Myocardial Fibrosis
Myocardial Fibrosis - Related Videos
11:12
Induction of Myocardial Infarction in Adult Zebrafish Using Cryoinjury
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Cited by 63 •
2012
Zebrafish represents a valuable model to study the mechanisms of heart regeneration in vertebrates. Here, we present a protocol for induction of a heart infarct in adult zebrafish using cryoinjury. This method results in massive cell death within 20% of the ventricular wall, similar to that observed in mammalian infarcts.
07:45
Acute Myocardial Infarction in Rats
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Cited by 103 •
2011
The rat model of acute myocardial infarction (AMI) is useful to study the consequence of a MI on cardiac pathophysiological and physiological function.
08:23
LAD-Ligation: A Murine Model of Myocardial Infarction
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Cited by 81 •
2009
This video demonstrates how to use a fast and reliable model to study pathobiological and pathophysiological processes of myocardial ischemia.
09:45
Histological Quantification of Chronic Myocardial Infarct in Rats
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Cited by 14 •
2016
The post-mortem assessment of myocardial infarction (MI) in rodents is based on quantification of the infarct on stained heart sections. We describe an accurate method to quantify the infarct size using systematic sampling of harvested rat hearts from base to apex and image analyses of trichrome-stained histological sections.
07:48
Myocardial Infarction in Neonatal Mice, A Model of Cardiac Regeneration
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Cited by 37 •
2016
This protocol describes a highly reproducible model of cardiac regeneration by surgical induction of myocardial infarction in the left ventricle of postnatal day 1 mice. The method involves induction of hypothermic anesthesia and ligation of the left anterior descending coronary artery.
FAQs
Persistent injury or stress activates cardiac fibroblasts, the cells responsible for producing extracellular-matrix proteins. These cells can increase production of collagen, causing matrix accumulation within the myocardium. This response may initially accompany tissue repair, but continued activation promotes maladaptive remodeling that can reduce myocardial performance and alter the structural environment surrounding surviving cardiomyocytes.
Replacement fibrosis develops where myocardial cells have been lost, with fibrous tissue occupying the damaged region. Interstitial fibrosis instead increases the connective tissue between surviving cardiomyocytes, thickening spaces that normally support myocardial structure. Distinguishing these patterns helps explain how different forms of remodeling may influence cardiac function and the heart’s electrical stability.
Fibrotic remodeling can disrupt the organized structural environment required for stable electrical activity in cardiac muscle. Areas of cell loss, collagen accumulation, or thickened interstitial spaces may therefore accompany reduced electrical stability. In clinical medicine, detecting this remodeling is relevant because fibrosis can help estimate arrhythmia risk alongside the possibility of progressive heart failure.
Cardiac magnetic resonance imaging, tissue analysis, and circulating biomarkers provide complementary ways to identify myocardial fibrosis. Imaging can support assessment within the heart, tissue analysis can examine structural changes directly, and blood-based biomarkers can provide circulating evidence associated with remodeling. Together, these approaches help clarify disease progression and support risk estimation.
Evaluation combines evidence of fibrotic remodeling with the broader clinical question of how the heart is changing over time. Cardiac magnetic resonance imaging, tissue analysis, and circulating biomarkers can each contribute information about fibrosis. Their use helps clinicians and researchers connect structural remodeling with myocardial performance and estimate risks related to heart failure or arrhythmias.
Therapeutic research focuses on limiting maladaptive remodeling rather than allowing persistent fibroblast activity and collagen accumulation to compromise the myocardium. Studying the mechanisms that drive fibrosis may reveal ways to preserve myocardial performance and reduce downstream electrical or functional instability. This makes fibrosis relevant both as a marker of disease progression and as a potential treatment target.