What are Premature Ventricular Contractions (PVCs) on an Electrocardiogram (ECG)?

What are Premature Ventricular Contractions (PVCs) on ECG?

PVCs are early depolarizations of the myocardium originating from an ectopic focus within the ventricles, appearing on ECG as abnormal, wide QRS complexes that occur before the expected normal beat. 1, 2

Definition and ECG Characteristics

• PVCs are defined as premature ventricular complexes that originate from the ventricles rather than the normal conduction system. 1
• On ECG, PVCs appear as wide QRS complexes (typically >120 ms) that occur earlier than expected in the cardiac cycle. 3, 4
• The QRS morphology differs from the patient's normal sinus beats because the electrical impulse spreads through ventricular muscle rather than the His-Purkinje system. 3, 2
• PVCs are typically followed by a compensatory pause as the ventricle resets before the next normal beat. 2

Epidemiology and Prevalence

• PVCs are extremely common, found in approximately 50% of all people on long-term monitoring, regardless of whether they have heart disease. 1
• On standard 12-lead ECG, PVCs are detected in only 0.6% of people <20 years of age and 2.7% of those >50 years of age, but this dramatically underestimates true prevalence. 1, 5
• The frequency of PVCs increases with age. 1
• In athletes, PVCs are uncommon and present in <1% of 12-lead ECGs. 5

Clinical Spectrum: Benign vs. Concerning Features

Generally Benign PVCs

• Isolated, infrequent PVCs (<10% burden on 24-hour monitoring) in patients without structural heart disease are typically benign. 5, 6
• PVCs that suppress with exercise are generally benign. 5, 6
• A PVC burden <2.1% represents very low clinical significance. 6

High-Risk Features Requiring Further Evaluation

• Multiple (≥2) PVCs on a standard 12-lead ECG suggest potential pathology. 5, 6
• PVC burden >10-15% of total heartbeats increases risk of PVC-induced cardiomyopathy. 5, 6
• Multifocal PVCs (originating from different ventricular sites) indicate higher cardiovascular risk. 1, 5, 6
• Wide QRS duration >160 ms may indicate arrhythmogenic right ventricular cardiomyopathy. 5, 6
• PVCs that increase rather than suppress with exercise are concerning. 5, 6
• Very frequent PVCs (>10,000-20,000 per day) can be associated with depressed left ventricular function. 1

Risk Stratification by Absolute Count

• <100 PVCs/24 hours: 0% risk of structural heart disease. 6
• <2,000 PVCs/24 hours: 3% risk of structural heart disease. 6
• ≥2,000 PVCs/24 hours: up to 30% risk of structural heart disease. 6

Clinical Significance and Outcomes

• In the general population, frequent PVCs (≥1 PVC on 12-lead ECG or >30 PVCs per hour) are associated with increased cardiovascular risk and mortality. 1
• PVCs are associated with increased risk of stroke in population studies. 1
• In patients with cardiovascular disease, PVCs and nonsustained ventricular tachycardia (NSVT, defined as ≥3 consecutive ventricular beats) are associated with adverse outcomes including death. 1
• In post-MI patients, PVCs remain an independent predictor of total mortality and sudden cardiac death (RR=1.62 for total mortality). 6

Evaluation Algorithm

Initial Assessment

1. Obtain 12-lead ECG to assess QRS morphology, duration, and frequency of PVCs. 4
2. Perform 24-hour Holter monitoring to quantify PVC burden as percentage of total heartbeats. 5, 6, 4
3. Order echocardiography to exclude structural heart disease (hypertrophic cardiomyopathy, dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, myocarditis, sarcoidosis). 5, 7, 4
4. Conduct exercise stress testing to determine if PVCs suppress (benign) or worsen (concerning) with exercise. 5, 6

Advanced Testing When Indicated

• Cardiac MRI should be performed if >2,000 PVCs/24 hours, NSVT present, or echocardiography is abnormal. 7
• Check serum potassium, magnesium, and calcium, particularly in patients with prolonged QTc or symptoms suggesting electrolyte abnormalities. 7
• Consider thyroid function testing and toxicology screening based on clinical presentation. 7

Treatment Principles

Critical Pitfall to Avoid

• Class I antiarrhythmic drugs (flecainide, encainide, quinidine) and d-sotalol INCREASE mortality in patients with post-MI or reduced LVEF and should NOT be used. 1
• The CAST trial definitively showed that despite suppressing PVCs, these medications increased death risk. 1

When Treatment is Indicated

• Treatment is indicated for: symptomatic PVCs, high PVC burden (>10-15%) with risk of cardiomyopathy, or PVCs associated with structural heart disease. 5
• Beta-blockers are first-line therapy for symptomatic PVCs. 4
• Nondihydropyridine calcium channel blockers can be considered as second-line agents. 4
• Catheter ablation is recommended for patients who fail medical therapy or cannot tolerate medications, with good success rates in reducing PVC burden and improving LVEF in PVC-induced cardiomyopathy. 4

When Treatment is NOT Indicated

• Asymptomatic patients with normal cardiac structure and PVC burden <10% require only clinical follow-up in 6-12 months with repeat ECG. 6
• Repeat Holter monitoring in 1-2 years to assess for changes in PVC burden. 6

Common Locations of Origin

• Most idiopathic PVCs originate from the right ventricular outflow tract (RVOT) or left ventricular outflow tract, including the aortic root. 3
• Other typical locations include the tricuspid or mitral valve annulus, papillary muscles, and Purkinje fibers. 3
• The mechanism is typically delayed post-depolarization (triggered activity). 3