Left Ventricle Remodeling
Left Ventricle Remodeling - Related Videos
02:37
Surgical Aortic Debanding: A Procedure to Study Left Ventricular Reverse Remodeling in Murine Model of Aortic Constriction
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2025
This video demonstrates the technique of aortic debanding, which can lead to reverse remodeling to limit the progression towards heart failure in a murine model. Post debanding, a significant reduction of ventricular afterload triggers regression of ventricular hypertrophy and fibrosis, causing a recovery in cardiac function.
04:38
Transverse Aortic Arch Banding in Mouse Model: A Minimally Invasive Technique in Mice for Induction of High Pressure in the Left Ventricle
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2025
In this video, we demonstrate an experimental protocol for minimally invasive transverse aortic constriction in mice to examine pressure overload-induced heart failure.
02:54
Nucleosome Remodeling
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2020
Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure. Nucleosome remodeling complex Eukaryotic cells have specialized enzymes called ATP-dependent nucleosome remodeling enzymes. These enzymes...
07:26
Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents
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Cited by 2 •
2021
Here we describe a step-by-step protocol of surgical aorta debanding in the well-established mice model of aortic-constriction. This procedure not only allows studying the mechanisms underlying the left ventricular reverse remodeling and regression of hypertrophy but also to test novel therapeutic options that might accelerate myocardial recovery.
08:28
Zebrafish Brain Ventricle Injection
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Cited by 72 •
2009
After neural tube formation, the neuroepithelium constricts and folds while the tube fills with embryonic cerebrospinal fluid (eCSF) to form the embryonic brain ventricles. We developed this ventricle injection technique to better visualize the fluid filled space in contrast to the neuroepithelial shape in a live embryo.
FAQs
Pressure overload, such as that associated with hypertension, can promote concentric hypertrophy, characterized by increased wall thickness. Volume overload can instead favor ventricular dilation, in which chamber size increases. These patterns reflect different mechanical stresses on the ventricle and may alter contractility and pumping performance in distinct ways, helping clinicians interpret structural changes in disease.
Increased wall stress and neurohormonal signaling can drive structural and functional changes beyond the original cardiac injury or loading condition. Their effects may influence ventricular size, shape, wall thickness, and contractility. Understanding these mechanisms is important because adverse remodeling can contribute to declining cardiac function, whereas therapies aimed at limiting these changes may help preserve performance.
After myocardial infarction, scar-related distortion can alter the ventricle’s shape and contractile behavior. The injured region may therefore contribute to broader changes in chamber geometry and pumping function rather than remaining an isolated abnormality. Evaluating these structural consequences helps clinicians assess disease progression and identify patients at greater risk of heart failure and related complications.
Echocardiography and cardiac magnetic resonance imaging are important methods for assessing remodeling. They can help evaluate changes in ventricular size, shape, wall thickness, and function, while other methods may provide additional assessment. Repeated imaging can also support evaluation of disease progression or treatment response, making structural measurements relevant to ongoing clinical management.
Assessment provides information about structural distortion and functional change in the heart’s main pumping chamber. Findings such as hypertrophy, dilation, altered shape, or reduced contractility can support evaluation of disease progression. In medicine, these observations contribute to risk stratification and help clinicians judge whether the ventricle is responding favorably to treatment.
Adverse remodeling can alter ventricular geometry and contractility in ways that impair cardiac function and increase the likelihood of heart failure and related complications. For this reason, clinicians monitor remodeling as part of disease assessment rather than focusing only on symptoms. Strategies that limit these structural changes aim to preserve ventricular function and improve clinical outlook.
Comparing ventricular assessments over time can show whether chamber size, shape, wall thickness, or contractility are changing after treatment. Echocardiography, cardiac magnetic resonance imaging, and other assessment methods may therefore be used longitudinally. Evidence of limited adverse change or preserved function can support a favorable response, while progression may prompt closer evaluation of disease status.