Premature Ventricular Complexes

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Background

Premature ventricular complexes (PVCs) (also known as ventricular premature complexes [VPCs]) are ectopic impulses originating from an area distal to the His Purkinje system. PVCs are the most common ventricular arrhythmia.[1] Assessment and treatment of PVCs is challenging and complex, and these are highly dependent on the clinical context. The prognostic significance of PVCs is variable and, again, best interpreted in the context of the underlying cardiac condition.

The approach to the evaluation and management of PVCs has undergone dramatic changes in the last decade. Observational studies and inferences from typical electrophysiology studies were initially focused on ventricular ectopy triggering ventricular tachycardia which, in turn, can degenerate into ventricular fibrillation, as a mechanisms for sudden cardiac death—particularly post myocardial infarction (MI).[1] The treatment paradigm in the 1970s and 1980s was to eliminate PVCs in patients after MI. The Cardiac Arrhythmia Suppression Trial (CAST) and other arrhythmia suppression studies have demonstrated that eliminating PVCs with available antiarrhythmic drugs increases the risk of death to patients without providing any measurable benefit.[2]

Pathophysiology

The fundamental underlying etiology of PVCs remain to be determined.[3] Very few studies have evaluated the pathophysiology of PVCs in human subjects; most of the information is derived from animal studies. However, what is known is that ventricular monocytes at the cellular level spontaneously depolarize, leading to a cardiac cycle that is an out-of-sync extrasystole.[1]  The most prevalent PVCs are from the outflow tract and appear to be due to triggered activity from excess calcium and afterdepolarizations.[4]

Three common mechanisms exist for PVCs: automaticity, reentry, and triggered activity.[3, 4]

 

Etiology

Cardiac causes of PVCs include the following:

Noncardiac causes of PVCs include the following:

Epidemiology

United States data

Although the reported prevalence of PVCs varies between studies, depending on the population studied, duration of observation, and method of detection, PVCs are very common in most patients with long-term ambulatory monitoring.[1, 3]  PVCs appear on standard electrocardiograms (ECGs) in an estimated 1% of clinically normal individuals and in 40-75% of healthy people evaluated by short-term ambulatory monitoring.[1, 6] The Atherosclerosis Risk in Communities (ARIC) trial found a higher PVC prevalence with increasing age, Black ethnicity, male sex, and lower education, as well with the presence of structural heart disease, hypertension, and lower levels of serum magnesium or potassium.[1, 7]

In asymptomatic patients, PVCs are infrequently noted when only a single 12-lead ECG is used for ascertainment. The Framingham heart study (with 1-h ambulatory ECG) suggested that the prevalence rate of 1 or more PVCs per hour was 33% in men without coronary artery disease (CAD) and 32% in women without CAD. Among patients with CAD, the prevalence rate of 1 or more PVCs was 58% in men and 49% in women. Other studies using 24-hour ambulatory monitoring showed a PVC prevalence rate of 41% in healthy teenage boys aged 14-16 years, 50-60% in healthy young adults, and 84% in healthy elderly persons aged 73-82 years. PVCs also are common in patients with hypertension, ventricular hypertrophy, cardiomyopathy, and mitral valve prolapse.

International data

Data from the Gruppo Italiano per lo Studio della Sopravvivenza dell'Infarto Miocardico 2 study demonstrated that 64% of patients who had MI then had ventricular arrhythmia and 20% of patients had more than 10 PVCs per hour when 24-h Holter monitoring was used.[8, 9]

In a study evaluating the features of frequent idiopathic PVCs in the Korean, investigators reported a mean patient age of 54.7 ± 16.8 years and a slight female preponderance (54.8%).[10]  The most common typical PVCs-related symptoms/signs were palpitation and a dropped beat (59.2%), whereas the most common ECG features were left bundle branch block, an inferior axis, and late precordial R-wave transition.

Sex- and age-related demographics

The Framingham heart study demonstrated increased prevalence of PVCs in men compared with women. The difference was especially higher in men with CAD than in women with CAD.

In a 2024 report, of 1067 participants from the Women's Health Initiative Strong and Healty (WHISH) trial without a history of atrial fibrillation (AF) but had a 5-year predicted risk of incident of at least 5% by CHARGE-AF score, 4.3% of postmenopausal women had at least 1 patch of frequent PVCs, and 1.1% had at least 1 episode of nonsustained ventricular tachycardia.(NSVT).[11] Gomez et al found a direct correlation between CHARGE-AF score and NSVT and PVC frequency. Sequential monitoring increased identification of PVC frequency.

The ARIC trial found that over 6% of middle-aged adults have PVCs on 2-minute ECGs.[7] As noted above, the study also showed Black ethnicity and male sex are associated with a greater prevalence of PVCs.

PVCs are uncommon in children (suggested prevalence rate of 0.8-2.2% from the Vanderbilt Medical Center; exact prevalence not known). Prevalence increases with age.

Prognosis

The prognosis depends on the frequency and characteristics of PVCs and on the type and severity of associated structural heart disease.[1, 3, 12] Overall, PVCs are associated with an increased risk of death, especially when CAD is diagnosed, but the relationship between PVC frequency and mortality, even in this group, is not robust. Importantly, no survival benefit in in any population has been convincingly demonstrated as a consequence of suppressing PVCs.

In asymptomatic patients, frequent ventricular ectopy (defined as a run of 2 or more consecutive premature ventricular depolarizations or with premature ventricular depolarizations constituting over 10% of all ventricular depolarizations on any of the ECG recordings with the subject at rest, during exercise, or during recovery) recorded during exercise testing was associated with 2.5-fold increased risk of cardiovascular death.[13] Less frequent PVCs did not increase the risk.

In general, multimorphic PVCs connote a poorer prognosis than uniform morphologic PVCs. In patients post-MI, frequent PVCs (>10/h) are associated with increased mortality in the prethrombolytic era, but the association in patients receiving thrombolysis is weak.

In two studies, frequent or complex ventricular ectopy (defined as the presence of 7 or more ventricular premature beats per minute during any given stage, ventricular bigeminy, ventricular trigeminy, ventricular couplets, ventricular triplets, sustained or nonsustained ventricular tachycardia, ventricular flutter, torsade de pointes, or ventricular fibrillation) during exercise was an independent predictor of death.[13, 14] However, in another study, frequent PVCs only during exercise did not independently predict an increased risk; instead frequent PVCs during recovery was a stronger predictor of death.[15]

Frequent PVCs, especially when they occur in a bigeminal pattern, can cause or contribute to tachycardia-induced cardiomyopathy, which reversed by elimination of the PVCs through catheter ablation.[13, 16, 17, 18]  However, the extent to which this can be generalized to larger populations remains uncertain. Caution is in order, primarily because prior attempts at pharmacologic suppression were associated with unexpected and deleterious outcomes.[19]

In a study that evaluated the prognostic value of PVC burden in 1767 individuals with persistent atrial fibrillation (AF), Yen et al reported a significant association of 24-hour PVC burden and the presence of consecutive PVCs, with an independent association with all-cause and cardiovascular mortality in the presence of persistent AF.[12]  Multivariate analysis determined significant baseline predictors of all-cause and cardiovascular mortality were increasing age; the presence of heart failure and/or stroke; the use of ACEIs/ARBs, beta blockers, digoxin, and/or anticoagulants; and lower estimated glomerular filtration rate.[12]

History

Various symptoms are associated with PVCs, however, many patients with PVCs are asymptomatic and don't have significal clinical issues.[3, 20] However, in patients with symptoms, there may be underlying structural heart disease.[3, 6] Typical symptoms include palpitations, light-headedness, syncope, atypical chest pain, or fatigue. Palpitations may feature fluttering, pounding, skipping beats or a strange fluttering sensation in the neck, or even dyspnea.[1] Palpitations are due to an augmented post-PVC beat and may be sensed as a pause rather than an extra beat.

Physical Examination

PVCs frequently are associated with variable or decreased intensity of heart sounds. An augmented beat following a dropped beat is heard frequently. Bounding jugular pulse (cannon a wave) from a loss of atrioventricular (AV) synchrony may be present. The follow-up beat after a PVC is stronger due to the postextrasystolic compensatory pause, allowing greater left ventricular (LV) filling, which usually causes greater intensity of that beat. This is known as extrasystolic potentiation. Conversely, the PVC itself may be underperfused and consequently not perceived by radial pulse, resulting in a spurious documentation of bradycardia.

Approach Considerations

Obtain laboratory studies to evaluate or correctable causes of PVCs, such as medications, electrolyte disturbances, infection, and myocardial ischemia or MI. Obtain serum electrolyte and magnesium levels.

A population-based study of 498 individuals with ventricular ectopy activity, including PVCs, found that elevated levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) were independently associated with ventricular ectopy but not with levels of high sensitivity-troponin I (hs-TnI) or hs-C-reactive protein (hs-CRP).[21] Obtaining levels of NT-proBNP may help in the evaluation of potential adverse cardiovascular events in persons with asymptomatic ventricular arrhythmias.

Imaging studies, such as echocardiography (particularly in the presence of frequent PVCs) and cardiac magnetic resonance imaging (CMRI), may help to identify any underlying structural heart abnormalities that can predispose to PVCs.[3, 22, 23] Assess the degree of LV dysfunction by noninvasive techniques such as echocardiography or radionuclide imaging. Echocardiography may be the preferred imaging modality because it also provides structural information about the heart.

Exercise stress testing should be performed to look for coronary ischemia, exercise-induced arrhythmia, or both.

In patients suspected of having coronary artery disease, a noninvasive evaluation to rule out this possibility or even a cardiac catheterization may be helpful diagnostically. This is based on not just the presence of PVCs, but on all risk factors and symptoms. Onset in an elderly patient should be a red flag to consider the possibility of progressive structural heart disease.

Electrocardiography

The diagnosis of PVCs is typically established by electrocardiography. The presence of a PVC on a 12-lead ECG provides essential information about the origin of that extrasystole, as well as providing important information about the ventricular site-of-origin of the PVC. Accordingly, an ECG should be performed to look for pathophysiologic cardiac abnormalities as well as documenting the presence of PVCs and potentially providing information about their specific mechanism and frequency.

Diagnostic criteria include the following:

Noninvasive mapping of cardiac arrhythmias is also possible with a 252-lead ECG and computed-tomography scan–based three-dimensional electroimaging.[24]

Newer monitoring devices

Newer monitoring devices are generally categorized in two groups. Wearable ambulatory electrocardiographic (AECG) devices and smaller cardiac implantable electronic devices (CIEDs) may be useful in patients with previously undiagnosed arrhythmias of significance.

More recent advances with miniaturized devices, rapidly expanding mobile technology (mobile cardiac telemetry [MCT]), and the availability of wearable ambulatory devices with microelectronics (eg, ZIO Patch, NUVANT MCT, and SEEQ MCT) have the potential to change the work-up algorithm for PVCs in near future.[25]

 

Holter Monitoring

In high-risk patients, ie, those with reduced ejection fraction (EF) and PVCs, a 24-hour Holter monitor may help establish the degree of electrical instability. Extending ambulatory monitoring beyond 24 hours to 7 days or longer appears to improve accuracy of assessing PVC burden.[26]

The severity of LV dysfunction, along with the complexity and frequency of the PVC, determines the aggressiveness of management.

Suppression of PVCs by beta-blocker or calcium blocker, together with a typical PVC morphology (inferior axis, LBBB morphology) can be helpful in establishing typical right ventricular outflow tract ectopy.

Suppressing the PVCs themselves is not the focus of treatment unless patients are significantly symptomatic.

Treatment of the underlying structural heart disease also is extremely important. This includes acute syndromes, such as ischemia and infarction, the treatment of which involves reperfusion.[27]

Electrophysiologic Study

Electrophysiologic study (EPS) may be indicated for 2 types of patients with PVCs, (1) those with a structurally normal heart with symptomatic PVCs, for whom pharmacological treatment or catheter ablation is indicated and (2) those with PVCs and structural heart disease, for whom risk stratification for sudden cardiac death is indicated.

According to the American College of Cardiology/American Heart Association guidelines,[28, 29] class I indications for EPS are patients with CAD, low EF (< 0.36), and nonsustained VT on ambulatory ECG. Class II indications for catheter ablation apply to patients with a highly symptomatic uniform morphology of PVCs, couplets, and nonsustained VT.

Other Tests

PVC mapping

Intracardiac mapping to determine accurate localization of the anatomic origin site is essential to catheter ablation elimination of PVCs.[30]

ECG localization of PVCs

12-lead ECGs are useful in predicting the likely site of PVC origin, particularly in structurally normal hearts.[30]

Artificial intelligence arrythmia mapping

In a 2024 report of findings from a retrospective study that evaluated the impact of artificial intelligence electrocardiographic (ECG) mapping to localize arrhythmia source in 28 patients with cardiac arrhythmias, Fox et al noted its use reduced time to ablation by 19.0%, lowered procedure duration by 22.6%, and reduced fluoroscopy by 43.7% relative to matched control subjects.[31] 6-Month arrhythmia-free survival in the study patients was 73.5% versus 63.5% in the control group. Atrial fibrillation, PVCs, and ventricular tachycardia were the most common arrhythmias in the study cohort.[31] Further investigation is needed to evaluate these data and the potential use of artificial intelligence ECG mapping.

Classification of Ventricular Premature Contractions

PVCs can be classified in different ways. The Lown classification was introduced to gauge effects of antiarrhythmic drugs and widely assumed to encapsulate prognostic significance—it is not clear that it fulfills either of these goals, but this classification is still employed.

Table 1. Lown Classification



View Table

See Table

 

The Lown classification does not necessarily imply a continuum of increasing risk.

Clinical classification is as follows:

Classification according to frequency is as follows:

Classification according to relationship to normal beats is as follows:

Classification according to origin is as follows:

Medical Care

Deciding when to treat PVCs is difficult because not all patients with PVCs are at risk of sudden death and treatment is associated with risk. The approach to PVCs depends on the frequency of PVCs, attributable symptoms, the presence or absence of underlying structural heart disease, and the estimated risk of sudden cardiac death.[3, 6, 32]

In the absence of significant structural heart disease (eg, normal ventricular function, no coronary or valvular heart disease) and the presence of asymptomatic PVCs, no therapy is required.[3]

For symptomatic PVCs associated with reduced LVEF, first-line treatment involves either medical therapy or catheter ablation.[3]

Recommended medical treatment usually involves the following:

Step 1: Beta-blockers and nondihydropyridine calcium channel blockers (eg, verapamil, diltiazem) can be used to treat symptomatic patients.[3] Beta-blockers with intrinsic sympathomimetic activity may be particularly helpful.[33, 34]

Step 2: The use of antiarrhythmic therapy is not typically recommended and best targeted to address limiting symptoms. The risk of the drug (including the risk of arrhythmic death from proarrhythmia) must be weighed against the benefits of PVC suppression. The risk of adverse events is higher in patients with structural heart disease.

In patients without structural heart disease who have refractory symptoms and are using beta-blockers and/or calcium channel blockers, cautious use of antiarrhythmic drugs is the appropriate next step. Class IC drugs (flecainide and propafenone) are effective in such patients without structural heart disease or coronary heart disease.

More recently, results from a study by Raad et al suggest that class IC agents are effective in suppressing PVCs in patients with nonischemic cardiomyopathy (NICM) and implantable cardioverter-defibrillators (ICDs)[35]  Of 34 study patients receiving flecainide (n = 23) and propafenone (n = 11), there was a 14% fall in PVC burden (20% to 6%), 4% rise in LVEF (33% to 37%), and 8% increase in biventricular pacing (85% to 93%).[35] More investigation is needed to evaluate the safety of this approach these patients.

Step 3: The next step in patients who cannot take flecainide or propafenone is to consider amiodarone or sotalol.

Because interest in PVC supression decreased when it was shown to be typically deleterious in patients with coronary artery disease, this literature is not current, and specifically the role of newer class III antiarrhythmic like dofetilide and azimilide for PVCs is unclear at present.

Presence of underlying heart disease (eg, PVCs in patients post MI)

Management in these patients Various strategies, both invasive and noninvasive, predict prognosis in patients with PVCs post-MI.

The most powerful combination of noninvasive prognostic variables that identify patients in whom invasive strategies are suitable includes the presence of two or more of the following variables, (1) LV EF less than 0.40, (2) ventricular late potentials (on signal-averaged ECG), and (3) repetitive PVCs.

Supportive management

Treatment should include limiting transient ischemia.

Optimal treatment for congestive heart failure (CHF), CAD, or both should be instituted.

Maintain electrolyte balance.

Blood pressure control should be obtained because LV hypertrophy is associated with increased PVCs.[36]

Ablation therapy

Catheter ablation can eradicate PVCs, but there are higher risks associated with the procedure (eg, disabling symptoms, LV systolic dysfunction, PVC-induced VF),[3, 30]  including proximity to vital structures (coronary arteries, conduction system) and an intramural origin.[30] Consider ablation therapy in the following[29] :

PVCs arising from the outflow tract (OT) are the most common subtype of idiopathic PVCs; more than 70-80% of premature ventricular contractions (PVCs) originate from the right ventricular (RV) OT. The remaining PVCs originate from other sites (left and right coronary cusp, mitral annulus, and on the epicardium near the left ventricular [LV] OT). Highly symptomatic and refractory cases of PVCs especially from RVOT are appropriate for ablation therapy, with success rates over 70%.

The selection of an endocardial versus an epicardial approach to target ventricular arrythmia depends on the patient’s underlying disease substrate, as well as the location of the arrhythmogenic substrate within the myocardial wall, which can be best assessed with a cardiac MRI.[37]

In a 2024 European tertiary care center study of real-world data from 120 patients who underwent catheter ablation for ventricular tachycardias (VTs) and PVCs, Schlatzer et al found acute success rates of 94.2% for VTs and 92.2% for PVCs, and complications rates of 10.1% and 7.8%, respectively.[38]  Of note, only patients with structural heart disease had complications.

In a 2024 retrospective (2019-2020) report, a multicenter study by Mugnai et al found a "zero fluoroscopy" catheter ablation of PVCs approach to be safe in 131 patients.[39]  One-fifth of patients had cardiomyopathy, and the most frequent source of PVCs were right ventricular outflow tract (55%), LV (16%), LV outflow tract and cusps (13.7%), and aortomitral continuity (5.3%). Acute PVC suppression occurred in 96.9% of patients (n = 127), with 12-month complete success in 83.2% (n = 109) and reduced PVC burden in 13.7% (n = 18). Four patients (3.1%) experienced failure. The investigators noted two minor complications, femoral hematoma and arteriovenous fistula, which received conservative management.[39]

Diet

Recommendations depend on the underlying cardiac disease; avoidance of caffeine, nicotine, and alcohol may reduce the frequency of PVCs.

Surgical Care

Patients deemed to be at high risk of sudden cardiac death may benefit from implantable cardioverter defibrillator (ICD) implantation.

Catheter-based renal sympathetic denervation (RSD) may have a role in reducing the arrhythmic burden of ventricular arrhythmias, including PVCs, that are refractory to pharmacotherapy.[40] In a preliminary study of 34 patients with PVCs and structurally normal hearts (20 underwent ablation RSD, 14 served as controls), investigators noted that at 3-, 6- (first month after RSD, without drugs), 7-, and 12-month (sixth month after RSD, without drugs) follow-up, those treated with RSD had significantly reduced numbers of polymorphic PVCs compared to baseline. Although neither patient group showed any changes in mean 24-hour ambulatory blood pressure monitoring (ABPM) and renal function at 12 months, the control group demonstrated a decrease in 24-hour Holter mean heart rate. The change in number of polymorphic PVCs at 6 months post RSD was significantly associated with the total number of RSD ablated sites.[40]

 

Consultations

Consultation with a cardiac electrophysiologist may be beneficial. As described above, select patients with symptomatic idiopathic PVCs may benefit from catheter ablation. EPS may help define risk for sudden death in some patients with structural heart disease. ICD implantation is beneficial in patients at high risk of sudden cardiac death, which is typically assessed by the presence of any associated cardiovascular disease, rather than the presence of PVCs per se.

Medication Summary

Treatment steps for PVCs include looking for and correcting the reversible causes (eg, hypoxia, hypokalemia, hypomagnesemia).

The long-term treatment of PVCs is highly controversial. Class I drugs affect fast sodium channels; they are classified into A, B, and C groups according to effects on phase 0 of the action potential, repolarization, and conduction.

Class IA drugs (eg, procainamide, quinidine, disopyramide) are moderately effective but have proarrhythmic effects. Procainamide is associated with a high incidence of allergic reactions, and quinidine is poorly tolerated due to adverse effects.

Class IB drugs (eg, mexiletine) may have less proarrhythmic effect (although one post-MI trial showed higher mortality for mexiletine than placebo) than class I antiarrhythmic drugs. They have a high incidence of adverse noncardiac effects. These drugs may show reasonable efficacy in some patients.

Class IC drugs (eg, flecainide, propafenone) are effective for reducing ventricular ectopy and are relatively well tolerated in patients with normal or minimally reduced LV function and no ischemic heart disease. They are not recommended in patients with ischemic heart disease because of the adverse outcome observed in the Cardiac Arrhythmia Suppression Trial (CAST). In CAST II, moricizine (Ethmozine) demonstrated neither benefits nor adverse effects long term, but, in the early use of the drug, increased mortality on moricizine occurred. Moricizine was discontinued in July 2007 because of diminished market demand.

Class II drugs (beta-blockers) are the drugs of choice in patients who are symptomatic but do not have structural heart disease. Also, class II drugs are considered the first choice of therapy for patients with underlying heart disease, especially if their EF is reduced. Beta-blockers or calcium blockers often suppress PVCs of right ventricular outflow tract origin.

Class III drugs (eg, amiodarone, sotalol) are approved for use only in life-threatening arrhythmia. Recent data suggest that amiodarone is safe post-MI for patients with PVCs, but does not reduce mortality. Amiodarone is the drug of choice in patients who can not tolerate beta-blockers. A meta-analysis comparing efficacy and safety of amiodarone and metoprolol in the treatment of PVC concluded that the response rate of amiodarone did not seem to be superior to metoprolol; amiodarone was associated with higher incidence of adverse reactions.[41, 42]

Class IV drugs (calcium channel blockers), in general, have a limited role in the treatment of PVCs. However, occasionally, these drugs may suppress triggered automaticity or idiopathic PVCs. Verapamil is recommended for treatment of idopathic LVOT PVCs. 

Currently, no evidence supports treatment of asymptomatic PVCs after MI with medication other than beta-blockers. Treatment considerations include symptoms caused by PVCs, other prognostic variables (ie, presence or absence and type of structural heart disease, CAD, and LV dysfunction), and adverse effects (specifically proarrhythmic effects of medications).

Clinical trials have suggested that type I antiarrhythmic agents and racemic sotalol increase mortality in patients post-MI. Amiodarone may have no adverse effect on mortality in this setting.[43]

Amiodarone (Cordarone, Pacerone)

Clinical Context:  Class III antiarrhythmic. Has antiarrhythmic effects that overlap all 4 Vaughn-Williams antiarrhythmic classes. May inhibit A-V conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation. Only agent proven to reduce incidence and risk of cardiac sudden death, with or without obstruction to LV outflow. Very efficacious in converting atrial fibrillation and flutter to sinus rhythm and in suppressing recurrence of these arrhythmias.

Has low risk of proarrhythmia effects, and any proarrhythmic reactions generally are delayed. Used in patients with structural heart disease. Most clinicians are comfortable with inpatient or outpatient loading with 400 mg PO tid for 1 wk because of low proarrhythmic effect, followed by weekly reductions with goal of lowest dose with desired therapeutic benefit (usual maintenance dose for AF 200 mg/d). During loading, patients must be monitored for bradyarrhythmias. Prior to administration, control the ventricular rate and CHF (if present) with digoxin or calcium channel blockers.

Oral efficacy may take weeks. With exception of disorders of prolonged repolarization (eg, LQTS), may be DOC for life-threatening ventricular arrhythmias refractory to beta-blockade and initial therapy with other agents.

Metoprolol (Lopressor, Toprol XL)

Clinical Context:  Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions.

Class Summary

Alter the electrophysiologic mechanisms responsible for arrhythmia.

What are ventricular premature complexes (VPCs)?What is the pathophysiology of ventricular premature complexes (VPCs)?What causes ventricular premature complexes (VPCs)?What is the prevalence of ventricular premature complexes (VPCs) in the US?What is the global prevalence of ventricular premature complexes (VCPs)?What are the sexual predilections of ventricular premature complexes (VPCs)?Which age groups have the highest prevalence of ventricular premature complexes (VPCs)?What is the prognosis of ventricular premature complexes (VPCs)?What are the signs and symptoms of ventricular premature complexes (VPCs)?Which physical findings are characteristic of ventricular premature complexes (VPCs)?How are ventricular premature complexes (VPCs) diagnosed?How are atrial premature complexes differentiated from ventricular premature complexes (VPCs)?How is a fusion beat differentiated from ventricular premature complexes (VPCs)?How are premature junctional contractions differentiated from ventricular premature complexes (VPCs)?How are idioventricular escape rhythms differentiated from ventricular premature complexes (VPCs)?How is ventricular tachycardia differentiated from ventricular premature complexes (VPCs)?How is parasystole differentiated from ventricular premature complexes (VPCs)?What is the significance of a variable coupling finding in the workup of ventricular premature complexes (VPCs)?What is interpolated ventricular premature complex (VPC)?Which factors increase the risk of torsades de pointes in ventricular premature complexes (VPCs)?What is the role of lab tests in the workup of ventricular premature complexes (VPCs)?What is the role of imaging studies in the workup of ventricular premature complexes (VPCs)?What is the role of stress testing in the workup of ventricular premature complexes (VPCs)?What is the role of cardiac catheterization in the workup of ventricular premature complexes (VPCs)?What is the role of ECG in the workup of ventricular premature complexes (VPCs)?What are the diagnostic criteria for ventricular premature complexes (VPCs)?Which electrocardiographic modalities are used in the workup of ventricular premature complexes (VPCs)?What is the role of Holter monitoring in the workup of ventricular premature complexes (VPCs)?What is the role of EPS in the workup of ventricular premature complexes (VPCs)?How are ventricular premature complexes (VPCs) classified?How are ventricular premature complexes (VPCs) treated?How are ventricular premature complexes (VPCs) treated following myocardial infarction (MI)?What is included in supportive care of ventricular premature complexes (VPCs)?What is the role of ablation therapy in the treatment of ventricular premature complexes (VPCs)?Which dietary modifications are used in the treatment of ventricular premature complexes (VPCs)?What is the role of surgery in the treatment of ventricular premature complexes (VPCs)?Which specialist consultations are beneficial to patients with ventricular premature complexes (VPCs)?How are acute ventricular premature complexes (VPCs) treated?What is the role of medications in the treatment of ventricular premature complexes (VPCs)?What is the role of medications in the treatment of ventricular premature complexes (VPCs) following myocardial infarction?Which medications in the drug class Antiarrhythmic agents are used in the treatment of Premature Ventricular Complexes?

Author

Jatin Dave, MD, MPH, Part-Time Clinical Instructor, Department of Medicine, Harvard Medical School; Attending Physician, Division of Aging, Department of Medicine, Brigham and Women's Hospital; Medical Director of Geriatrics, Tufts Health Plan

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Tufts Health Plan, a not for profit organization.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Brian Olshansky, MD, FESC, FAHA, FACC, FHRS, Professor Emeritus of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Jose M Dizon, MD, Professor of Clinical Medicine, Clinical Electrophysiology Laboratory, Division of Cardiology, Columbia University College of Physicians and Surgeons; Attending Physician, Department of Medicine, New York-Presbyterian/Columbia University Medical Center

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous authors John Michael Gaziano, MD, MPH; Revat Lakhia, MD; and Shivkumar H Jha, MD, to the development and writing of this article.

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Premature Ventricular Complexes (PVCs). Ventricular trigeminy is present. Note that the PVCs are unimorphic and that a compensatory pause follows each PVC. This patient has asymptomatic idiopathic PVCs originating from the right ventricular outflow tract.

Premature Ventricular Complexes (PVCs). Ventricular trigeminy is present. Note that the PVCs are unimorphic and that a compensatory pause follows each PVC. This patient has asymptomatic idiopathic PVCs originating from the right ventricular outflow tract.

Class Arrhythmia
0None
1Unifocal; < 30/h
2Unifocal; ≥ 30/h
3Multiform
4A2 consecutive
4B≥ 3 consecutive
5R-on-T phenomenon