In a test of this theory, researchers have demonstrated that mice harboring a human SCN1A gene mutation that results in Dravet Syndrome (DS), a severe and intractable genetic epilepsy, have electrical disturbances in the heart that culminate
in ventricular fibrillation and sudden cardiac death.
Not exact matches
Defibrillation is a technique used
in emergency medicine to terminate
ventricular fibrillation or pulseless
ventricular tachycardia.
However, if not enough energy is used for defibrillation, the heart may not be completely depolarized,
in which case the
ventricular tachycardia or
fibrillation may not be terminated.
Francis Kim, M.D., of Harborview Medical Center, Seattle, and colleagues evaluated whether early prehospital cooling (lowering body temperature) improved survival to hospital discharge and neurological outcome
in cardiac arrest patients with or without
ventricular fibrillation (VF).
Previous research has shown carbon monoxide, which is produced naturally
in heart cells, can guard against
ventricular fibrillation, however the mechanism behind why this happens was unknown.
Study participation was restricted to patients with either
ventricular fibrillation or
ventricular tachycardia who did not achieve a stable heart rhythm after at least one defibrillator shock and, therefore, represent the typical group of those who receive such medications for cardiac arrest
in clinical practice.
We also aim,
in the model of cardiomyocyte, decipher implication of mutations identified
in cardiomyopathies such as inherited hypertrophic cardiomyopathies (HCM), Atrial
fibrillation (AF) or Arrhythmogenic right
ventricular cardiomyopathy (ARVC).
Atrial
fibrillation affects almost 5 million Americans and sudden cardiac death,
in part caused by
ventricular arrhythmias, is the leading cause of mortality
in industrialized nations.
In severe cases, this can lead to atrial
fibrillation, supraventricular tachycardia, and premature
ventricular contractions.
In fact, according to the Heart Rhythm Society 2004, more than 50 % of deaths from cardiovascular disease can be blamed on arrhythmia (
ventricular fibrillation).
An average human dose equivalent of 500 mg of tyrosine given intravenously reduces susceptibility to life - threatening
ventricular fibrillation in experimental animals.
Pets with
ventricular fibrillation or digitalis overdose Cats with hypertrophic cardiomyopathy Use with caution
in Collie - breed dogs as they may be more sensitive to Central Nervous System effects Use with caution
in obese pets and those with kidney or thyroid disease, severe lung disease or those with an electrolyte imbalance Safety has not been determined
in breeding, pregnant or nursing animals If your pet has had an allergic reaction to digoxin or like products Directions:
Cardiac dilation, decreased oxygen supply, and increased oxygen demand secondary to elevated heart rate and
ventricular wall stress may predispose to the development of cardiac arrhythmias arising
in either the atria (atrial
fibrillation, supraventricular tachycardia) or
in the ventricles (
ventricular premature complexes,
ventricular tachycardia).
Alternatively, it could cause
ventricular fibrillation which essentially refers to disorganized and useless fluttering of the ventricles found
in the heart.