Premature Ventricular Contractions and Non-sustained Ventricular Tachycardia: Association with Sudden Cardiac Death, Risk Stratification, and Management Strategies

Abstract

Premature ventricular contractions (PVCs) and non-sustained ventricular tachycardia (NSVT) are frequently encountered and a marker of electrocardiomyopathy. In some instances, they increase the risk for sustained ventricular tachycardia, ventricular fibrillation, and sudden cardiac death. While often associated with a primary cardiomyopathy, they have also been known to cause tachycardia-induced cardiomyopathy in patients without preceding structural heart disease. Medical therapy including beta-blockers and class III anti-arrhythmic agents can be effective while implantable cardiac defibrillators (ICD) are indicated in certain patients. Radiofrequency ablation (RFA) is the preferred, definitive treatment in those patients that improve with anti-arrhythmic therapy, have tachycardia-induced cardiomyopathy, or have certain subtypes of PVCs/NSVT. We present a review of PVCs and NSVT coupled with case presentations on RFA of fascicular ventricular tachycardia, left-ventricular outflow tract ventricular tachycardia, and Purkinje arrhythmia leading to polymorphic ventricular tachycardia.

Keywords: PVC; ablation; premature ventricular contractions; sudden death; ventricular tachycardia.

Figure 1

Electrocardiogram demonstrating sinus rhythm with a five beat run of nonsustained ventricular tachycardia with left bundle branch block morphology (negative in V1).

Figure 2

The upper portion of this figure depicts ectopy that can occur after myocardial injury has caused ventricular dysfunction. Frequent PVC's may also cause ventricular remodeling as seen in the lower portion of the figure. VT = ventricular tachycardia; PVCs = premature ventricular contractions

Figure 3

Characteristics of primary cardiomyopathy versus tachycardia-induced cardiomyopathy

Figure 4

Management algorithm for PVCs or NSVT.

Figure 5

Electrocardiogram demonstrating underlying sinus rhythm with frequent monomorphic PVCs. The morphology of the PVCs suggests a LVOT focus. The first clue is the right bundle branch block morphology of the PVCs suggests left-sided origin. The second clue is that the PVCs are strongly positive in inferior leads (II, III, aVF) and strongly negative in aVR and aVL which suggests the origin is superior in the outflow tracts.

Figure 6

Intracardiac electrograms and EKG in a patient with an unusual supravalvar origin for PVCs. EKG shows PVCs occurring in a begiminal pattern. LS is a circumferential multielectrode catheter placed in the aortic route. Note: small, spike-like signals that occur with or without related exit to the ventricle producing PVCs. RVT = right ventricular; HRA = high right atrium; HBE1 and HBE2 = His bundle recording catheters; RVOT uni = right ventricular outflow tract unipola; AORT ablation = ablation catheter placed in the distal aortic outflow tract; CS = coronary sinus.

Figure 7

Typical electrocardiographic pattern of idiopathic left ventricular tachycardia (fascicular VT). A typical right bundle morphology is noted in lead V1. Unlike outflow tract VT, however, leads AVl and AVr are both positive. A strong superior axis is noted, and the positive R wave dominates in lead one.

Figure 8

Intracardiac tracings obtained when mapping a constant PVC that initiated ventricular fibrillation. Note the spike-like signals on the ablation electrodes (ABLD = ablation distal; ABLP = ablation proximal). In this instance, these signals represented the depolarization of the arrhythmogenic Purkinje fibers responsible for the arrhythmia. HBE = His bundle; RV = right ventricle; HRA = high right atrium; CS = coronary sinus

Figure 9

EP tracing demonstrating the onset of ventricular fibrillation provoked by a PVC. The arrow points to a Purkinje potential that precedes the PVC. Note that the time interval from the Purkinje potential to the onset of the QRS varies likely because of different exit sites)