Ventricular tachycardia in the absence of structural heart disease

Recurrent ventricular fibrillation with different tyrosine kinase inhibitors for chronic myeloid leukemia

“…6 The QTc interval in our case has consistently been normal and there has been no evidence of early repolarization to suggest an inherited channelopathy as a cause for our patient's VF. 7 The appearance of isolated PVCs prior to arrest does raise the possibility that direct TKI arrhythmogenic effect may underpin our patient's presentations. Importantly, the lack of arrhythmia recurrence on asciminib demands explanation.…”

The Genetics and Epigenetics of Ventricular Arrhythmias in Patients Without Structural Heart Disease

“…The vast majority of ventricular arrhythmias occurs in structurally diseased hearts, however, a proportion of patients with ventricular tachycardia is free of cardiac structure alterations ( 1 ). Ventricular arrhythmias without structural heart disease mainly includes monomorphic ventricular tachycardia classified by location of origin, polymorphic ventricular tachycardia dominated by primary hereditary arrhythmia syndrome, and ventricular fibrillation, i.e., Brugada syndrome (BrS), congenital long QT syndrome (LQTS), short QT syndrome (SQTS), catecholaminergic polymorphic ventricular tachycardia (CPVT) ( 2 , 3 ). The clinical presentations vary, including palpitations, vertigo, syncope, seizure-like activity and sudden cardiac death.…”

“…Triggered activity, abnormal automaticity, and re-entry are the three mechanisms of ventricular arrhythmias, in ventricular arrhythmias without structural heart disease, usually due to trigger activity ( 3 ). Triggered activity that occurs in phase 2 and early phase 3 is called early afterdepolarization (EAD), in late phase 3 and phase 4 are called delayed after-depolarization (DAD) ( 11 ), The trigger activity is generated by the membrane depolarisation induced by the I NCX and/or Ica,l ( 12 , 13 ).…”

“…Once I K1 is inhibited, the membrane potential cannot reach the resting potential, which may lead to the generation of abnormal inward currents, such as I f , causing abnormal automaticity. Re-entry refers to a cardiac impulse that repeatedly runs and activates the cardiac muscle surrounding around the center of anatomical or functional disorders, usually the pathogenesis of structural ventricular arrhythmias, but specific arrhythmias induced by EAD (Torsades de Pointes in LQTS) or DAD (bidirectional ventricular tachycardia in CPVT) may be caused by re-entry involving fascicles of the Purkinje system ( 3 ).…”

Heartbeat: Bicuspid aortic valve heritability and association with aortopathy

“…The Education in Heart article in this issue7 discusses the mechanisms and types of ventricular tachycardia (VT) occurring in the absence of structural heart disease (figure 4). The three main mechanisms are re-entry (such as scar-mediated VT), triggered activity (such as right ventricular outflow VT) and automaticity (such as idiopathic focal VT) with clinical presentations varying from palpitations to sudden cardiac death.…”