Mouse models of myocardial infarction are essential tools for the study of cardiac injury, repair, and remodeling. Our current investigation establishes a systematic approach for quantitative evaluation of the inflammatory and reparative response, cardiac function, and geometry in a mouse model of reperfused myocardial infarction. Reperfused mouse infarcts exhibited marked induction of inflammatory cytokines that peaked after 6 hr of reperfusion. In the infarcted heart, scar contraction and chamber dilation continued for at least 28 days after reperfusion; infarct maturation was associated with marked thinning of the scar, accompanied by volume loss and rapid clearance of cellular elements. Echocardiographic measurements of end-diastolic dimensions correlated well with morphometric assessment of dilative remodeling in perfusion-fixed hearts. Hemodynamic monitoring was used to quantitatively assess systolic and diastolic function; the severity of diastolic dysfunction following myocardial infarction correlated with cardiomyocyte hypertrophy and infarct collagen content. Expression of molecular mediators of inflammation and cellular infiltration needs to be investigated during the first 72 hr, whereas assessment of dilative remodeling requires measurement of geometric parameters for at least four weeks after the acute event. Rapid initiation and resolution of the inflammatory response, accelerated scar maturation, and extensive infarct volume loss are important characteristics of infarct healing in mice.
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http://dx.doi.org/10.1369/0022155413493912 | DOI Listing |
Eur J Prev Cardiol
January 2025
Department of Occupational and Environmental Medicine, Bispebjerg Hospital, Copenhagen, Denmark.
Aims: Exposure to air pollution including diesel engine exhaust (DEE) is associated with increased risk of acute myocardial infarction (AMI). Few studies have investigated the risk of AMI according to occupational exposure to DEE. The aim of this study was to evaluate the association between occupational exposure to DEE and the risk of first-time AMI.
View Article and Find Full Text PDFJ Cardiothorac Surg
January 2025
Department of General Internal Medicine, Hangzhou Xixi Hospital, Hangzhou Sixth People's Hospital, Hangzhou Xixi Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, 310023, China.
Background: Gout is a metabolic disease caused by decreased blood uric acid excretion and purine metabolism disorders. Long-term and persistent metabolic dysfunction gradually affects other organ functions and is the main factor inducing Myocardial Infarction (MI) and Heart Failure (HF), seriously affecting the health of patients. This study adopts a meta-analysis to analyze the risk of MI and HF in gout patients.
View Article and Find Full Text PDFCell Commun Signal
January 2025
Department of Vascular & Cardiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Purpose: Cardiomyocyte death is a major cytopathologic response in acute myocardial infarction (AMI) and involves complex inflammatory interactions. Although existing reports indicating that mixed lineage kinase domain-like protein (MLKL) is involved in macrophage necroptosis and inflammasome activation, the downstream mechanism of MLKL in necroptosis remain poorly characterized in AMI.
Methods: MLKL knockout mice (MLKL), RIPK3 knockout mice (RIPK3), and macrophage-specific MLKL conditional knockout mice (MLKL) were established.
BMC Public Health
January 2025
Grupo de Investigación en Servicios Sanitarios de Aragón (GRISSA), Fundación Instituto de Investigación Sanitaria de Aragón (IIS Aragón), Zaragoza, Spain.
Background: European guidelines recommend the prescription of certain drugs after acute myocardial infarction (AMI). The existence of gender differences in pharmacological treatment after an AMI has been described. This study aims to describe and analyse, using real-world data (RWD), whether there are gender differences in the prescribing patterns and initiation of treatment in secondary prevention after a first AMI, and which are the factors that explain these differences.
View Article and Find Full Text PDFBMC Anesthesiol
January 2025
Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Anesthesiology and Intensive Care Medicine, Campus Benjamin Franklin, Hindenburgdamm 30, Berlin, 12203, Germany.
Background: Postcardiotomy cardiogenic shock (PCCS) in cardiac surgery is associated with a high rate of morbidity and mortality. Beside other therapeutic measures (e.g.
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