Ventricular Fibrillation Research Articles

Arrhythmias from the ventricular myocardium or the His-Purkinje system are grouped under ventricular arrhythmia (AV). This includes a subset of arrhythmias such as ventricular tachycardia (VT), ventricular fibrillation (VF), premature ventricular contractions (PVC) and ventricular flutter. Large complex tachycardia (WCT) is used to define all tachyarrhythmias with a complex QRS duration greater than 0.12 seconds. VF is a WCT caused by irregular electrical activity and characterized by a ventricular rate generally greater than 300 with discrete QRS complexes on the electrocardiogram (ECG). The morphology of QRS in VF varies in shape, amplitude and duration with a large irregular rhythm. [1] VF is an extremely dangerous rhythm that significantly compromises cardiac output and ultimately leads to sudden cardiac death (SCD).

VF is often linked to an underlying structural heart disease. 3 to 12% of myocardial infarction (MI) cases develop VF during the acute phase. [2] Patients with MI with complete coronary occlusion on angiography, infarction of the anterior wall, atrial fibrillation and angina before the infarction are more likely to develop VF. [3] Many common conditions associated with VF include electrolyte abnormalities (hypokalemia / hyperkalemia, hypomagnesemia), acidosis, hypothermia, hypoxia, cardiomyopathies, family history of sudden cardiac death, birth defects QT interval, Brugada syndrome and alcohol consumption. Patients with a history of particularly sustained VA monomorphic or polymorphic VT may switch to VF in susceptible patients. [4] The genetic predisposition to FV is now increasingly recognized. The first genome-wide association was reported in the AGNES study identifying the locus of susceptibility to FV at 21q21.