Causes and Risk Stratification of Premature Ventricular Contractions in Young Patients

High-Risk Underlying Conditions

The American Heart Association suggests that young patients with congenital heart disease are at increased risk for clinically significant PVCs and sudden cardiac death 3, 2
The American College of Cardiology recommends that cardiomyopathies (dilated, hypertrophic, or arrhythmogenic) be considered as a potential cause of symptomatic ventricular arrhythmias in young patients 2
Myocardial tumors, particularly in infants, can cause incessant ventricular tachycardia and PVCs, according to the European Society of Cardiology 1, 2
Coronary artery anomalies represent an important structural cause of PVCs in young patients, as stated by the American Heart Association 3, 2

The European Society of Cardiology states that long QT syndrome (LQTS) and other ion channel defects are critical causes of PVCs, particularly forms with AV block or digital syndactyly 1, 2
Wolff-Parkinson-White (WPW) syndrome with short refractory periods (≤240 ms) can cause PVCs and carries SCD risk, according to the American College of Cardiology 1, 3
Short-coupled torsade de pointes predominantly affects young patients, with PVCs having extremely short coupling intervals (<300 ms) initiating polymorphic VT, as reported by the European Heart Journal 4, 5

Myocarditis from viral infections (Coxsackie B, adenovirus, parvovirus B19, HHV-6) causes active inflammatory destruction of myocytes with resultant PVCs, according to the European Heart Journal 4, 5
HIV-related cardiotoxicity and opportunistic infections can cause myocarditis and PVCs, as stated by the European Society of Cardiology 5

Hyperkalemia is a specific cause of sustained VT and PVCs in infants and young patients, according to the American Heart Association 1, 2
Digoxin toxicity can cause ventricular arrhythmias, particularly dangerous when misdiagnosed as SVT in infants, as reported by the European Heart Journal 1, 2, 7

Accelerated idioventricular rhythm is the most common sustained ventricular arrhythmia in infants, typically benign and self-resolving within the first year, according to the American College of Cardiology 1, 2
Incessant VT from myocardial tumors or cardiomyopathy represents a high-risk scenario requiring urgent evaluation in infants, as stated by the American Heart Association 1, 2
PVC prevalence increases from <5% in children to 10% by age 10 and 25% during late adolescence, according to the American Academy of Pediatrics 1, 3, 2

The American College of Cardiology recommends exercise stress testing to determine if PVCs suppress with exercise (benign) or increase (concerning for underlying pathology) 8
The European Society of Cardiology suggests that 24-hour Holter monitoring be used to quantify PVC burden and identify non-sustained VT 8

A PVC burden of <100 PVCs/24h is associated with 0% risk of structural heart disease, according to the American Heart Association 8
A PVC burden of <2,000 PVCs/24h is associated with 3% risk of structural heart disease, as reported by the American College of Cardiology 8
A PVC burden of ≥2,000 PVCs/24h is associated with up to 30% risk of structural heart disease, according to the European Society of Cardiology 8

The American Heart Association warns that administering digoxin or verapamil for presumed SVT in infants without excluding VT can precipitate ventricular fibrillation and sudden death 1, 2, 7
Symptomatic ventricular arrhythmias may be the initial presentation of previously undiagnosed cardiomyopathy, as stated by the American College of Cardiology 2