What causes premature ventricular contractions (PVCs) and how are they managed, especially in cases with triplet PVCs and occasional PVC runs?

Management of Premature Ventricular Contractions (PVCs) and PVC Runs

Beta blockers are the first-line treatment for symptomatic PVCs, while catheter ablation is recommended for frequent PVCs (>15% of beats) causing symptoms or declining ventricular function when medications are ineffective or not tolerated. 1, 2

Causes of PVCs

• PVCs are common cardiac arrhythmias that increase in frequency with age, present in approximately 50% of all people with or without heart disease 3
• Common causes include:
  • Structural heart disease (ischemic heart disease, cardiomyopathy) 3
  • Electrolyte abnormalities (hypokalemia, hypomagnesemia) 4
  • Medications (stimulants, certain antiarrhythmics) 2
  • Caffeine, alcohol, or sympathomimetic agents 2
  • Idiopathic (no identifiable cause) 4
• Risk factors for adverse outcomes include:
  • Multifocal PVCs 3
  • Frequent PVCs (>30 PVCs per hour) 3
  • Underlying cardiovascular disease 3

Evaluation of PVCs

• Assessment should include:
  • PVC burden (percentage of total heartbeats) 1, 2
  • QRS morphology and coupling interval 2
  • Presence of symptoms (palpitations, dyspnea, presyncope, fatigue) 4, 5
  • Evaluation for structural heart disease with echocardiography 2, 4
• High-risk features requiring more aggressive management:
  • PVC burden >15% of total beats (risk of PVC-induced cardiomyopathy) 3, 2
  • Wider QRS complexes (>160 ms) 2
  • Short coupling interval (<300 ms) 2
  • Declining left ventricular function 3, 1

Management Algorithm for PVCs

For Asymptomatic Patients with Occasional PVCs:

• Reassurance if PVC burden is low (<10%) and no structural heart disease 2, 6
• Periodic follow-up with reassessment of ventricular function if PVC burden is moderate (10-15%) 2
• Consider treatment if PVC burden is high (>20%) even if asymptomatic, to prevent PVC-induced cardiomyopathy 2, 7

For Symptomatic Patients:

1. First-line approach:

   • Avoidance of triggers (caffeine, alcohol, sympathomimetic agents) 2
   • Beta-blockers (e.g., metoprolol) 3, 1, 5
   • Non-dihydropyridine calcium channel blockers if beta-blockers are contraindicated 2, 5

2. Second-line approach (if first-line fails):

   • Amiodarone for patients with structural heart disease 3, 2
   • Catheter ablation for patients with:
     • Frequent PVCs (>15% of beats) causing symptoms 3, 2
     • Declining ventricular function due to PVCs 3, 1
     • Medication intolerance or preference for non-pharmacological treatment 3

For Triplet PVCs and PVC Runs:

• More aggressive evaluation and management is warranted 3
• Beta-blockers are first-line therapy 1, 2
• Consider amiodarone if beta-blockers are ineffective 3, 2
• Electrophysiology study may be indicated, especially with unexplained syncope 3
• ICD may be considered if associated with sustained ventricular arrhythmias or cardiac arrest 3

Treatment Efficacy and Follow-up

• Catheter ablation success rates of up to 80% have been reported 2
• Left ventricular function typically normalizes within 6 months in 82% of patients with PVC-induced cardiomyopathy after successful treatment 2
• Follow-up should include:
  • Monitoring of PVC burden reduction after initiating therapy 2
  • Serial echocardiography to document improvement in left ventricular function 2
  • Reassessment for need of continued therapy 1

Important Caveats

• Class I sodium channel-blocking antiarrhythmic medications (e.g., flecainide, quinidine) should be avoided in post-MI patients or those with reduced LVEF as they increase mortality risk 3, 1
• It may be difficult to determine whether PVCs caused LV dysfunction or whether progressive LV dysfunction caused frequent PVCs 1
• Catheter ablation, while effective for idiopathic VF triggered by PVCs, may still have a substantial recurrence risk requiring ICD protection 3
• PVCs in athletes, especially in the absence of structural heart disease, are generally benign 2