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 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...
Mechanism of Cardiac Arrhythmias01:28

Mechanism of Cardiac Arrhythmias

Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.
Coronary Artery Disease III: Clinical Manifestations01:30

Coronary Artery Disease III: Clinical Manifestations

Coronary Artery Disease (CAD) is a primary health risk worldwide, leading to significant morbidity and mortality. The condition arises from the buildup of atherosclerotic plaques within the coronary arteries, resulting in diminished blood supply to the heart muscle.The clinical manifestations of CAD vary widely, from asymptomatic stages to severe, life-threatening conditions. Understanding these manifestations is crucial for early diagnosis and effective management.Angina Pectoris: The Warning...
Coronary Artery Disease I: Introduction01:30

Coronary Artery Disease I: Introduction

Coronary Artery Disease (CAD): An Overview with Scientific InsightsCoronary Artery Disease (CAD), often referred to as C-A-D, is a prevalent blood vessel disorder classified under the broader category of atherosclerosis. Atherosclerosis is a pathological process characterized by the hardening and narrowing of arteries due to the accumulation of atherosclerotic plaques. These plaques are composed of cholesterol, fatty substances, inflammatory cells, calcium, and fibrin, reducing blood flow to...
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
Human Genetics01:28

Human Genetics

Human genetics provides a profound framework for understanding the interplay between genetic predispositions and human psychology. At the heart of this discipline lies the study of how genes influence physical traits, behaviors, and susceptibility to diseases. Each person carries a unique genetic code that subtly or significantly shapes their psychological and behavioral landscape.
The complex relationship between genetics and psychology is observable through common biological components such...

You might also read

Related Articles

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

Sort by
Same author

Natural History of Asymptomatic Phenotypically Mild HCM: Insights From the SHaRe Registry.

Journal of the American College of Cardiology·2026
Same author

Catheter ablation of atrial fibrillation in transthyretin and light-chain cardiac amyloidosis: results from the multicentre AMYL-AF study.

Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology·2026
Same author

Invasive exercise hemodynamics in obstructive and non-obstructive hypertrophic cardiomyopathy.

Journal of applied physiology (Bethesda, Md. : 1985)·2026
Same author

How Many CPVT Patients Need an ICD?: The Impact of Left Cardiac Sympathetic Denervation.

JACC. Clinical electrophysiology·2026
Same author

Machine learning-guided risk stratification for long QT syndrome genetic variants with hiPSC-derived cardiomyocytes.

Cardiovascular research·2026
Same author

MTMR4 variants have opposite gene-specific impact on life-threatening arrhythmic risk in type 1 and 2 long QT syndrome.

European heart journal·2026

Related Experiment Video

Updated: Jun 6, 2026

Determining the Likelihood of Variant Pathogenicity Using Amino Acid-level Signal-to-Noise Analysis of Genetic Variation
07:15

Determining the Likelihood of Variant Pathogenicity Using Amino Acid-level Signal-to-Noise Analysis of Genetic Variation

Published on: January 16, 2019

Genetic predisposition to sudden cardiac death.

Lia Crotti1

  • 1University of Pavia and IRCCS Fondazione Policlinico San Matteo, Pavia, Italy. l.crotti@smatteo.pv.it

Current Opinion in Cardiology
|November 25, 2010
PubMed
Summary

Genetic factors significantly contribute to sudden cardiac death (SCD). Recent advances focus on primary ventricular fibrillation and channelopathies like Long QT syndrome, with molecular autopsy becoming standard for SCD assessment.

More Related Videos

Implantation of Electroencephalogram and Electrocardiogram Telemetry Devices in Neonatal Rabbit Kits
06:46

Implantation of Electroencephalogram and Electrocardiogram Telemetry Devices in Neonatal Rabbit Kits

Published on: February 28, 2025

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

Related Experiment Videos

Last Updated: Jun 6, 2026

Determining the Likelihood of Variant Pathogenicity Using Amino Acid-level Signal-to-Noise Analysis of Genetic Variation
07:15

Determining the Likelihood of Variant Pathogenicity Using Amino Acid-level Signal-to-Noise Analysis of Genetic Variation

Published on: January 16, 2019

Implantation of Electroencephalogram and Electrocardiogram Telemetry Devices in Neonatal Rabbit Kits
06:46

Implantation of Electroencephalogram and Electrocardiogram Telemetry Devices in Neonatal Rabbit Kits

Published on: February 28, 2025

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

Area of Science:

  • Cardiovascular Genetics
  • Molecular Cardiology
  • Sudden Cardiac Death Research

Background:

  • Sudden cardiac death (SCD) poses a significant public health challenge.
  • Genetic factors are increasingly recognized as crucial contributors to SCD risk.
  • Inherited arrhythmogenic syndromes highlight the genetic basis of SCD.

Purpose of the Study:

  • To review recent advancements in the genetic predisposition to sudden cardiac death (SCD).
  • To focus specifically on genetic factors in primary ventricular fibrillation and channelopathies.
  • To discuss the implications of new genetic findings for clinical practice and research.

Main Methods:

  • Review of recent scientific literature on genetic SCD.
  • Analysis of genome-wide association studies for primary ventricular fibrillation.
  • Examination of advances in understanding genetic channelopathies (e.g., Long QT, Brugada syndrome).

Main Results:

  • Coronary artery disease remains the primary determinant of SCD, with a complex genetic background.
  • Initial genome-wide association studies for primary ventricular fibrillation require larger cohorts for conclusive results.
  • Significant progress has been made in understanding Long QT syndrome and Brugada syndrome genetics.
  • Early repolarization syndrome and J wave syndromes have been recently described.
  • Molecular autopsy is now a standard requirement in autopsy investigations for SCD.

Conclusions:

  • Recent genetic research offers valuable insights into the basis of sudden cardiac death.
  • Genetic findings in channelopathies are being integrated into clinical guidelines and practice.
  • Further research is needed to fully elucidate the genetic underpinnings of SCD related to coronary artery disease.