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Related Concept Videos

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...
Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
Cardiomyopathy I: Introduction and Classification01:25

Cardiomyopathy I: Introduction and Classification

Cardiomyopathy, or CMP, is a group of diseases affecting the myocardial structure, impairing its ability to pump blood effectively. This condition can lead to arrhythmias, heart failure, or sudden cardiac death.Cardiomyopathies are classified into primary and secondary categories:Primary Cardiomyopathy refers to conditions involving only the heart muscle that are often idiopathic (of unknown cause) or genetic. They primarily affect the myocardium without the involvement of other systemic...
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,...
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...

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Related Experiment Video

Updated: Jun 30, 2026

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

Myosin Inhibition in Non-obstructive Hypertrophic Cardiomyopathy: Lessons from ODYSSEY-HCM.

Koji Hasegawa1, Moritake Iguchi1, Hiromichi Wada1

  • 1National Hospital Organization Kyoto Medical Center Kyoto, Japan.

European Cardiology
|June 29, 2026
PubMed
Summary

The cardiac myosin inhibitor mavacamten showed no significant clinical benefit in non-obstructive hypertrophic cardiomyopathy patients. Biomarker improvements were observed, but clinical outcomes and systolic function require further investigation for this heart condition.

Keywords:
Hypertrophic cardiomyopathydiastolic dysfunctionmavacamtenmyosin inhibitor

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Last Updated: Jun 30, 2026

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

Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples
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Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples

Published on: April 21, 2014

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

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Area of Science:

  • Cardiology
  • Pharmacology
  • Clinical Trials

Background:

  • Hypertrophic cardiomyopathy (HCM) is a primary genetic heart muscle disease.
  • Non-obstructive HCM presents unique challenges in therapeutic development.
  • Cardiac myosin inhibitors represent a novel therapeutic class for HCM.

Purpose of the Study:

  • To evaluate the efficacy and safety of mavacamten in symptomatic non-obstructive hypertrophic cardiomyopathy.
  • To assess the impact of mavacamten on clinical endpoints and biomarkers.
  • To critically appraise the ODYSSEY-HCM trial findings and inform future research.

Main Methods:

  • Phase III, randomized, placebo-controlled trial (ODYSSEY-HCM).
  • Inclusion of symptomatic patients with non-obstructive hypertrophic cardiomyopathy.
  • Assessment of clinical endpoints (KCCQ, peak VO2), biomarkers (pro-BNP), and echocardiographic parameters.

Main Results:

  • Mavacamten did not significantly improve primary clinical endpoints like Kansas City Cardiomyopathy Questionnaire (KCCQ) score or peak oxygen consumption (VO2).
  • Significant reductions in pro-B-type natriuretic peptide (pro-BNP) levels were observed.
  • Improvements in echocardiographic indices of diastolic function and left atrial function were noted.

Conclusions:

  • A dissociation exists between biomarker improvements and clinical outcomes with mavacamten in non-obstructive HCM.
  • Concerns regarding patient selection, endpoint selection, and dosing strategies warrant further investigation.
  • Potential decline in left ventricular systolic function and arrhythmic vulnerability require careful consideration in myosin inhibition therapy.