ArticleESC heart failure2015
In vivo and ex vivo functional characterization of left ventricular remodelling after myocardial infarction in mice.
Article in ESC heart failure, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Left ventricle strain and T1 mapping evaluation in a mouse model with myocardial infarction.Scientific reports · 2025Article
- Tenascin-C drives cardiovascular dysfunction in a mouse model of diabetic cardiomyopathy.Cardiovascular diabetology · 2025Article
- The isolated, perfused working heart preparation of the mouse-Advantages and pitfalls.Acta physiologica (Oxford, England) · 2025Review
- Cardioprotection in cardiovascular surgery.Basic research in cardiology · 2024Review
- Tenascin-C aggravates ventricular dilatation and angiotensin-converting enzyme activity after myocardial infarction in mice.ESC heart failure · 2020Article
- Endothelial progerin expression causes cardiovascular pathology through an impaired mechanoresponse.The Journal of clinical investigation · 2019Article
- In Vivo Imaging With Confirmation by Histopathology for Increased Rigor and Reproducibility in Translational Research: A Review of Examples, Options, and Resources.ILAR journal · 2018Article
- In vivo and ex vivo functional characterization of left ventricular remodelling after myocardial infarction in mice.ESC heart failure · 2015Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsThe interest in cardiac remodelling (REM) has steadily increased during recent years. The aim of this study was to functionally characterize REM following myocardial infarction (MI) in mice using high-end in vivo and ex vivo methods. METHODS AND
resultsMyocardial infarction or sham operation was induced in A/J mice. Six weeks later, mice underwent cardiac magnetic resonance imaging and were subsequently sacrificed for ex vivo measurements on the isolated heart. Thereafter, hearts were trichrome stained for infarction size calculation. Magnetic resonance imaging showed significantly reduced ejection fraction (P < 0.01) as well as increased end-systolic and end-diastolic volumes (P < 0.01) after MI. The mean infarct size was 48.8 ± 6.9% of left ventricle. In the isolated working heart coronary flow (time point 20': 6.6 ± 0.9 vs. 13.9 ± 1.6 mL/min, P < 0.01), cardiac output (time point 20': 17.5 ± 2.6 vs. 36.1 ± 4.3 mL/min, P < 0.01) and pump function (80 mmHg: 2.15 ± 0.88 vs. 4.83 ± 0.76, P < 0.05) were significantly attenuated in MI hearts during all measurements. Systolic and diastolic wall stress were significantly elevated in MI animals.
conclusionThis two-step approach is reasonable, since data quality increases while animals are not exposed to major additional interventions. Both the working heart and magnetic resonance imaging offer a reliable characterization of the functional changes that go along with the development of post-MI REM. By combining these two techniques, additional information such as wall stress can be evaluated.
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