Sudden Cardiac Death
Sudden Cardiac Death - Related Videos
07:49
Large-Animal Model of Donation after Circulatory Death and Normothermic Regional Perfusion for Cardiac Assessment
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Cited by 6 •
2022
The protocol describes a large-animal (porcine) model of donation after circulatory death, followed by thoracoabdominal normothermic regional perfusion that closely simulates the clinical scenario in heart transplantation, and has the potential to facilitate therapeutic studies and strategies.
06:26
Pre-clinical Model of Cardiac Donation after Circulatory Death
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Cited by 4 •
2019
This protocol shows a simple and flexible approach for the evaluation of new conditioning agents or strategies to increase the feasibility of cardiac donation after circulatory death.
09:44
Neuro-rehabilitation Approach for Sudden Sensorineural Hearing Loss
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Cited by 10 •
2016
This article reports the development of a neuro-rehabilitation approach, "constraint-induced sound therapy (CIST)" for sudden sensorineural hearing loss. The aim of CIST is to prevent maladaptive cortical reorganization by using an enriched acoustic environment. CIST represents a safe, easy, inexpensive, and effective approach to treat sudden sensorineural hearing loss.
10:06
An Introduction to Cell Death
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2023
Necrosis, apoptosis, and autophagic cell death are all manners in which cells can die, and these mechanisms can be induced by different stimuli, such as cell injury, low nutrient levels, or signaling proteins. Whereas necrosis is considered to be an “accidental” or unexpected form of cell death, evidence exists that apoptosis and autophagy are both programmed and “planned” by cells.In this introductory video, JoVE highlights key discoveries pertaining to cell death, including recent work done...
08:28
Methods for ECG Evaluation of Indicators of Cardiac Risk, and Susceptibility to Aconitine-induced Arrhythmias in Rats Following Status Epilepticus
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Cited by 3 •
2011
Techniques for measurement of electrical activity of the heart by electrocardiogram (ECG), and analysis of cardiac risk factors and susceptibility to arrhythmias following status epilepticus (SE) in the rat are described.
FAQs
Ventricular tachycardia reflects a rapid ventricular rhythm, whereas ventricular fibrillation represents disorganized ventricular activity. In either case, abnormal excitability and impulse conduction prevent the ventricles from contracting effectively. This distinction matters pharmacologically because therapies must be evaluated for their ability to suppress dangerous electrical activity without creating additional electrical instability.
These conditions can converge on a shared electrical pathway while disturbing the heart in different ways. Ischemia and structural heart disease can disrupt myocardial function, whereas inherited channel abnormalities alter properties governing excitability or impulse conduction. Recognizing the underlying trigger helps investigators interpret why a medicine may be beneficial in one setting yet hazardous in another.
QT prolongation signals altered cardiac repolarization, the electrical recovery phase of the heart. When medicines lengthen this process, they may increase electrical instability and the potential for dangerous ventricular rhythms. Pharmacological evaluation therefore considers not only whether a compound suppresses arrhythmias, but also whether its effects on repolarization could raise risk.
These systems provide important pharmacological points of control over cardiac electrical behavior. Medicines that alter ion channels can change excitability and impulse conduction, while effects on autonomic signaling or repolarization can modify rhythm stability. Examining all three helps distinguish compounds that may control dangerous rhythms from those that could unintentionally promote electrical disturbances.
Evaluation focuses on whether a medicine changes the electrical mechanisms associated with dangerous ventricular rhythms. Investigators consider effects on ion channels, autonomic signaling, and cardiac repolarization, including the possibility of QT prolongation. This risk assessment supports safer drug development by identifying compounds whose rhythm-related effects could outweigh their intended therapeutic benefit.
Understanding the electrical basis of sudden cardiac death helps connect emergency treatment with the mechanisms producing ventricular tachycardia or fibrillation. Pharmacological strategies can then be considered in relation to abnormal excitability, impulse conduction, and repolarization rather than cardiac performance alone. This mechanistic context supports more informed treatment planning and evaluation of antiarrhythmic approaches.