What are the causes of premature ventricular contractions (PVCs)?

Causes of Premature Ventricular Contractions

PVCs arise from both cardiac and non-cardiac causes, with structural heart disease being the most clinically significant etiology, though they commonly occur in healthy individuals as a benign finding.

Structural Heart Disease Causes

The most important cardiac causes to identify include:

• Coronary artery disease and ischemic heart disease are among the most common pathologic causes of PVCs, particularly in older patients 1
• Previous myocardial infarction creates scar tissue that serves as substrate for PVCs 1
• Heart failure (both reduced and preserved ejection fraction) significantly increases PVC frequency 1
• Hypertrophic cardiomyopathy is a well-established cause of PVCs 1
• Valvular heart disease can trigger PVCs through hemodynamic stress and chamber dilation 1

The presence of structural heart disease is the strongest predictor of adverse outcomes in patients with PVCs, making this distinction critical 2.

Metabolic and Electrolyte Disturbances

Reversible causes that must be evaluated include:

• Hypokalemia, hypomagnesemia, and hypocalcemia are common electrolyte triggers 1
• Hyperthyroidism increases adrenergic tone and PVC frequency 1
• Acute infections and inflammatory conditions affecting the myocardium (including myocarditis) can manifest as PVCs 1, 3

Lifestyle and Pharmacologic Triggers

Modifiable factors include:

• Excessive caffeine consumption acts as a sympathomimetic trigger 1
• Alcohol use can provoke PVCs through multiple mechanisms 1
• Sympathomimetic agents (including decongestants, stimulants) increase catecholamine-mediated PVCs 1

Ischemia-Related PVCs

In the acute setting:

• Reperfusion after coronary intervention commonly triggers PVCs as a marker of restored blood flow 1
• Incomplete revascularization or recurrent ischemia in acute coronary syndrome patients may manifest as new or increased PVCs 1
• Approximately 5-10% of patients with acute MI develop VF or sustained VT before hospital presentation, with another 5% developing these arrhythmias within 48 hours of admission 4

PVCs in Structurally Normal Hearts

PVCs are extremely common in healthy individuals and increase with age:

• Approximately 50% of all people demonstrate PVCs on long-term monitoring 1
• Prevalence ranges from 0.6% in those under 20 years to 2.7% in those over 50 years on standard 12-lead ECG 1
• In young adults with high functional capacity, isolated PVCs are generally benign 1

Risk Factors for PVC-Induced Cardiomyopathy

When PVC burden becomes pathologic:

• High PVC burden (>10-15% of total heartbeats or >10,000-20,000 PVCs/day) can cause reversible left ventricular dysfunction 4, 1, 5
• Short coupling interval (<300 ms) increases risk of cardiomyopathy 1
• Wide QRS complexes (>160 ms) suggest greater myocardial involvement and higher risk 1

Special Clinical Contexts

Important caveats:

• Multifocal PVCs (originating from different ventricular sites) suggest higher cardiovascular risk even in young adults and warrant thorough evaluation 1, 2
• PVCs in athletes are uncommon and require evaluation when present, particularly if complex morphology 4, 1
• PVCs that worsen with exercise may indicate underlying pathology, while those suppressing with exercise are generally benign 1, 5
• In patients with idiopathic ventricular fibrillation, PVCs from injured Purkinje fibers can act as triggers for life-threatening arrhythmias 1

Risk Stratification by Absolute Count

The European Heart Journal provides specific thresholds:

• <100 PVCs/24 hours: 0% risk of structural heart disease 5
• <2,000 PVCs/24 hours: 3% risk of structural heart disease 5
• ≥2,000 PVCs/24 hours: Up to 30% risk of structural heart disease 5

Common pitfall: Assuming all PVCs are benign without quantifying burden or excluding structural disease. Even in asymptomatic patients, very frequent PVCs (>10,000-20,000/day) can cause reversible cardiomyopathy that requires intervention 4, 6.