A Systematic Approach to the Evaluation of Patients with Ventricular Ectopy

Cardiologists and electrophysiologists are commonly asked to evaluate and manage patients with premature ventricular contractions (PVCs). A systematic flow diagram summarizing the evaluation and treatment of patients with PVCs is below (Figure 1).

Patients with PVCs can present with palpitations and be highly symptomatic, but can also present with PVCs detected incidentally. The first step in the evaluation is to confirm the diagnosis. It is important to rule out premature atrial beats with aberrant conduction, and to exclude electrocardiographic artifact. Once the diagnosis is established, the first and probably most important step is to exclude structural heart disease. The goals at the initial encounter are not only to reduce symptoms, but to risk stratify patients to prevent sudden cardiac death and avoid a PVC-induced cardiomyopathy. The type of testing that needs to be performed at this stage is variable and depends on the pretest probability of underlying heart disease, but at the minimum should include an electrocardiogram (ECG) and echocardiogram. Follow-up stress testing or cardiac magnetic resonance imaging should be done when indicated. Arrhythmogenic right ventricular cardiomyopathy (ARVC) must be excluded in patients with frequent PVCs that are of a left bundle branch block morphology, particularly when they do not appear to be arising from the outflow tract, where most idiopathic PVCs come from. Patients who are found to have structural heart disease need to have appropriate targeted therapy initiated. For example, patients who are diagnosed with a dilated cardiomyopathy will need treatment specific for their cardiomyopathy and not necessarily for the ventricular ectopy. Patients with no structural heart disease are usually at very low risk of sustained ventricular arrhythmias. However, there are case reports of patients with what appear to be idiopathic PVCs who suffered from a ventricular fibrillation cardiac arrest, particularly when the PVCs are tightly coupled.

Next, determine if the PVCs are polymorphic in morphology. If so, the patient may have a primary electrical disorder that, even in the absence of structural heart disease, can be associated with a high risk of sustained ventricular arrhythmias. Diseases that must be excluded include catecholaminergic polymorphic ventricular tachycardia (CPVT) and long QT syndrome. These patients are often treated with beta-blockers and occasionally ICD therapy. If it is clear that the PVCs are not polymorphic, then the next step is to determine if the patient has symptoms from the PVCs. Continuous monitoring can be very useful to correlate symptoms, such as palpitations, with the occurrence of PVCs. Patients who are asymptomatic generally do not require more than simple reassurance. However, patients who are unaware of their PVCs should have their PVC burden quantified. Patients with a high PVC burden (approximately over 20,000 PVCs in a 24-hour period) must be evaluated closely for a PVC-induced cardiomyopathy. If they have ventricular dysfunction, then they should be treated. Patients with frequent asymptomatic PVCs and preserved ventricular function should be reassured and followed periodically to be sure their ventricular function continues to be stable. Although these patients are often offered medical therapy and catheter ablation, there is no evidence to support such approaches.

Patients who are symptomatic or who have a possible PVC-induced cardiomyopathy should be offered therapy to eliminate their PVCs. Even for patients whose ventricular dysfunction is the primary process rather than the PVCs, elimination of the PVCs can improve their ventricular function. Although beta-blockers generally do little to reduce the number of PVCs, they can improve the symptoms that are often related to the post-PVC pause and the subsequent beat that is associated with a stronger contraction. Patients who fail beta-blocker therapy should be considered for catheter ablation if amenable. This leads to the question of whether their PVCs can be targeted for ablation: are they unifocal and frequent enough to map in the EP lab? Again, continuous monitoring can help determine the burden of PVCs and the frequency of each morphology. Inspection of the QRS morphology can help determine if they are likely to be accessible with endocardial ablation. For difficult cases arising from the outflow tract, mapping and ablation within the anterior interventricular vein and bipolar ablation can be used.

The flow diagram provided here can be useful in the initial and subsequent evaluations of patients with PVCs. Patients who are symptomatic from unifocal PVCs and those who have developed a PVC-induced cardiomyopathy as a result of a high burden of unifocal PVCs, even when asymptomatic, are often good candidates for catheter ablation. As experience has increased, and as mapping systems have improved, the ability to cure these patients has greatly increased.