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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...
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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,...
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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...
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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...
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Typical heart performance is influenced by heart rate, rhythm, myocardial contraction, and metabolism or blood flow. The cardiac muscle exhibits distinct electrophysiological features, including pacemaker activity and calcium channel control, which play a vital role in the heart's response to various drugs. The autonomic nervous system, comprising the sympathetic and parasympathetic branches, regulates heart rate. Sympathetic activation increases heart rate, while parasympathetic activation...

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Real-Time Electrocardiogram Monitoring During Treadmill Training in Mice
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Precision Cardiogenomics in Athletes.

Pari Goyal1, Alwaleed Aljohar1,2, Reid A Mitchell1,3

  • 1SportsCardiologyBC, The University of British Columbia Hospital, Vancouver, BC V6T 2B5, Canada.

International Journal of Molecular Sciences
|June 26, 2026
PubMed
Summary
This summary is machine-generated.

Sudden cardiac death in athletes stems from inherited disorders exacerbated by exercise. Understanding the molecular links between genes and heart conditions is key to preventing these tragic events.

Keywords:
athletescardiomyopathieschannelopathiesexercisegenomicssudden cardiac death

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Area of Science:

  • Cardiovascular Genetics
  • Exercise Physiology
  • Molecular Cardiology

Background:

  • Sudden cardiac death (SCD) in athletes often signals underlying inherited cardiovascular disorders.
  • Intense exercise acts as a trigger by increasing adrenergic stress, altering calcium cycling, and imposing mechanical and metabolic demands.

Purpose of the Study:

  • To review the molecular mechanisms linking genetic predispositions to arrhythmogenic phenotypes in athletes.
  • To explore how exercise-induced physiological remodeling interacts with these genetic pathways.
  • To discuss strategies for risk stratification and prevention of SCD in athletes.

Main Methods:

  • Review of molecular pathways involved in hypertrophic cardiomyopathy, arrhythmogenic cardiomyopathy, and inherited channelopathies.
  • Examination of exercise-related signaling cascades including IGF-1/PI3K/AKT, mitochondrial biogenesis, and oxidative stress.
  • Integration of genetic data, polygenic risk scores, and digital phenotyping for risk assessment.

Main Results:

  • Specific molecular defects in sarcomeric proteins, desmosomes, and ion channels predispose athletes to SCD.
  • Exercise modulates pathways like IGF-1/PI3K/AKT, inflammation, and epigenetics, influencing disease expression.
  • Genotype-positive/phenotype-negative states and variable penetrance highlight the complexity of exercise-mediated disease.

Conclusions:

  • Understanding the genotype-phenotype link in inherited heart conditions is crucial for preventing SCD in athletes.
  • Integrating molecular, genetic, and digital data can improve risk stratification and identify therapeutic targets.
  • Further research into exercise's role in disease expression is needed for effective prevention strategies.