Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

707
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...
707
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

789
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...
789
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

803
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,...
803
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

1.5K
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...
1.5K
Heart Failure IV: Classification and Diagnostic Evaluation01:30

Heart Failure IV: Classification and Diagnostic Evaluation

624
Heart failure can be classified in various ways, with the most common classifications based on physical activity limitations, disease progression, severity, and treatment strategies.The Functional Classification of Heart Failure divides patients into four categories based on physical activity limitation due to symptom burden.Class I: Patients in this class have cardiac disease but no physical activity limitations. Ordinary activities like walking, climbing stairs, or routine tasks do not cause...
624
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

4.8K
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...
4.8K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Sex difference in nocturnal blood pressure dipping in adolescents with varying degrees of adiposity.

BMC pediatrics·2024
Same author

Predicting stroke and myocardial infarction risk in Takayasu arteritis with automated machine learning models.

iScience·2023
Same author

Intestinal <i>Cckbr</i>-specific knockout mouse as a novel model of salt-sensitive hypertension via sodium over-absorption.

Journal of geriatric cardiology : JGC·2023
Same author

Childhood-Onset Refractory Hypertension Results from Neurofibromatosis Type 1 Caused by a Splicing NF1 Mutation.

Kidney & blood pressure research·2023
Same author

Clinical characteristics and management of coexistent cardiomyopathy in patients with bicuspid aortic valve.

Journal of geriatric cardiology : JGC·2023
Same author

A novel AGK splicing mutation in a patient with Sengers syndrome and left ventricular non-compaction cardiomyopathy.

Pediatric research·2023

Related Experiment Video

Updated: Apr 14, 2026

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
10:21

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix

Published on: June 14, 2016

10.8K

Recent progress in end-stage hypertrophic cardiomyopathy.

Yan Xiao1, Kun-Qi Yang, Yong Jiang

  • 1Departments of Cardiology (YX, K-QY, X-LZ) and Echocardiology (YJ), State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

The American Journal of the Medical Sciences
|April 23, 2015
PubMed
Summary

End-stage hypertrophic cardiomyopathy (ES-HCM) involves left ventricular enlargement and dysfunction, posing high risks for heart failure and sudden death. Early recognition and new management strategies are crucial for improving outcomes in this challenging condition.

More Related Videos

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
03:45

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model

Published on: August 8, 2022

4.4K
An Approach to Study Shape-Dependent Transcriptomics at a Single Cell Level
06:02

An Approach to Study Shape-Dependent Transcriptomics at a Single Cell Level

Published on: November 2, 2020

6.3K

Related Experiment Videos

Last Updated: Apr 14, 2026

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
10:21

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix

Published on: June 14, 2016

10.8K
Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
03:45

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model

Published on: August 8, 2022

4.4K
An Approach to Study Shape-Dependent Transcriptomics at a Single Cell Level
06:02

An Approach to Study Shape-Dependent Transcriptomics at a Single Cell Level

Published on: November 2, 2020

6.3K

Area of Science:

  • Cardiology
  • Genetics
  • Internal Medicine

Background:

  • Hypertrophic cardiomyopathy (HCM) is a spectrum of diseases.
  • A subset, end-stage HCM (ES-HCM), presents with left ventricular enlargement and systolic dysfunction.
  • ES-HCM carries a high risk of refractory heart failure and sudden cardiac death.

Purpose of the Study:

  • To review the evolving clinical features of ES-HCM.
  • To discuss the elucidated underlying mechanisms of ES-HCM.
  • To highlight the importance of early recognition and novel management strategies for ES-HCM.

Main Methods:

  • Literature review of studies on ES-HCM over the past two decades.
  • Analysis of clinical features, underlying mechanisms, and treatment strategies.
  • Synthesis of evidence for early detection and intervention.

Main Results:

  • Clinical features of ES-HCM have expanded over 20 years.
  • Underlying mechanisms of ES-HCM are becoming clearer.
  • Evidence supports earlier identification and intervention for ES-HCM.

Conclusions:

  • ES-HCM is an underestimated entity within hypertrophic cardiomyopathy.
  • Improved understanding of ES-HCM facilitates early recognition.
  • New insights into prevention and management promise better clinical outcomes for ES-HCM patients.