What are the causes of premature ventricular contractions (PVCs) in patients with and without underlying cardiovascular disease, such as hypertension or coronary artery disease?

Causes of Premature Ventricular Contractions (PVCs)

Primary Etiologic Categories

PVCs arise from multiple mechanisms including triggered activity, automaticity, and reentry, with causes broadly categorized into structural heart disease, metabolic/toxic factors, and idiopathic origins. 1

Structural Heart Disease

The most clinically significant causes of PVCs involve underlying cardiac pathology:

• Ischemic heart disease is a leading cause, particularly in older patients, where PVCs may indicate underlying coronary artery disease and are associated with increased mortality risk 2, 3
• Cardiomyopathy of any etiology (ischemic or nonischemic) predisposes to PVCs, with the frequency and complexity correlating with disease severity 4, 5
• Left ventricular hypertrophy from hypertension or other causes creates substrate for ventricular ectopy 3
• Heart failure is commonly associated with PVCs, though the PVCs themselves may not provide incremental prognostic information beyond clinical variables in this population 4
• Myocarditis can manifest with PVCs as a marker of the underlying inflammatory process 5
• Valvular heart disease creates hemodynamic and structural abnormalities that promote ectopy 5

Metabolic and Toxic Causes

Reversible factors frequently trigger PVCs and should be systematically evaluated:

• Electrolyte disturbances, particularly hypokalemia, hypomagnesemia, and hypercalcemia, directly affect myocardial excitability 2, 6
• Acute myocardial ischemia causes electrical instability and PVCs 2
• Caffeine, alcohol, and stimulant use (including sympathomimetics) are common precipitants 7, 6
• Drug toxicity, notably digitalis, can cause characteristic bidirectional ventricular tachycardia and PVCs 2
• Hypoglycemia in diabetic patients increases nocturnal bradycardia and ventricular ectopy 2

Autonomic and Functional Causes

• High adrenergic tone from stress, anxiety, or catecholamine excess promotes PVCs 7
• Autonomic, electromechanical, and structural remodeling contributes to arrhythmogenesis, particularly in diabetic patients 2
• Glycemic fluctuations in diabetes are implicated in PVC pathophysiology 2

Age-Related and Idiopathic Causes

• Increasing age is the strongest predictor of PVC frequency, with prevalence rising from 0.6% in those under 20 years to 2.7% in those over 50 years on standard ECG, and approximately 50% of all individuals showing PVCs on extended monitoring 2, 1
• Idiopathic PVCs occur in structurally normal hearts without identifiable cause, most commonly originating from the right ventricular outflow tract (RVOT) with characteristic left bundle branch block morphology and inferior axis 2, 6

Risk Stratification by Underlying Cause

The risk of adverse cardiac events is dictated primarily by underlying heart disease rather than the ectopic beats themselves. 2

High-Risk Scenarios Requiring Aggressive Evaluation

• Post-myocardial infarction patients with PVCs, especially with LVEF <35%, face substantially increased sudden cardiac death risk 2, 4
• Structural heart disease with reduced ejection fraction (LVEF ≤40%) and nonsustained ventricular tachycardia warrants electrophysiology study and potential ICD implantation 4
• PVC burden >10,000-20,000 per day (>10-15% of total beats) can cause or worsen cardiomyopathy regardless of initial etiology 2, 7, 5
• Multifocal PVCs indicate higher risk even without sustained VT, associated with increased death and cardiovascular events including stroke 8

Lower-Risk Presentations

• Isolated PVCs in structurally normal hearts are generally benign, particularly RVOT origin PVCs that suppress with exercise 2, 7
• Asymptomatic patients without structural disease require only surveillance and reassurance 7

Clinical Pitfalls in Identifying Causes

• Failing to quantify PVC burden through 24-48 hour Holter monitoring, as symptoms correlate poorly with frequency 7, 9
• Dismissing PVCs as benign without echocardiography to exclude structural disease, which is the strongest predictor of adverse events 8, 5
• Missing reversible causes such as electrolyte abnormalities or substance use that require correction before considering antiarrhythmic therapy 7, 6
• Confusing complete AV block with AV dissociation in the setting of frequent PVCs, which requires different management 2