In many cases the mechanism of PVCs is unknown and more than one process may ultimately be responsible. There are three basic mechanism that might be at play:³

• Triggered activity.
• Automaticity.
• Re-entry.  

The mechanism may have clinical relevance when considering behavioural triggers, other underlying diseases, the potential effectiveness of certain medicines, and understanding the approaches (and therefore patient experiences) pertinent to catheter ablation procedures, explain Marcus et al.³

What are PVCs?

PVCs are extra heartbeats that begin in one of the heart's two lower pumping chambers (ventricles), which leads to a prolonged QRS complex duration of >120ms because of the delay in the spread of activation to the contralateral ventricle through the non-specialised myocardium.⁴

However, in certain instances, a QRS complex duration of <120ms can occur, leading to the activation of both ventricles synchronously because of electrical stimulus from one of the fascicles through a specific conduction system.⁴

Prevalence, risk factors, and symptoms

The prevalence of PVCs is estimated to be ~0.5% in patients <20-years and 2.2% in those >50-years. In the majority of cases, the cause of PVCs is unknown. Risk factors include increasing age, a taller height, high blood pressure, a history of heart disease, sedentary lifestyles, and smoking.^2,3,4 

Some patients experience no symptoms, while others may complain about palpitations (fluttering, pounding, skipping beats, or often a strange sensation in the neck), fatigue, shortness of breath, change of stamina and endurance, light-headedness or dizziness.^1,4

Diagnosing and treating PVCs

Patients with no or mild symptoms, a low PVC burden (see table 1), and normal ventricular function may be best served with simple reassurance. The decision to initiate additional management beyond reassurance should be based on:³

• Symptoms.
• The burden of the PVCs (a percentage of all beats).
• The presence or absence of SHD.

Patients who experience frequent symptoms should be referred for an echocardiogram.Furthermore, cardiac magnetic resonance imaging (cMRI) may be helpful when the evaluation suggests the presence of associated SHD. Ambulatory monitoring is required to assess symptom frequency, which may be a risk factor for heart failure and mortality.³

Pharmacotherapy or catheter ablation are considered first-line therapies in most patients with symptoms or a reduced left ventricular ejection fraction (LVEF). Patient preference plays a role in determining which to try first.³

The 2022 European Society of Cardiology (ESC) guidelines for the management of patients with ventricular arrhythmia and the prevention of sudden cardiac death, recommend catheter ablation as first-line treatment for symptomatic PVCs from the right ventricular outflow tract (RVOT) or the left fascicles.⁵

β-blockers or non-dihydropyridine calcium channel blockers (CCBs) are indicated in symptomatic patients with PVCs from an origin other than the RVOT or the left fascicles, recommends the ESC.⁵

The ESC guidelines recommend using β-blockers, non-dihydropyridine CCBs, or flecainide when catheter ablation is not available, not desired, or is particularly risky. Catheter ablation or flecainide should also be considered in symptomatic patients with PVCs from an origin other than the RVOT or the left fascicles.⁵

PVC-induced cardiomyopathy should be considered in patients with an unexplained reduced ejection fraction and a PVC burden of ≥10%. In patients with cardiomyopathies suspected to be caused by frequent and predominantly monomorphic PVCs, the ESC recommends catheter ablation.⁵

The latest American Heart Association/American College of Cardiology/Heart Rhythm Society guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death (2017), recommend β-blockers, non-dihydropyridines CCBs, and some AADs for the relieve of symptoms.⁶

Efficacy and safety of AADs

The success of PVC ablation procedures ranges from 80% to 95%, while the efficacy of β-blockers or CCB is in the range of 20%. Flecainide has been reported to achieve a higher rate of PVC reduction (≥85%) compared to β-blockers or CCB.^3,7,8

In the past, class IC AADs were contraindicated in patients with significant SHD. A 2018 study by Hyman et al, investigated whether class IC AADs can be safely used to treat PVC-induced cardiomyopathy.⁹

This was a small cohort (n=20) with suspected PVC-induced cardiomyopathy and who had undergone an average of 1.3 ± 0.2 previous unsuccessful ablations.⁹

In patients treated with flecainide or propafenone, mean PVC burden decreased from 36.2% ± 3.5% to 10.0% ± 2.4%. Mean LVEF increased from 37.4%±2% to 49% ± 1.9%. Seven patients with myocardial delayed enhancement on cMRI (all <5% of the total myocardium) experienced similar improvement in LVEF (from 36.8% ± 4.3% before AAD treatment to 51.7%±3.7% afterward. Over an average 3.8±0.9 treatment-years, no sustained ventricular arrhythmias or sudden cardiac deaths occurred.⁹

The team concluded that in patients suspected of having PVC-induced cardiomyopathy, AADs effectively suppressed PVCs, leading to LVEF recovery in the majority of patients. No adverse events occurred in this small cohort.⁹

According to Bunch et al (2019) broad exclusion of the use of class IC AADs to treat all patients with ventricular arrhythmias in the setting of coronary artery disease (CAD) has been advocated, despite the fact that it is unclear if this exclusion is justified in patients without a prior MI.¹⁰

Their study showed that flecainide in patients with stable CAD and a preserved ejection for PVCs and VT has a favourable safety profile compared to class III AADs. These data suggest the need for prospective trials of flecainide in CAD patients to determine if the guideline-recommended exclusion is justified.¹⁰

Conclusions

For patients without symptoms, the prognosis is excellent. However, asymptomatic patients with an EF of <40% may have a slightly higher risk of developing ventricular arrhythmias and even cardiac arrest.¹¹ 

Those with frequent PVCs (>1000/day) are at risk of developing dilated cardiomyopathy. For those with heart disease, PVCs are an indicator of increased mortality risk.¹¹

PVCs occurring during a period of exercise have a varying prognosis, depending on when they occur. If the PVCs occur during exercise, the prognosis is very good. If they occur during the recovery phase of exercise, the long-term risk of mortality is higher than the general population.¹¹

In general, PVCs that occur in patients with left ventricular dysfunction are associated with high mortality. In addition, PVCs that are not inducible during electrophysiology studies are associated with a low risk for sudden death.¹¹

Table 1: The Lown grading system for PVCs¹¹

PVCs usually are described in terms of the Lown grading system for premature beats, as follows (the higher the grade, the more serious the ectopy):

References