Summary
A premature ventricular complex (PVC) is an abnormal early electrical firing caused by an ectopic focus in the ventricles. PVCs do not always lead to a contraction. Common causes of PVCs include electrolyte imbalances, cardiovascular disease, and certain medications. PVCs occur in the majority of adults, and prevalence increases with age. They are often discovered incidentally during an ECG for another indication. Most PVCs are asymptomatic, but some individuals present with symptoms such as dizziness or palpitations. ECG findings include wide QRS complexes and compensatory pauses that can be random or have consistent patterns, such as couplets or bigeminy. Most individuals do not require treatment unless they have an underlying condition (e.g., myocarditis, electrolyte abnormalities). Antiarrhythmic drugs or, in some cases, catheter ablation should be considered for individuals with frequent PVCs that cause significant symptoms, as they are at risk for sudden cardiac death.
Etiology
- Modifiable [1][2]
- Electrolyte imbalances (e.g., hypokalemia, hypomagnesemia)
- Caffeine [2]
- Alcohol
- Drugs (e.g., digoxin)
- High blood pressure
- Physical inactivity
- Smoking
- Nonmodifiable [1][2]
- Cardiovascular disease (e.g., coronary artery disease, myocarditis)
- Older age
- Above-average height
- Reduced LVEF
- Idiopathic [1][2]
Pathophysiology
- The extra, abnormal heartbeats in PVC are caused by ectopic foci within the ventricles.
- ↓ Diastolic filling time → ↓ stroke volume
Classification
Clinical features
- Most patients are asymptomatic. [3]
- Frequent PVCs may lead to lightheadedness, dizziness, and/or palpitations. [3]
- Irregular heartbeat
- Skipped or forceful beat [2]
- Syncope (rare) [2]
- Heart failure symptoms (in patients with PVC-induced cardiomyopathy) [3]
Diagnosis
Approach [2][3][4]
A 12-lead ECG confirms the diagnosis.
- Obtain BMP and magnesium levels to asses for electrolyte imbalances.
- Consider additional laboratory studies (e.g., TSH, urine drug screen).
- Specialized testing (e.g., Holter monitor, cardiac imaging) may be indicated to:
- Rule out underlying structural disease
- Assess PVC burden, i.e., the proportion of PVCs per total number of beats
ECG [2][3]
-
Common characteristics
-
QRS duration ≥ 120 ms with a blocklike QRS morphology
- Right ventricular premature beat: similar configuration to left bundle branch block
- Left ventricular premature beat: similar configuration to right bundle branch block
- There is no P wave before a premature QRS complex.
- Compensatory pause after the PVC
- Prematurity: The complex occurs earlier than predicted by the prior sinus pattern.
- T wave and ST segment abnormalities
-
QRS duration ≥ 120 ms with a blocklike QRS morphology
-
Additional characteristics [3]
- PVC patterns
-
R-on-T phenomenon and short-coupled PVCs: PVCs before the peak of the T wave [1]
- Occur during the vulnerable phase of the ventricular action potential
- Can lead to torsades de pointes or ventricular fibrillation
A 1-minute rhythm strip may help identify PVCs on ECG. [2]
Laboratory studies [3]
- All patients: BMP and magnesium level
- Symptomatic patients with no identified cause
- TSH
- Urine drug screen
- Cardiac biomarkers
- Serum digoxin level (if indicated)
Specialized testing [2][3]
Indications [2][3]
- Frequent PVCs: e.g., > 30 PVCs per hour or PVC burden > 20% [3][4]
- Symptomatic PVCs: especially symptoms that limit physical activity or are otherwise concerning (e.g., syncope)
- Concerning patient history [2]
- PVCs arising from the right ventricle [2]
PVCs are a common incidental finding on routine ECGs. No advanced workup is required in asymptomatic patients without indications for additional testing.
Modalities [2]
- Ambulatory ECG monitoring: : e.g., 24-hour Holter monitor, wearable ECG patch
-
Exercise stress test
- To determine morphology and risk for developing other ventricular arrhythmias
- PVCs occurring during exercise testing are associated with an increased risk of death. [4]
-
Cardiac imaging
- Echocardiography: to evaluate cardiac structure and function in all patients referred for clinical evaluation of PVCs
-
Cardiac MRI
- To evaluate for structural abnormalities or underlying cardiac infiltrative disease (e.g., sarcoidosis)
- Can help ablation procedure planning
Treatment
Approach [2]
- Treat underlying diseases (e.g., CAD, myocarditis, heart failure).
- Treat electrolyte abnormalities (e.g., hypokalemia, hypomagnesemia).
- Specific treatment, i.e., antiarrhythmic drugs, and/or catheter ablation
-
Expectant management: Consider for asymptomatic patients with normal LVEF.
- Low PVC burden (< 5%): routine monitoring during primary care visits
- High PVC burden (> 5–10%): refer to cardiology for annual clinical evaluation and echocardiogram
Beta blockers, CCBs, or catheter ablation are considered first-line strategies for treating PVCs. The optimal approach should be based on shared decision-making. [2]
Antiarrhythmic drugs [2][4]
- Indications include:
-
First line
- Beta blockers, e.g., bisoprolol (off-label) OR metoprolol (off-label) [2][4]
- OR nondihydropyridine calcium channel blockers: diltiazem OR verapamil
-
Second line: if first-line treatment is unsuccessful and catheter ablation is not possible or unsuccessful [2]
- Class IC antiarrhythmics, e.g., flecainide, propafenone [2][5]
- Sotalol
- Amiodarone
- Mexiletine
Catheter ablation [2][4]
Indications for catheter ablation include:
- Symptomatic patients who prefer nonpharmacological treatment
- Frequent PVCs (PVC burden ≥ 5–10%) in patients with reduced LVEF [2]
- Lack of response to or intolerance of first-line pharmacotherapy
Catheter ablation has higher success rates in patients with monomorphic PVCs than in patients with polymorphic PVCs. [2]
Complications
- PVC-induced cardiomyopathy, potentially leading to left ventricular systolic dysfunction [6]
- Torsades de pointes [2]
- Ventricular fibrillation [2]
We list the most important complications. The selection is not exhaustive.
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