Heart Remodeling
Heart Remodeling - Related Videos
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...
07:31
A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
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Cited by 26 •
2016
A rat model of abdominal aortic constriction that induces cardiac hypertrophy and remodeling is described. An efficient, highly-reproducible, and minimally-invasive method is used to provide a simple yet useful platform for research in myocardial hypertrophy and dysfunction.
07:27
Implantation of Total Artificial Heart in Congenital Heart Disease
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Cited by 40 •
2014
This is a case report of a patient with congenitally corrected transposition of the great arteries (CCTGA) who received a total artificial heart (TAH) as a bridge to heart transplant. The TAH was successfully implanted with modifications to accommodate the patient's congenitally malformed heart.
07:41
A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats
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Cited by 2 •
2022
The present protocol describes a surgical procedure to remove ascending-aortic banding in a rat model of pulmonary hypertension due to left heart disease. This technique studies endogenous mechanisms of reverse remodeling in the pulmonary circulation and the right heart, thus informing strategies to reverse pulmonary hypertension and/or right ventricular dysfunction.
07:13
A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
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Cited by 1 •
2020
We describe the creation of a rat model of pressure overload induced moderate remodeling and early systolic dysfunction where signal transduction pathways involved in the initiation of the remodeling process are activated. This animal model will aid in identifying molecular targets for applying early therapeutic anti-remodeling strategies for heart failure.
FAQs
Early structural adjustments can help the heart maintain performance when pressure or volume increases or tissue is injured. Persistent stress, however, may cause continuing cardiomyocyte hypertrophy, chamber dilation, and changes in ventricular geometry. As these adaptations progress, the heart may lose efficient contraction and relaxation, shifting remodeling from compensation toward functional impairment.
Persistent neurohormonal activation contributes to the progression of heart remodeling by sustaining signals that alter myocardial structure and function. These signals act alongside hemodynamic stress, encouraging changes such as cardiomyocyte enlargement and fibrosis. Their importance makes neurohormonal activity a therapeutic target, because reducing it can help limit adverse structural change and support reverse remodeling.
These changes affect the heart in different but connected ways. Cardiomyocyte hypertrophy alters the size and workload of individual muscle cells, while chamber dilation changes ventricular geometry. Myocardial fibrosis adds structural tissue changes within the heart. Together, they can initially accompany compensation but eventually interfere with effective contraction and relaxation when remodeling becomes progressive.
The initiating condition shapes the resulting structural response. Altered pressure or volume places different mechanical demands on the heart, whereas myocardial injury directly changes affected tissue. In each setting, remodeling may include hypertrophy, dilation, altered ventricular geometry, and fibrosis, but the balance and progression of these changes depend on the underlying stress or damage.
Assessment combines imaging, biomarkers, and functional evaluations rather than relying on a single measurement. Imaging can track structural changes such as chamber dimensions and ventricular geometry, while biomarkers provide biological information related to cardiac stress or injury. Functional assessments show how remodeling affects performance. Repeated evaluation helps identify progression, stability, or improvement over time.
Monitoring is particularly relevant in heart failure, hypertension, and recovery after myocardial infarction, where structural changes can influence cardiac performance and prognosis. Tracking remodeling helps clinicians connect underlying injury or hemodynamic stress with changes in function. It also provides a way to evaluate whether treatment is reducing adverse changes or promoting reverse remodeling.
Reverse remodeling refers to improvement in adverse structural and functional changes rather than continued progression. Treatments that reduce hemodynamic stress and neurohormonal activation can promote this response. Its clinical importance lies in the possibility of improving contraction, relaxation, and overall cardiac performance, making remodeling measures useful for evaluating therapeutic benefit.
These conditions represent different clinical settings in which remodeling helps explain changes in cardiac function. Hypertension can impose persistent pressure-related stress, myocardial infarction can initiate injury-related structural change, and heart failure reflects impaired performance associated with progressive remodeling. Studying the process across these conditions supports assessment, treatment selection, and evaluation of recovery.