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Related Concept Videos

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...
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
Imbalances in Cardiac Output01:26

Imbalances in Cardiac Output

The heart's primary function is to pump blood throughout the body, maintaining a balance between blood sent out (cardiac output) and blood returning (venous return). If this balance is disrupted, it can result in congestive heart failure (CHF), a severe condition where the heart becomes an inefficient pump, leading to inadequate blood circulation.
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send blood...
Mitral Regurgitation I: Introduction01:20

Mitral Regurgitation I: Introduction

Mitral regurgitation is characterized by the backward circulation of blood from the left ventricle to the left atrium during systole, a phase of the cardiac cycle when the heart contracts and pumps blood out of the chambers. This abnormal flow occurs primarily due to the dysfunction of the mitral valve or its supporting structures, which include the mitral leaflets, chordae tendineae, annulus, and papillary muscles.Etiology and Mechanisms:Primary Mitral Regurgitation: This type arises from...
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...
Myocarditis I: Introduction01:21

Myocarditis I: Introduction

Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...

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Related Experiment Video

Updated: Jun 5, 2026

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

Published on: December 2, 2014

The aging heart and post-infarction left ventricular remodeling.

Henry Shih1, Brian Lee, Randall J Lee

  • 1Department of Medicine, Division of Cardiology, University of California San Francisco, San Francisco, California 94143, USA.

Journal of the American College of Cardiology
|December 28, 2010
PubMed
Summary

Aging impairs heart cell repair after heart attacks, increasing heart failure risk in older adults. Cellular changes like reduced autophagy and stem cell function worsen outcomes in the aged heart.

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Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
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Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs

Published on: April 17, 2021

Related Experiment Videos

Last Updated: Jun 5, 2026

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

Published on: December 2, 2014

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
14:35

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs

Published on: April 17, 2021

Area of Science:

  • Cardiology
  • Gerontology
  • Cellular Biology

Background:

  • Aging is a significant risk factor for heart failure, a leading global cause of death.
  • Elderly patients face higher risks of myocardial infarction (MI) and subsequent heart failure compared to younger individuals.
  • Cellular aging processes in cardiomyocytes contribute to poor cardiovascular disease outcomes.

Purpose of the Study:

  • To review the cellular and molecular mechanisms of post-infarction remodeling in the aged heart.
  • To connect cellular changes with clinical outcomes in elderly patients experiencing MI.
  • To elucidate how aging impacts cardiomyocyte biology and cardiac function post-MI.

Main Methods:

  • Review of existing literature on cellular and molecular aging.
  • Analysis of age-related changes in cardiomyocyte signaling pathways.
  • Examination of impaired autophagy and apoptosis in aged cardiomyocytes.
  • Investigation of reduced cardiomyocyte renewal and stem cell function in the elderly.

Main Results:

  • Increased cellular stress and altered signaling pathways in aged cardiomyocytes.
  • Impaired autophagy due to metabolic waste accumulation, promoting apoptosis.
  • Reduced cardiomyocyte division and stem cell function contribute to cardiac dysfunction.
  • Aged hearts exhibit maladaptive remodeling responses to MI and stress.

Conclusions:

  • Cellular aging profoundly impacts the heart's ability to recover from myocardial infarction.
  • Impaired cellular repair mechanisms, including autophagy and regeneration, are key in aged hearts.
  • Understanding these cellular changes is crucial for improving clinical outcomes in elderly patients with heart failure post-MI.