Infarcted myocardium decreased on the first 30 days (from 18.09% ± 7.26% to 9.9% ± 5.68%) and then stabilized (10.2% ± 4.21%). Pathology revealed increasing collagen content and fibrous organization over time, with a rim of preserved endocardial cells. In conclusion, intracoronary ethanol administration in swine consistently results in infarction. The sustained compromise in heart function and myocardial thinning over time indicate that the model may be useful for the preclinical evaluation of and training in therapeutic approaches to heart failure.

Noncontact Mapping of Ventricular Tachycardia in a Closed-Chest Animal Model of Chronic Myocardial Infarction

2003 ◽  
Vol 26 (12) ◽  
pp. 2253-2263 ◽  
Author(s):  
SVEN REEK ◽  
J. CHRISTOPH GELLER ◽  
ANTJE MITTAG ◽  
FRANK GROTHUES ◽  
ANDREAS HESS ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Animal Model ◽  
Ventricular Tachycardia ◽  
Chronic Myocardial Infarction ◽  
Closed Chest ◽  
Noncontact Mapping

Aerobic training prior to myocardial infarction increases cardiac GLUT4 and partially preserves heart function in spontaneously hypertensive rats

2017 ◽  
Vol 42 (3) ◽  
pp. 334-337 ◽  
Author(s):  
Maximiliano Isoppo Schaun ◽  
Rafael Aguiar Marschner ◽  
Thiago Rodrigues Peres ◽  
Melissa Medeiros Markoski ◽  
Alexandre Machado Lehnen
Keyword(s):  
Myocardial Infarction ◽  
Spontaneously Hypertensive Rats ◽  
Glucose Transporter ◽  
Aerobic Training ◽  
Heart Function ◽  
Glucose Transporter 4 ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Glut4 Expression ◽  
And Training

We assessed cardiac function (echocardiographic) and glucose transporter 4 (GLUT4) expression (Western blot) in response to 10 weeks of aerobic training (treadmill) prior to acute myocardial infarction (AMI) by ligation of the left coronary artery in spontaneously hypertensive rats. Animals were allocated to sedentary+sham, sedentary+AMI, training+sham, and training+AMI. Aerobic training prior to AMI partially preserves heart function. AMI and/or aerobic training increased GLUT4 expression. However, those animals trained prior to AMI showed a greater increase in GLUT4 in cardiomyocytes.

Nucleolin Improves Heart Function During Recovery From Myocardial Infarction by Modulating Macrophage Polarization

2021 ◽  
pp. 107424842198957
Author(s):  
Yuting Tang ◽  
Xiaofang Lin ◽  
Cheng Chen ◽  
Zhongyi Tong ◽  
Hui Sun ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Early Phase ◽  
Heart Function ◽  
Macrophage Polarization ◽  
Late Phase ◽  
Macrophage Infiltration ◽  
Enzyme Linked Immunosorbent Assay ◽  
M2 Macrophage ◽  
M2 Macrophage Polarization ◽  
Nucleolin Expression

Background: Nucleolin has multiple functions within cell survival and proliferation pathways. Our previous studies have revealed that nucleolin can significantly reduce myocardial ischemia-reperfusion injury by promoting myocardial angiogenesis and reducing myocardial apoptosis. In this study, we attempted to determine the role of nucleolin in myocardial infarction (MI) injury recovery and the underlying mechanism. Methods: Male BALB/c mice aged 6–8 weeks were used to set up MI models by ligating the left anterior descending coronary artery. Nucleolin expression in the heart was downregulated by intramyocardial injection of a lentiviral vector expressing nucleolin-specific small interfering RNA. Macrophage infiltration and polarization were measured by real-time polymerase chain reaction, flow cytometry, and immunofluorescence. Cytokines were detected by enzyme-linked immunosorbent assay. Results: Nucleolin expression in myocardium after MI induction decreased a lot at early phase and elevated at late phase. Nucleolin knockdown impaired heart systolic and diastolic functions and decreased the survival rate after MI. Macrophage infiltration increased in the myocardium after MI. Most macrophages belonged to the M1 phenotype at early phase (2 days) and the M2 phenotype increased greatly at late phase after MI. Nucleolin knockdown in the myocardium led to a decrease in M2 macrophage polarization with no effect on macrophage infiltration after MI. Furthermore, Notch3 and STAT6, key regulators of M2 macrophage polarization, were upregulated by nucleolin in RAW 264.7 macrophages. Conclusions: Lack of nucleolin impaired heart function during recovery after MI by reducing M2 macrophage polarization. This finding probably points to a new therapeutic option for ischemic heart disease.

scholarly journals Trends in mortality, co-morbidity and treatment after acute myocardial infarction in patients with rheumatoid arthritis 1998–2013

2020 ◽  
Vol 9 (8) ◽  
pp. 931-938 ◽  
Author(s):  
Mattias Skielta ◽  
Lars Söderström ◽  
Solbritt Rantapää-Dahlqvist ◽  
Solveig W Jonsson ◽  
Thomas Mooe
Keyword(s):  
Rheumatoid Arthritis ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Atrial Fibrillation ◽  
Acute Myocardial Infarction ◽  
Congestive Heart Failure ◽  
Cox Regression Analysis ◽  
Co Morbidity ◽  
One Year ◽  
Over Time

Aims: Rheumatoid arthritis may influence the outcome after an acute myocardial infarction. We aimed to compare trends in one-year mortality, co-morbidities and treatments after a first acute myocardial infarction in patients with rheumatoid arthritis versus non-rheumatoid arthritis patients during 1998–2013. Furthermore, we wanted to identify characteristics associated with mortality. Methods and results: Data for 245,377 patients with a first acute myocardial infarction were drawn from the Swedish Register of Information and Knowledge about Swedish Heart Intensive Care Admissions for 1998–2013. In total, 4268 patients were diagnosed with rheumatoid arthritis. Kaplan-Meier analysis was used to study mortality trends over time and multivariable Cox regression analysis was used to identify variables associated with mortality. The one-year mortality in rheumatoid arthritis patients was initially lower compared to non-rheumatoid arthritis patients (14.7% versus 19.7%) but thereafter increased above that in non-rheumatoid arthritis patients (17.1% versus 13.5%). In rheumatoid arthritis patients the mean age at admission and the prevalence of atrial fibrillation increased over time. Congestive heart failure decreased more in non-rheumatoid arthritis than in rheumatoid arthritis patients. Congestive heart failure, atrial fibrillation, kidney failure, rheumatoid arthritis, prior diabetes mellitus and hypertension were associated with significantly higher one-year mortality during the study period 1998–2013. Conclusions: The decrease in one-year mortality after acute myocardial infarction in non-rheumatoid arthritis patients was not applicable to rheumatoid arthritis patients. This could partly be explained by an increased age at acute myocardial infarction onset and unfavourable trends with increased atrial fibrillation and congestive heart failure in rheumatoid arthritis. Rheumatoid arthritis per se was associated with a significantly worse prognosis.

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