Causes of Premature Ventricular Contractions
PVCs arise from both structural cardiac disease and non-cardiac triggers, with ischemic heart disease being the most common pathological cause in older adults, while benign idiopathic PVCs predominate in younger individuals without structural abnormalities. 1, 2
Structural Cardiac Causes
Ischemic and Coronary Disease
- Coronary artery disease and ischemic heart disease are the most common pathological causes of PVCs, particularly in middle-aged and older patients 2
- Previous myocardial infarction creates scar tissue that serves as substrate for ventricular ectopy 2
- In acute coronary syndromes, PVCs may indicate incomplete revascularization or recurrent ischemia 2
Cardiomyopathies and Structural Disease
- Heart failure with both reduced (HFrEF) and preserved ejection fraction (HFpEF) significantly increases PVC frequency 2
- Hypertrophic cardiomyopathy generates PVCs through myocardial disarray and fibrosis 2
- Left ventricular hypertrophy from any cause (hypertension, valvular disease) predisposes to PVCs 3
- Valvular heart disease, particularly mitral valve prolapse and aortic stenosis, can trigger PVCs 2
Metabolic and Electrolyte Disturbances
Electrolyte abnormalities are critical reversible causes that must be identified and corrected before considering other interventions 2:
Endocrine and Systemic Conditions
- Hyperthyroidism increases sympathetic tone and PVC frequency 2
- Acute infections and inflammatory conditions affecting the myocardium (myocarditis) 2
Lifestyle and Pharmacological Triggers
Eliminating aggravating factors should be the initial management step alongside any pharmacotherapy 4:
- Excessive caffeine consumption 2, 4
- Alcohol intake 2, 4
- Sympathomimetic agents (decongestants, stimulants, cocaine) 2, 4
Idiopathic PVCs in Structurally Normal Hearts
PVCs are extremely common in healthy individuals, affecting approximately 50% of all people on long-term monitoring, with frequency increasing with age 1, 2:
- Only 0.6% prevalence in those under 20 years on standard 12-lead ECG 1, 2
- Increases to 2.7% in those over 50 years on standard ECG 1, 2
- Most idiopathic PVCs originate from the right ventricular outflow tract (RVOT) with characteristic left bundle branch block morphology and inferior axis 1
Iatrogenic and Procedural Causes
- Reperfusion after coronary intervention can transiently increase PVC burden 2
- Cardiac catheterization or electrophysiology procedures may mechanically trigger PVCs 2
Critical Thresholds for Clinical Significance
The burden and characteristics of PVCs determine their clinical significance more than their mere presence 1:
- Frequent PVCs (>10,000-20,000 per day or >10-15% of total beats) can cause PVC-induced cardiomyopathy, a reversible form of left ventricular dysfunction 1, 2
- PVC burden >24% with short coupling intervals (<300 ms) strongly suggests PVC-induced cardiomyopathy 1, 2
- Multifocal PVCs indicate higher cardiovascular risk even in structurally normal hearts 1, 2
Special Populations
Athletes
- PVCs are uncommon in athletes (<1% on 12-lead ECG) and warrant evaluation when present 1
- Multiple PVCs (≥2) on resting ECG require comprehensive workup including Holter monitoring, echocardiography, and exercise testing 1
- Among athletes with ≥2,000 PVCs per 24 hours, up to 30% have underlying structural heart disease 1
Idiopathic Ventricular Fibrillation
- In rare cases, PVCs from injured Purkinje fibers act as triggers for polymorphic ventricular tachycardia/ventricular fibrillation 1, 2
- These typically have short coupling intervals and consistent morphology 1
Common Pitfalls
Do not dismiss PVCs as benign without quantifying burden and excluding structural disease 5:
- Symptoms correlate poorly with PVC frequency—24-hour monitoring is essential 5
- Exercise-induced PVCs or those that increase with exertion may indicate underlying pathology, while suppression with exercise is generally benign 2
- Even asymptomatic frequent PVCs (>15% burden) require surveillance for development of cardiomyopathy 4, 2