Causes of Premature Ventricular Contractions (PVCs)
PVCs arise from abnormal impulse formation or reentry in the ventricular myocardium or Purkinje system, with causes ranging from benign idiopathic mechanisms in structurally normal hearts to serious underlying cardiac pathology, particularly ischemic heart disease in older patients. 1, 2
Structural Heart Disease
The most clinically significant causes of PVCs involve underlying cardiac pathology:
- Coronary artery disease and ischemic heart disease are the most common causes, particularly in older patients, and represent the primary substrate for life-threatening ventricular arrhythmias 1, 2
- Heart failure (both reduced and preserved ejection fraction) significantly increases PVC frequency and risk 2
- Previous myocardial infarction creates scar tissue that serves as a substrate for reentrant circuits 2
- Hypertrophic cardiomyopathy and valvular heart disease are additional structural causes requiring evaluation 2
Metabolic and Electrolyte Disturbances
Reversible metabolic factors frequently trigger PVCs:
- Hypokalemia, hypomagnesemia, and hypocalcemia alter myocardial excitability and should be corrected first 2
- Hyperthyroidism increases cardiac stimulation and PVC burden 2
Lifestyle and Exogenous Factors
Multiple modifiable triggers contribute to PVC occurrence:
- Excessive caffeine consumption precipitates heightened cardiac stimulation 2, 3
- Alcohol disturbs electrical pathways even in moderate amounts 2, 3
- Nicotine and smoking disrupt normal conduction 2, 3
- Sympathomimetic agents (including illicit drugs like cocaine and amphetamines) directly increase PVC frequency 2, 3
- Stress and elevated cortisol levels create autonomic imbalance favoring PVC generation 3
- Sleep deprivation and insomnia increase PVC burden through autonomic dysregulation 3
- Obesity is associated with higher PVC rates 3
Idiopathic PVCs in Structurally Normal Hearts
In the absence of structural disease, PVCs typically originate from specific anatomic locations:
- Right ventricular outflow tract (RVOT) is the most common site, producing PVCs with left bundle branch block morphology and inferior axis 1, 4
- Left ventricular outflow tract and aortic root are the second most common locations 4
- Tricuspid or mitral valve annulus, papillary muscles, and Purkinje fibers represent other typical focal origins 4
- The mechanism is usually delayed afterdepolarization rather than reentry 4
Age-Related and Population Factors
PVC prevalence increases dramatically with age:
- In healthy individuals, PVCs occur in only 0.6% of those under 20 years but 2.7% of those over 50 years on standard ECG 1, 5
- Long-term monitoring reveals PVCs in approximately 50% of all people regardless of heart disease status 1, 5, 2
- In athletes, PVCs are uncommon, present in less than 1% of 12-lead ECGs, and when present warrant evaluation for underlying pathology 1, 5
Clinical Context Matters
The significance of PVCs depends heavily on burden and associated conditions:
- Frequent PVCs (>10,000-20,000 per day or >10-15% of total beats) can themselves cause cardiomyopathy through chronic dyssynchrony 2, 6, 7
- Multifocal PVCs indicate higher cardiovascular risk even in younger adults 1, 5
- PVCs during acute coronary syndromes may signal incomplete revascularization or recurrent ischemia 2
- In patients with idiopathic ventricular fibrillation, PVCs from injured Purkinje fibers act as triggers for life-threatening arrhythmias 2
Common Pitfall
Do not assume all PVCs are benign simply because they are common. The American College of Cardiology emphasizes that detection of PVCs, particularly if multifocal and frequent, mandates evaluation to exclude underlying conditions like ischemic heart disease or left ventricular dysfunction that warrant treatment to reduce mortality risk 1. The widespread assumption that PVCs are insignificant is not supported by research evidence, as frequent PVCs (>10% of heartbeats) can cause fatigue, dyspnea, and when exceeding 20% of beats, may lead to cardiomyopathy and heart failure 6.