Polymorphic Ventricular Tachycardia

This section will be devoted to covering polymorphic ventricular tachycardia (PMVT), which is a rhythm originating from the ventricles but with constantly-changing QRS morphologies. 

Topics included will be:

• Pathobiology of PMVT: A discussion on the vulnerable period of the heart and the risk of unstable reentrant circuits being formed with excitation during this period (i.e. R-on-T PVCs). 

• Torsades de pointes (TdP): A subtype of PMVT associated with pathologic long QT that cannot appropriately accomodate to changes in heart rate. This discussion will include:

  • The congenital and acquired causes of long QT syndrome, and the pathophysiology of QT prolongation. We will also discuss the different phenotypical subtypes of long QT syndrome (i.e. Type 1, Type 2, Type 3).

  • The pathogenesis of TdP, including the role of early afterdepolarizations in triggering PMVT.

  • The phenotypes of TdP and their characteristic features, such as:

    • Pause-dependent TdP, which occurs in the context of bradycardia. Characterized by a typical short-long-short initiation pattern, giant TU waves.

    • Tachycardia-dependent TdP, which occurs in the context of tachycardia and failure of accommodation of the action potential duration to heart rate acceleration. Characterized by T wave alternans.

  • A discussion on pseudo-TdP, a type of PMVT that occurs in patients with long QT but not because of this, and how to differentiate it from TdP by examining the baseline QT, the coupling interval of the inciting PVC, and examining the ventricular rate of the PMVT itself.

• Ischemic VF: A subtype of PMVT associated with acute ischemia, and typically STEMIs. We will discuss the mechanism of ischemic VF (phase 2 reentry, delayed afterdepolarizations) as well an overview of the characteristic features and how to differentiate it from TdP (for example, the presence of a normal baseline QTc, very short coupling interval of the inciting PVC).

• PMVT related to other channelopathy: We will cover PMVT associated with the following genetic channelopathies: Brugada syndrome, short QT syndrome, and catecholaminergic polymorphic VT (CPVT). We will discuss the characteristic clinical and ECG features of each channelopathy, as well as acquired causes that can mimic them, and go over diagnostic manoeuvres that can uncover channelopathies in patients with PMVT.

• Idiopathic VF: Another subtype of PMVT that may originate from the Purkinje fibres and has a stereotypic phenotype: PMVT triggered by a PVC with an ultrashort coupling interval, with an otherwise normal baseline ECG. We will also discuss the association with J wave syndromes and the proposed mechanisms.

• Differential diagnosis of PMVT: Such as preexcited AF and artefact, along with practical tips on differentiating the rhythms.

• We will also cover VTs characterized by more than 1 QRS morphology (so not strictly monomorphic) but lacking the characteristic continuously-changing QRS axis of PMVT:

  • Bidirectional VT: While not a true "polymorphic" VT, this is a distinct type of VT with beat-to-beat alternation of the QRS axis and typically associated with a short list of causes, most commonly being CPVT and digoxin toxicity.

  • Pleomorphic VT: While not a true "polymorphic" VT, this is a type of VT with more than 1 morphologically distinct QRS complex during the same episode of VT. However, there is no continuous change in the QRS axis, and no alternation like in bidirectional VT.