Medicine, via pristina

Medicine, via pristina

Premature Ventricular Complexes (PVCs)

1. Knuuti J, Wijns W, Saraste A, Capodanno D, Barbato E, Funck-Brentano C, et al. 2019 ESC Guidelines for the diagnosis and management of chronic coronary syndromes. Eur Heart J. 2020;41(3):407-477.
PMID: 31504439
DOI: https://doi.org/10.1093/eurheartj/ehz425


2. Fihn SD, Gardin JM, Abrams J, Berra K, Blankenship JC, Dallas AP, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease. J Am Coll Cardiol. 2012;60(24):e44-e164.
PMID: 23182125
DOI: https://doi.org/10.1016/j.jacc.2012.07.013


3. Khan MA, Hashim MJ, Mustafa H, Baniyas MY, Al Suwaidi SKBM, AlKatheeri R, et al. Global epidemiology of ischemic heart disease: Results from the Global Burden of Disease Study. Cureus. 2020;12(7):e9349.
PMID: 32742886
DOI: 10.7759/cureus.9349


4. Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2018;39(2):119-177.
PMID: 28886621
DOI: https://doi.org/10.1093/eurheartj/ehx393


5. Amsterdam EA, Wenger NK, Brindis RG, Casey DE Jr, Ganiats TG, Holmes DR Jr, et al. 2014 AHA/ACC guideline for the management of patients with non–ST-elevation acute coronary syndromes. J Am Coll Cardiol. 2014;64(24):e139-e228.
PMID: 25260716
DOI: https://doi.org/10.1016/j.jacc.2014.09.017

Background 

Premature ventricular complexes (PVCs) are early depolarizations originating in the ventricles, occurring before the next expected sinus beat. They are characterized by wide and bizarre QRS complexes not preceded by a P wave. PVCs are common and usually benign, but frequent or symptomatic PVCs may indicate underlying structural heart disease or trigger ventricular arrhythmias. 


II) Classification/Types
 

By Morphology 

  • Unifocal PVCs: All PVCs look identical on ECG (same focus) 
  • Multifocal PVCs: PVCs vary in morphology (multiple foci) 

By Pattern 

  • Isolated PVCs: Occur sporadically 
  • Bigeminy: Every other beat is a PVC 
  • Trigeminy: Every third beat is a PVC 
  • Couplets/Triplets: Two or three consecutive PVCs 
  • Non-sustained VT: Three or more PVCs in a row lasting <30 seconds 

 

Pathophysiology 

PVCs result from enhanced automaticity, triggered activity, or reentry within the ventricular myocardium. They originate below the bundle of His and bypass the normal conduction pathway, causing early and wide QRS complexes. In the setting of myocardial irritation (ischemia, scarring, or electrolyte disturbance), PVCs may increase in frequency or become malignant. 

 

Epidemiology 

  • Seen in up to 50–60% of healthy adults on 24-hour Holter 
  • Prevalence increases with age 
  • More common in patients with ischemic or structural heart disease 
  • Frequent PVCs (>10,000–20,000/day) may cause or contribute to cardiomyopathy 

 


Etiology
 

I) Causes 

  • Stimulants: caffeine, alcohol, tobacco, sympathomimetics 
  • Electrolyte imbalances: hypokalemia, hypomagnesemia 
  • Hypoxia or ischemia (MI, CAD) 
  • Structural heart disease (cardiomyopathy, valvular disease) 
  • Drug-induced: digoxin toxicity, antiarrhythmics 
  • Increased sympathetic tone: stress, fever, pain 
  • Idiopathic (especially in younger patients with normal hearts) 


II) Risk Factors
 

  • Coronary artery disease 
  • Heart failure 
  • Electrolyte disorders 
  • Age > 50 
  • Male sex 
  • Stimulant or alcohol use 
  • Obstructive sleep apnea 

 


Clinical Presentation
 

I) History (Symptoms) 

  • Often asymptomatic 
  • Palpitations (“skipped beat” or “thumping” sensation) 
  • Dizziness or near-syncope (especially if frequent PVCs) 
  • Fatigue or exertional intolerance (PVC-induced cardiomyopathy) 
  • Chest discomfort (occasionally) 


II) Physical Exam (Signs)
 

  • Irregular heart rhythm with compensatory pause 
  • Variable intensity of first heart sound (S1) 
  • Cannon A waves (if AV dissociation occurs) 
  • May be normal between PVCs 

 


Differential Diagnosis (DDx)
 

  • Premature atrial complexes (PACs) 
  • Ventricular tachycardia (if PVCs occur in runs) 
  • Atrial fibrillation with aberrancy 
  • Bundle branch block 
  • Sinus arrhythmia 
  • Wolff-Parkinson-White (WPW) syndrome 

 


Diagnostic Tests
 

Initial Work-Up 

  • ECG: Wide QRS (>120 ms), no preceding P wave, full compensatory pause 
  • Holter monitor: Assess frequency and burden 
  • Event recorder: If symptoms are intermittent 
  • Electrolytes: Check K+, Mg++, Ca++ 
  • TSH: Rule out thyroid dysfunction 
  • Echocardiogram: Evaluate for structural heart disease 
  • Cardiac MRI: If cardiomyopathy or scar suspected 
  • Stress test: Evaluate for ischemia or exercise-induced PVCs 

 


Treatment
 

I) Initial Management 

  • Asymptomatic with normal heart: Reassurance only 
  • Avoid triggers: Reduce caffeine, alcohol, stress 
  • Electrolyte correction: Normalize K+, Mg++ 
  • Manage underlying conditions: e.g., ischemia, heart failure, sleep apnea 


II) Medications
 

Drug Class 

Examples 

Notes 

Beta-blockers 

Metoprolol, Atenolol 

First-line for symptomatic PVCs 

Calcium channel blockers 

Verapamil, Diltiazem 

Alternative in those who can’t tolerate beta-blockers 

Class IC antiarrhythmics 

Flecainide, Propafenone 

Use only if structurally normal heart and symptoms are disabling 

Class III antiarrhythmics 

Amiodarone, Sotalol 

Reserved for severe symptomatic cases or when other drugs fail 

Electrolyte supplements 

KCl, MgSO₄ 

Replete deficiencies to reduce ectopy 

 

Device Therapy 

  • Implantable loop recorder: For unexplained syncope 
  • ICD: If PVCs trigger sustained VT/VF in high-risk patients 
  • Pacemaker: Rare; considered in bradycardia or overdrive pacing 
  • Catheter ablation: Effective in symptomatic idiopathic PVCs or PVC-induced cardiomyopathy, especially with >10% PVC burden 

 


Patient Education, Screening, Vaccines
 

Education 

  • Reassure if PVCs are isolated and benign 
  • Identify and avoid PVC triggers (caffeine, alcohol, lack of sleep) 
  • Encourage adherence to medical therapy if prescribed 
  • Educate about signs of worsening arrhythmia or cardiomyopathy 


Screening/Prevention
 

  • Monitor frequency in patients with heart disease 
  • Holter monitoring if symptoms worsen or in presence of LV dysfunction 
  • Sleep study if OSA suspected 
  • Manage cardiovascular risk factors (HTN, CAD, obesity) 


Vaccinations
 

  • No PVC-specific vaccines 
  • Standard vaccinations (influenza, pneumococcal) per age and risk 

 


Consults/Referrals
 

  • Cardiology: For symptomatic, frequent, or high-burden PVCs 
  • Electrophysiology: For ablation consideration or suspected PVC-induced cardiomyopathy 
  • Sleep specialist: If OSA suspected 

 


Follow-Up
 

Short-Term 

  • Repeat ECG and electrolytes 
  • Holter or event monitor for PVC burden 
  • Initiate treatment and assess symptom response 


Long-Term
 

  • Monitor for development of PVC-induced cardiomyopathy 
  • Consider repeat echocardiogram for LV function if high burden 
  • Adjust therapy based on frequency and symptoms 

 

Prognosis 

  • Excellent if PVCs are isolated and in structurally normal hearts 
  • Frequent PVCs (>10% of total beats) may cause reversible cardiomyopathy 
  • Prognosis worsens with underlying structural heart disease 
  • Catheter ablation has high success rates in idiopathic PVCs 

 

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