Ventricular Remodeling
Ventricular Remodeling - Related Videos
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.
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.
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...
09:22
Chronic Thromboembolic Pulmonary Hypertension and Assessment of Right Ventricular Function in the Piglet
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Cited by 22 •
2015
Chronic Thromboembolic Pulmonary Hypertension (CTEPH) and Right Ventricular (RV) dysfunction were induced in piglets by progressive obstruction of the pulmonary arteries. Consequences were remarkably similar to those observed in CTEPH patients. This animal model would be a very useful tool for pathophysiology and therapeutic experiments on CTEPH and RV failure.
14:39
Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples
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Cited by 44 •
2014
Current knowledge on the cellular basis of cardiac diseases mostly relies on studies on animal models. Here we describe and validate a novel method to obtain single viable cardiomyocytes from small surgical samples of human ventricular myocardium. Human ventricular myocytes can be used for electrophysiological studies and drug testing.
FAQs
Increased wall stress places mechanical demand on the ventricle. After myocardial infarction or sustained pressure and volume overload, this stress participates in a progression that includes neurohormonal signaling, cardiomyocyte hypertrophy, chamber dilation, and fibrosis. As structure changes, the ventricle may contract and relax less effectively. Clinically, recognizing this sequence helps explain why remodeling can progress beyond the initial injury.
Neurohormonal signaling and cardiomyocyte hypertrophy are components of the response to sustained ventricular stress. Together with chamber dilation and fibrosis, they represent structural and regulatory changes that can shift the ventricle away from normal performance. Their clinical importance lies in the cumulative effect: as remodeling progresses, both pumping and filling functions may deteriorate, increasing concern for heart failure.
Fibrosis is important because it is one of the structural changes associated with progressive loss of ventricular performance. Fibrosis appears alongside hypertrophy and dilation as remodeling advances, and the combined process can impair contraction and relaxation. This matters clinically because adverse remodeling is linked not only to heart failure risk but also to a greater risk of arrhythmias.
Clinical assessment relies on echocardiography, cardiac magnetic resonance imaging, and other measures of cardiac function. These approaches provide complementary information about ventricular size, shape, wall structure, and performance. Using structural imaging together with functional measures helps clinicians characterize the extent of remodeling, estimate its prognostic significance, and support treatment decisions.
Imaging findings help translate structural change into clinically useful information. Echocardiography and cardiac magnetic resonance imaging can assess the ventricle, while other measures of cardiac function add functional context. Clinicians use these results to estimate prognosis and guide treatment, rather than viewing chamber size or wall structure in isolation. The goal is to identify the significance of remodeling for future cardiac performance.
Assessment is particularly relevant after myocardial infarction and when pressure or volume overload persists, because these settings can initiate or sustain adverse structural change. Clinical evaluation can then characterize ventricular size, shape, wall structure, and function through imaging and functional measures. This information supports decisions intended to limit progression and reduce later heart failure or arrhythmia risk.