Causes of Premature Ventricular Contractions (PVCs) on EKG
PVCs arise from multiple etiologies, but the most critical distinction is whether structural heart disease is present, as this fundamentally changes risk stratification and management. 1
Primary Causes and Mechanisms
Structural Heart Disease (Highest Risk)
- Ischemic heart disease is the most common cause of life-threatening PVCs, particularly in patients over 30 years of age, where coronary artery disease accounts for the majority of sudden cardiac death cases 1
- Cardiomyopathies including dilated, hypertrophic, and arrhythmogenic right ventricular cardiomyopathy (ARVC) are major structural causes, with ARVC particularly suspected when PVCs show LBBB morphology with QRS duration exceeding 160 ms 1
- Valvular heart disease such as mitral valve prolapse, aortic stenosis, and mitral regurgitation commonly trigger PVCs 2
- Prior myocardial infarction creates substrate for reentrant circuits and automaticity, with PVC frequency directly correlating with mortality risk 1, 3
Idiopathic PVCs (Lower Risk in Structurally Normal Hearts)
- Right ventricular outflow tract (RVOT) is the most common origin site for benign PVCs in structurally normal hearts, characterized by LBBB morphology with inferior axis 1, 4
- Left ventricular outflow tract (LVOT) accounts for substantial idiopathic PVCs, showing inferior axis with early R/S transition at V1/V2 4
- Papillary muscles and annular structures serve as less common but identifiable PVC origins 4
Reversible and Exacerbating Factors
- Stimulants and medications including caffeine, alcohol, sympathomimetic agents, and certain antiarrhythmics provoke PVCs 2
- Electrolyte abnormalities particularly hypokalemia and hypomagnesemia increase PVC frequency 5
- Increased sympathetic tone from anxiety, fever, infection, dehydration, anemia, or hyperthyroidism triggers PVCs 1
Genetic and Channelopathies
- Long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia cause PVCs with high sudden death risk 2
- Family history of sudden cardiac death significantly elevates risk even with apparently benign PVCs 6
Risk Stratification Based on PVC Burden
The frequency and characteristics of PVCs determine clinical significance:
Low-Risk Features
- <100 PVCs per 24 hours carries 0% risk of underlying structural heart disease 6
- <2,000 PVCs per 24 hours has only 3% risk of structural disease 1, 6
- PVC burden <10% is generally benign in structurally normal hearts and requires only surveillance 2, 6
High-Risk Features Requiring Aggressive Evaluation
- ≥2,000 PVCs per 24 hours carries up to 30% risk of underlying structural heart disease 1, 6
- PVC burden >15% significantly increases risk of PVC-induced cardiomyopathy and warrants intervention 2, 6
- Multifocal PVCs suggest potential pathology and mandate further workup 1, 6
- PVCs that increase with exercise rather than suppress are concerning and require comprehensive evaluation 1, 6
- Wide QRS duration >160 ms may indicate ARVC even with RVOT morphology 1
Critical Pitfalls to Avoid
Never dismiss multiple PVCs (≥2 on standard 12-lead ECG) as benign without proper evaluation, as this finding in athletes or general population warrants at minimum Holter monitoring, echocardiography, and exercise stress testing 1. The presence of ≥2 PVCs on a single ECG occurs in <1% of athletes but may herald underlying heart disease 1.
In post-MI patients, even low PVC burdens carry different risk thresholds: >10 PVCs per hour (approximately 1% burden) has 42-54% sensitivity for predicting arrhythmic events, and PVCs remain an independent predictor of mortality with relative risk of 1.62 at 6 months 6.
PVC-induced cardiomyopathy can develop with burdens as low as 10%, though risk substantially increases above 15%, with 82% of patients normalizing left ventricular function within 6 months after successful ablation 2, 6.