What are the causes of premature ventricular contractions (PVCs) on an electrocardiogram (ECG)?

Causes of Premature Ventricular Contractions (PVCs) on ECG

PVCs arise from structural heart disease, electrolyte disturbances, medications, stimulants, and idiopathic mechanisms, with ischemic heart disease and cardiomyopathy being the most clinically significant causes requiring immediate evaluation. 1

Primary Etiologic Categories

Structural Heart Disease

• Ischemic heart disease is the leading cause of PVCs in older patients and carries the highest mortality risk, particularly in post-myocardial infarction patients with reduced ejection fraction 1, 2
• Cardiomyopathies (dilated, hypertrophic, arrhythmogenic right ventricular) directly cause PVCs through myocardial scarring and electrical instability 3, 1
• Valvular heart disease including mitral valve prolapse, aortic stenosis, and mitral regurgitation generates PVCs through mechanical stretch and hemodynamic stress 3
• Left ventricular hypertrophy from chronic hypertension creates substrate for ventricular ectopy 4, 2

Metabolic and Electrolyte Disturbances

• Hypokalemia, hypomagnesemia, and hypercalcemia directly alter myocardial excitability and are reversible causes that must be corrected before considering antiarrhythmic therapy 1
• Hypoglycemia in diabetic patients increases nocturnal bradycardia and ventricular ectopy through autonomic dysfunction 1
• Glycemic fluctuations and autonomic remodeling in diabetes contribute to arrhythmogenesis 1

Medications and Substances

• Digitalis toxicity causes characteristic bidirectional ventricular tachycardia and frequent PVCs 1
• Stimulant medications (sympathomimetics, methylphenidate) trigger PVCs through increased adrenergic tone 3
• Certain antiarrhythmic drugs paradoxically cause PVCs through proarrhythmic effects 3
• Caffeine and alcohol consumption increase PVC frequency in susceptible individuals 3, 2

Acute Ischemia and Coronary Syndromes

• Acute myocardial ischemia causes electrical instability manifesting as PVCs, particularly during primary PCI for STEMI 3, 1
• Prolonged and frequent ventricular ectopy during acute coronary syndrome signals incomplete revascularization or recurrent ischemia 3
• PVCs during colonoscopy preparation occur through vagal stimulation, catecholamine release from anxiety/pain, and electrolyte shifts from bowel preparation 5

Autonomic and Catecholamine-Mediated Causes

• High adrenergic tone from stress, anxiety, or catecholamine excess promotes PVCs through enhanced automaticity 1, 2
• Vagal stimulation from hollow viscus distention (during endoscopy or colonoscopy) triggers PVCs through parasympathetic mechanisms 5
• Dehydration-induced catecholamine release increases ectopy frequency 5

Idiopathic PVCs

• Idiopathic PVCs originate most commonly from the right ventricular outflow tract (RVOT) in structurally normal hearts, displaying characteristic left bundle branch block morphology with inferior axis 1, 6
• These represent 60-70% of all PVCs in patients without structural disease and are generally benign when burden remains <10% 3, 6

Cardiac Channelopathies

• Long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia cause PVCs through abnormal ion channel function 3
• These require specific evaluation with genetic testing and specialized management 3

Critical Risk Stratification Factors

Age-Related Prevalence

• PVC frequency increases dramatically with age: 0.6% prevalence in those under 20 years versus 2.7% in those over 50 years on standard ECG 1
• Increasing age is the strongest predictor of PVC frequency independent of other factors 1, 2

High-Risk Features Requiring Aggressive Evaluation

• PVC burden >10,000-20,000 per day (>10-15% of total beats) can cause or worsen cardiomyopathy regardless of initial etiology 1, 6
• Multifocal PVCs indicate higher risk even without sustained VT, associated with increased death and cardiovascular events including stroke 1, 6
• Wide QRS duration >160 ms may indicate arrhythmogenic right ventricular cardiomyopathy 6
• PVCs that increase rather than suppress with exercise are concerning and require further evaluation 6

Important Clinical Pitfalls

• The risk of adverse cardiac events is dictated primarily by underlying heart disease rather than the ectopic beats themselves, making echocardiography mandatory in symptomatic patients or those with PVC burden >5-10% 3, 1
• Dismissing PVCs as benign without quantifying burden through 24-48 hour Holter monitoring leads to missed PVC-induced cardiomyopathy 1
• Missing reversible causes (electrolytes, medications, substances) before initiating antiarrhythmic therapy represents a fundamental management error 1
• In post-MI patients with PVCs and LVEF <35%, sudden cardiac death risk is substantially increased regardless of PVC frequency 1