Evaluation and management of premature ventricular complexes

Cleveland Clinic Journal of Medicine. 2013 June;80(6):377-387 | 10.3949/ccjm.80a.12168

June 1, 2013|Cleveland Clinic Journal of Medicine

ABSTRACTPremature ventricular complexes (PVCs) are a common cause of palpitations. Related symptoms include difficulty breathing, chest pain, fatigue, and dizziness. PVCs are also commonly detected incidentally on electrocardiography, outpatient ambulatory monitoring, and inpatient telemetry. Treatment goals include palliating symptoms, restoring cardiac function if affected, and preventing progression to tachycardia-related cardiomyopathy if the PVC burden is high, even in patients without symptoms. Responses to caffeine reduction, cessation of stimulants, and stress reduction are inconsistent. Aerobic exercise is rarely effective and can sometimes exacerbate PVCs.

KEY POINTS

Diagnostic evaluation should include an assessment for structural heart disease and quantification of the total PVC burden by ambulatory Holter monitoring.
Patients without structural heart disease and low-to-modest PVC burdens do not always require treatment. PVCs at higher burdens (typically more than 15% to 20% of heartbeats) or strung together in runs of ventricular tachycardia pose a higher risk of tachycardia-related cardiomyopathy and heart failure, even if asymptomatic.
When necessary, treatment for PVCs involves beta-blockers, calcium channel blockers, or other antiarrhythmic drugs and catheter ablation in selected cases.
Catheter ablation can be curative, but it is typically reserved for drug-intolerant or medically refractory patients with a high PVC burden.

Noninvasive cardiac evaluation

Surface echocardiography is indicated to look for overt structural heart disease and can reliably detect abnormalities in cardiac chamber size, wall thickness, and function. Valvular heart disease is concomitantly identified by two-dimensional imaging as well as by color Doppler. The finding of significant structural heart disease in conjunction with PVCs should prompt a cardiology referral, as this carries significant prognostic implications.^3–5

Exercise treadmill stress testing is appropriate for patients who experience PVCs with exercise or for whom an evaluation for coronary artery disease is indicated. The expected finding would be an increase in PVCs or ventricular tachycardia with exercise or in the subsequent recovery period. Exercise testing can be combined with either echocardiographic or nuclear perfusion imaging to evaluate the possibility of myocardial ischemia. For patients unable to exercise, pharmacologic stress testing with dobutamine or a vasodilator agent can be performed.

Advanced noninvasive cardiac imaging— such as computed tomography, magnetic resonance imaging, or positron-emission tomography—should be reserved for specific clinical indications such as congenital heart disease, suspected cardiac sarcoidosis, and infiltrative heart disease, and for specific cardiomyopathies, such as hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. For example, frequent PVCs with a left bundle branch block morphology and superior axis raise the concern for a right ventricular disorder and may prompt cardiac magnetic resonance imaging for either arrhythmogenic right ventricular cardiomyopathy or sarcoidosis.

PVCs WITHOUT STRUCTURAL HEART DISEASE

Outflow tract PVCs and ventricular tachycardia

The right or left ventricular outflow tracts, or the epicardial tissue immediately adjacent to the aortic sinuses of Valsalva are the most common sites of origin for ventricular ectopy in the absence of structural heart disease.^6–9 Affected cells often demonstrate a triggered activity mechanism due to cyclic adenosine monophosphate-mediated and calcium-dependent delayed after-depolarizations.^7,8

Figure 1. (A) A PVC originating in the right ventricular outflow tract with the classic left bundle branch block morphology, inferior axis with tall R waves in the inferior limb leads, and precordial transition between V3 and V4. (B) Complete elimination of the PVC after successful catheter ablation in the posteroseptal right ventricular outflow tract.

Most of these foci are in the right ventricular outflow tract, producing a left bundle branch block morphology with an inferior axis (positive R waves in limb leads II, III, and aVF) and typical precordial R-wave transition in V₃ and V₄ (Figure 1). A minority are in the left ventricular outflow tract, producing a right bundle branch block with an inferior axis pattern, or in the aortic sinuses with a left bundle branch block pattern but with early precordial R transition in V₂ and V₃.

A study in 122 patients showed that right and left outflow tract arrhythmias had similar electrophysiologic properties and pharmacologic sensitivities, providing evidence for shared mechanisms possibly due to the common embryologic origin of these structures.⁹

Such arrhythmias are typically catecholamine-sensitive and are sometimes inducible with burst pacing in the electrophysiology laboratory. The short ventricular coupling intervals can promote intracellular calcium overload in the affected cells, leading to triggered activity.

Therefore, outflow tract PVCs and ventricular tachycardia are commonly encountered clinically during exercise and, to an even greater extent, in the postexercise cool-down period. Similarly, they can be worse during periods of emotional stress or fatigue, when the body’s endogenous catecholamine production is elevated. However, it is worthwhile to note that there are exceptions to this principle in which faster sinus rates seem to overdrive the PVCs in some patients, causing them to become paradoxically more frequent at rest, or even during sleep.

Figure 2. Electroanatomic activation map created during a catheter ablation procedure of a right ventricular outflow tract PVC. The map is limited to only the region of interest, and is depicted in the right anterior oblique (RAO) projection, with a cartoon face on top and a heart model in the left lower corner provided for orientation. The PVC site of origin is marked by the white cross, and the red-to-blue color scheme depicts its electrical propagation away from its origin. The three red dots abutting the white cross represent the sites where radiofrequency energy was applied to successfully ablate and eliminate this PVC. These appear off the map as they were annotated on a sinus beat, rather than a PVC, as a reference to deliver additional lesions if desired at the successful site once the targeted PVC is eliminated, as was done in this case. The remaining white and yellow dots indicate locations where pace mapping was performed with the ablation catheter.

Outflow tract PVCs can be managed medically with beta-blockers, nondihydropyridine calcium channel blockers (verapamil or diltiazem), or, less commonly, class IC drugs such as flecainide. They are also highly curable by catheter ablation (Figure 2), with procedure success rates greater than 90%.^9.10

However, a subset of outflow tract PVCs nested deep in a triangle of epicardial tissue between the right and left endocardial surface and underneath the left main coronary artery can be challenging. This region has been labeled the left ventricular summit, and is shielded from ablation by an epicardial fat pad in the adjacent pericardial space.¹¹ Ablation attempts made from the right and left endocardial surfaces as well as the epicardial surface (pericardial space) sometimes cannot adequately penetrate the tissue deep enough to reach the originating focus deep within this triangle. While ablation cannot always fully eliminate the PVC, ablation from more than one of the sites listed can generally reduce its burden, often in combination with suppressive medical therapy (Figure 3).

Fascicular PVCs

Figure 3. (A) A very frequent PVC originating from the left ventricular summit. The PVC is occurring in bigeminy and has left bundle branch block morphology in V1, a very early precordial transition in V2, an overall broad QRS with a slurred rS appearance in limb lead I, and an overall inferior axis. Despite efforts to characterize this PVC prospectively, the pattern on ECG varies depending on the heart’s rotation, and the diagnosis cannot always established until the time of catheter ablation. (B) Catheter ablation from the right and the left endocardial and epicardial surfaces resulted in reduction of the PVC burden, but not a complete and curative elimination. The residual PVC burden required adjunctive medical suppressive therapy with flecainide.

Fascicular PVCs originate from within the left ventricular His-Purkinje system¹² and produce a right bundle branch block morphology with either an anterior or posterior hemiblock pattern (Figure 4). Exit from the posterior fascicle causes an anterior hemiblock pattern, and exit from the anterior fascicle a posterior hemiblock pattern. Utilization of the rapidly conducting His-Purkinje system gives these PVCs a very narrow QRS duration, sometimes approaching 120 milliseconds or shorter. This occasionally causes them to be mistaken for aberrantly conducted supraventricular beats. Such spontaneous PVCs are commonly associated with both sustained and nonsustained ventricular tachycardia and are usually sensitive to verapamil.¹³

Special issues relating to mapping and catheter ablation of fascicular arrhythmias involve the identification of Purkinje fiber potentials and associated procedural diagnostic maneuvers during tachycardia.¹⁴

Other sites for PVCs

Figure 4. (A) A PVC originating from the left posterior fascicle with a characteristic right bundle branch block pattern, left superior axis, and a relatively narrow QRS. (B) Successful catheter ablation from the endocardial surface of the left ventricle resulted in the curative elimination of this PVC.

Other sites of origin for PVCs in the absence of structural heart disease include ventricular tissue adjacent to the aortomitral continuity,¹⁵ the tricuspid annulus,¹⁶ the mitral valve annulus, ¹⁷ papillary muscles,¹⁸ and other Purkinje-adjacent structures such as left ventricular false tendons.¹⁹ An example of a papillary muscle PVC is shown in Figures 5 and 6.

Curable by catheter ablation

Any of these PVCs can potentially be cured by catheter ablation when present at a sufficient burden to allow for activation mapping in the electrophysiology laboratory. The threshold for offering ablation varies among operators, but is generally around 10% or greater. Pacemapping is a technique applied in the electrophysiology laboratory when medically refractory symptomatic PVCs occurring at a lower burden require ablation.

PVCs WITH AN UNDERLYING CARDIAC CONDITION

Coronary artery disease

Figure 5. (A) A papillary muscle PVC occurring in a bigeminal pattern and occasional couplets. The PVC has a right bundle branch morphology with a left superior axis and a slurred, notched appearance in the precordial leads. (B) After successful catheter ablation at the base of the posterior papillary muscle.

Tissue injury and death caused by acute myocardial infarction has long been recognized as a common cause of spontaneous ventricular ectopy attributed to infarct border zones of ischemic or hibernating myocardium.^20,21

Suppression has not been associated with improved outcomes, as shown for class IC drugs in the landmark Cardiac Arrhythmia Suppression Trial (CAST),²² or in the amiodarone treatment arm of the Multicenter Automatic Defibrillator Implantation Trial II (MADIT-II).²³ Therefore, treatment of ventricular ectopy in this patient population is usually symptom-driven unless there is hemodynamic intolerance, tachycardia-related cardiomyopathy, or a very high burden of PVCs in a patient who may be at risk of developing tachycardia-related cardiomyopathy. Antiarrhythmic drug treatment, when required, usually involves beta-blockers or class III medications such as sotalol or amiodarone.

Nonischemic dilated cardiomyopathy

Figure 6. Electroanatomic activation map created during catheter ablation of the papillary muscle PVC shown in Figure 5. The map shows both the right and left ventricles in the anterior projection. The successful ablation site is demarcated by the blue dots at the base of the posteromedial papillary muscle. The catheter tip is depicted in alignment with the annotated blue reference point, whereas the catheter body projects outside the shell of the map as can occur with this mapping software. Catheter positions are evaluated also in real time by fluoroscopy and sometimes by intracardiac echocardiography.

This category includes patients with a wide variety of disease states including valvular heart disease, lymphocytic and other viral myocarditis, cardiac sarcoidosis, amyloidosis and other infiltrative diseases, familial conditions, and idiopathic dilated cardiomyopathy (ie, etiology unknown). Although it is a heterogeneous group, a common theme is that PVCs in this patient cohort may require epicardial mapping and ablation.²⁴ Similarly, epicardial PVCs and ventricular tachycardia cluster at the basal posterolateral left ventricle near the mitral annulus, for unclear reasons.²⁵

While specific criteria have been published, an epicardial focus is suggested by slowing of the initial QRS segment, pseudo-delta waves, a wider overall QRS, and Q waves in limb lead I.²⁶

Treatment is symptom-driven unless the patient has a tachycardia-related cardiomyopathy or a high burden associated with the risk for its development. Antiarrhythmic drug therapy, when required, typically involves a beta-blocker or a class III drug such as sotalol or amiodarone. Sotalol is used in this population but has limited safety data and should be used cautiously in patients without an implantable cardioverter-defibrillator.

References

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