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Related Concept Videos

Aortic Regurgitation III: Medical Management01:25

Aortic Regurgitation III: Medical Management

Aortic regurgitation (AR) is when the aortic valve does not close or seal properly, leading to backward blood circulation from the aorta into the left ventricle during diastole. Common causes of AR include rheumatic heart disease, congenital valve defects, and aortic root dilation. Managing AR requires a multifaceted approach to alleviate symptoms, preserve left ventricular function, and address the underlying cause of the regurgitation. Patients with symptomatic AR or significant left...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
Heart Failure VI: Adjunct Therapies01:22

Heart Failure VI: Adjunct Therapies

Additional therapies for treating patients with heart failure (HF) may include procedural interventions, supplemental oxygen, the management of sleep disorders, and nutritional therapy.Procedural InterventionsImplantable Cardioverter-Defibrillator: For patients at risk of life-threatening arrhythmias due to severe left ventricular dysfunction, an Implantable Cardioverter-Defibrillator (ICD) can detect and terminate these arrhythmias, preventing sudden cardiac death and improving survival rates.
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...

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Related Experiment Video

Updated: Jul 1, 2026

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
07:24

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR

Published on: April 8, 2013

Ventricular remodelling: consequences and therapy

H N Sabbah1, S Goldstein

  • 1Department of Medicine, Henry Ford Heart and Vascular Institute, Detroit, Michigan.

European Heart Journal
|July 1, 1993
PubMed
Summary
This summary is machine-generated.

Mammalian heart remodeling, involving myocytes and fibrous structures, adapts to stimuli like tissue loss. Pharmacological agents can modify these adaptive mechanisms in myocardial infarction and heart failure.

More Related Videos

Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure
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Published on: December 2, 2014

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing
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Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing

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Related Experiment Videos

Last Updated: Jul 1, 2026

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
07:24

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR

Published on: April 8, 2013

Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure
09:37

Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure

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Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing
12:45

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing

Published on: December 11, 2017

Area of Science:

  • Cardiovascular Biology
  • Cardiac Pathophysiology
  • Pharmacology

Background:

  • The mammalian left ventricle undergoes significant changes in size and shape, termed remodeling, in response to various physiological and pathological stimuli.
  • Ventricular remodeling is a complex process involving cellular (myocyte) and extracellular matrix (interstitial fibrous structures) components.
  • These adaptive mechanisms are influenced by systemic factors and are targets for therapeutic intervention.

Purpose of the Study:

  • To review the process of myocardial remodeling in the context of myocardial infarction and heart failure.
  • To examine the impact of pharmacological agents on the remodeling process in these cardiac conditions.

Main Methods:

  • Literature review of studies on left ventricular remodeling.
  • Analysis of research on the effects of pharmacological interventions on cardiac remodeling.

Main Results:

  • Remodeling involves intricate interactions between myocytes and the interstitial matrix.
  • Humoral and cellular signals play crucial roles in mediating adaptive and maladaptive remodeling.
  • Pharmacological agents demonstrate potential to modify adverse remodeling pathways.

Conclusions:

  • Ventricular remodeling is a dynamic process critical to understanding heart disease progression.
  • Targeting remodeling pathways with pharmacological agents offers therapeutic potential for myocardial infarction and heart failure.
  • Further research is needed to fully elucidate and exploit the therapeutic benefits of modulating cardiac remodeling.