Premature ventricular complexes: Clinical presentation and evaluation

INTRODUCTION — 

Premature ventricular complexes/contractions (PVCs), also referred to as premature ventricular beats, premature ventricular depolarizations, or ventricular extrasystoles, are early beats arising from the ventricular myocardium in a variety of situations. PVCs are common and occur in a broad spectrum of the population. This includes patients without structural heart disease and those with any form of cardiac disease, independent of severity.

The prevalence, pathophysiology, associated symptoms, clinical presentation, electrocardiographic (ECG) appearance, and approach to evaluation for patients with known or suspected PVCs will be presented here. Discussions of the treatment and prognosis of PVCs, as well as a discussion of supraventricular premature beats (also known as premature atrial complexes), are presented separately. (See "Premature ventricular complexes: Treatment and prognosis" and "Premature atrial contractions and junctional premature beats in adults".)

PREVALENCE AND PATHOPHYSIOLOGY

●Prevalence – Occasional premature ventricular complexes (PVCs) are common, occurring in 6 percent of healthy adults who are monitored with an electrocardiogram (ECG) for two minutes, and in 40 to 80 percent of healthy adults who are monitored for 24 hours [1-4]. One observational study of 101 adults who had normal cardiac structure and function based on an extensive evaluation (ie, ECG, echocardiogram, exercise stress test, right- and left-heart catheterization, and coronary angiography) found that 39 percent of participants had at least one PVC in 24 hours and only 4 percent had more than 100 PVCs in 24 hours [4].

In a prospective multicenter study of PVC burden data from consecutive ambulatory monitors ordered in eight United States medical centers, the prevalence of PVCs was as follows [5]:

•<1 percent PVC burden: 70 percent of patients

•1 to 5 percent PVC burden: 21 percent of patients

•6 to 10 percent PVC burden: 4 percent of patients

•>10 percent PVC burden: 5 percent of patients

The average left ventricular ejection fraction (LVEF) was lower in patients with frequent PVCs than in those with infrequent PVCs. However, frequent PVCs were not limited to patients with low LVEF.

Older age, heart disease, hypertension, hypokalemia, hypomagnesemia, and a faster sinus rate are associated with an increased prevalence of PVCs [1,3,6-8]. PVCs are also seen in children and may decrease over time; a retrospective cohort study of 198 patients ≤21 years of age with frequent PVCs demonstrated that PVC burden decreased over time in most patients [9]. Those with <15 percent PVC burden and without complex ectopy (eg, couplets, triplets, nonsustained ventricular tachycardia, polymorphic PVCs) were very likely to have a spontaneous reduction in PVC burden.

●Pathophysiology

•Mechanism – There are three mechanisms by which PVCs may be generated [6]:

-Reentry – In patients with structural heart disease (eg, post-myocardial infarction, dilated cardiomyopathy, hypertrophic cardiomyopathy), PVCs are usually due to reentry in an area of myocardial fibrosis, which creates a circular anatomic pathway. PVCs may then develop under certain circumstances, such as the administration of a drug that prolongs conduction. Reentry is also thought to be the most common mechanism of PVC generation in patients without structural heart disease (see 'Associated conditions' below). Reentry is discussed in detail elsewhere. (See "Reentry and the development of cardiac arrhythmias".)

-Enhanced automaticity – In patients with electrolyte abnormalities or acute ischemia, PVCs may be due to abnormal automaticity. These conditions tend to lower the diastolic transmembrane voltage, resulting in premature depolarization. The principal site of PVC development due to abnormal automaticity is the Purkinje fiber layer. Enhanced automaticity is discussed in detail elsewhere. (See "Enhanced cardiac automaticity".)

-Triggered activity – Triggered activity refers to depolarization that occurs either early or late after the initial depolarization wavefront. Early (phase 3 of the action potential) or late (phase 4) afterdepolarizations may occur in Purkinje cells or in the ventricular myocardium. This type of electrical activity may arise in the setting of certain conditions (eg, hypokalemia, ischemia, infarction, cardiomyopathy, excess calcium, drug toxicity [such as digoxin or agents that prolong repolarization or the QT interval]). If repetitive firing allows these afterdepolarizations to reach threshold potential, PVCs will be generated and may perpetuate if the proper conditions are present. Triggered activity is discussed in detail elsewhere. (See "Cardiac excitability, mechanisms of arrhythmia, and action of antiarrhythmic drugs", section on 'Triggered activity'.)

•Location – Most benign PVCs (ie, PVCs that occur in patients without structural heart disease) originate in the right ventricular outflow tract (RVOT) (waveform 1) or left ventricular outflow tract (LVOT) (waveform 2) [10]. Patients with structural abnormalities of the right ventricle (eg, arrhythmogenic right ventricular cardiomyopathy) may have right-sided PVCs from sites other than the RVOT, while patients with structural abnormalities of the left ventricle (eg, myocardial infarction, hypertrophic cardiomyopathy) may have left-sided PVCs originating from sites other than the LVOT (eg, papillary muscle, left anterior or posterior fascicle, mitral annulus). The appearance of the PVC on ECG provides information about the site of origin. (See 'Describing PVCs' below.)

ASSOCIATED CONDITIONS — 

There are many conditions that are associated with increased prevalence and frequency of PVCs (table 1). Cardiac conditions that may cause or exacerbate PVCs include the following [11-19]:

●Left ventricular hypertrophy

●Acute myocardial infarction

●Heart failure with reduced ejection fraction

●Myocarditis

●Arrhythmogenic right ventricular cardiomyopathy

●Cardiac sarcoidosis

●Hypertrophic cardiomyopathy

●Congenital heart disease

Noncardiac conditions that may cause or exacerbate PVCs include the following [20-23]:

●Chronic obstructive pulmonary disease

●Sleep apnea syndromes

●Pulmonary hypertension

●Endocrinopathies (thyroid, adrenal, or gonadal abnormalities)

●Hypokalemia and hypomagnesemia

●Nicotine, alcohol, or stimulant use, including sympathomimetic medications (eg, beta-agonists, decongestants, antihistamines) and illicit drugs (eg, cocaine, amphetamines)

●Digitalis toxicity

Caffeine does not appear to be associated with increased PVCs, although some patients report an increase in symptomatic PVC frequency with caffeine ingestion [24-26]. In an observational study of 1388 participants in the Cardiovascular Health Study who self-reported their caffeine intake, the frequency of PVCs was comparable between caffeine users and nonusers [27].

CLINICAL PRESENTATION — 

The majority of individuals with premature ventricular complexes (PVCs) experience no symptoms. Asymptomatic patients are usually diagnosed with PVCs based on an electrocardiogram (ECG), stress test, ambulatory ECG monitor, or inpatient telemetry monitor. Occasionally, patients with frequent PVCs (eg, ventricular bigeminy) may report that their smartwatch has alerted them to rhythm irregularity; alternatively, the smartwatch may alert for bradycardia because it may fail to detect PVCs, which have a reduced stroke volume compared with normal beats.

A minority of patients with PVCs present with symptoms, usually palpitations. Patients with symptomatic PVCs typically describe a sensation of a skipped beat (due to the post-PVC pause) or a prominent heartbeat (due to the increased stroke volume generated during a post-PVC beat). Some patients are symptomatic only when resting in a quiet environment, such as in bed. Others can provoke symptoms by lying on their left side, which brings the heart closer to the chest wall. In some cases, frequent PVCs can result in a pounding sensation in the neck, lightheadedness, or near syncope.

INITIAL EVALUATION OF ALL PATIENTS — 

For all patients with premature ventricular complexes (PVCs) identified on electrocardiography (ECG) or monitoring, we perform a history and physical examination.

History — For all patients with PVCs, we take a history to assess their symptoms and determine if they have an underlying condition associated with PVCs. We ask about the following:

●Palpitations, including the nature, frequency, and any relationship to activity. Palpitations that do not fit the typical description of PVC-induced palpitations (see 'Clinical presentation' above) may be due to a different etiology and may merit further evaluation as discussed elsewhere. (See "Evaluation of palpitations in adults".)

●Syncope, because this is not typically caused by PVCs and thus may indicate a more significant arrhythmia. (See "Syncope in adults: Clinical manifestations and initial diagnostic evaluation".)

●Chest pain or dyspnea, which may be due to a condition (eg, coronary artery disease, heart failure, chronic obstructive pulmonary disease) that is associated with PVCs. (See "Outpatient evaluation of the adult with chest pain" and "Approach to the patient with dyspnea".)

●Psychological stress and anxiety, which may trigger PVCs or increase awareness of PVCs. (See "Generalized anxiety disorder in adults: Epidemiology, pathogenesis, clinical manifestations, course, assessment, and diagnosis".)

●Use of recreational drugs (eg, alcohol, cocaine, amphetamines) or prescription drugs (eg, methylphenidate, digoxin) that may trigger PVCs.

●History of myocardial infarction, cardiomyopathy, hypertension, chronic lung disease, or any other conditions that are associated with PVCs. (See 'Associated conditions' above.)

●Family history of either cardiomyopathy or sudden cardiac death at a young age (<40 years of age), either of which increases the risk of an inherited condition that may predispose to sustained ventricular arrhythmias (See "Cardiac evaluation of the survivor of sudden cardiac arrest", section on 'Evaluation of family members' and "Familial dilated cardiomyopathy: Prevalence, diagnosis and treatment".)

Physical examination — For all patients with PVCs, we perform a physical examination, looking for the following findings:

●Hypoxemia, which may trigger PVCs.

●Tachycardia, which may be due to certain conditions (eg, stimulant drugs, hyperthyroidism, anemia, anxiety) that are associated with PVCs.

●Severe hypertension, which is associated with PVCs.

●Signs of heart failure, which suggest an underlying condition (eg, cardiomyopathy) that is associated with PVCs.

●Certain cardiac findings that may be present if a patient is having PVCs during the examination. The most common of these include an irregular pulse and a prolonged pause (ie, compensatory pause) after a premature beat. Less commonly, there can be signs of atrioventricular (AV) dissociation (eg, variable intensity of the first heart sound secondary to a changing PR interval, cannon "A" waves due to almost simultaneous retrograde atrial and antegrade ventricular activation and subsequent contraction). A widely split second heart sound (S2) may occur if the PVC has a right bundle branch block (RBBB) morphology, which causes a delayed P2. (See "Auscultation of heart sounds".)

12-lead electrocardiogram — For all patients with suspected or confirmed PVCs, we perform a 12-lead ECG to characterize the PVCs.

Describing PVCs — Most PVCs have the following ECG characteristics (see "ECG tutorial: Ventricular arrhythmias"):

●QRS duration ≥120 ms – The QRS duration of PVCs is at least 120 ms. The duration is usually even longer (>130 ms) but can occasionally be <130 ms (eg, PVCs originating in the left posterior fascicle) [28]. Compared with a patient’s sinus complexes, most PVCs have a longer QRS duration; however, if a PVC originates from the contralateral ventricle in a patient with a preexisting bundle branch block, the PVC may have a shorter QRS duration than the sinus complexes.

●Atypical QRS morphology – The QRS morphology is usually different from a typical right bundle branch block (RBBB) or left bundle branch block (LBBB). As an example, in a typical RBBB, there is a broad S wave in V5 and V6, which is not the case in the PVCs in the sample waveform (waveform 2). However, PVCs may occasionally have typical RBBB- and LBBB-like morphologies.

●T wave vector in opposite direction – The T wave after a PVC is typically in the opposite direction from the main QRS vector. However, patients with a prior myocardial infarction may have a “pseudonormalized” T wave, meaning the T wave vector is in the same direction as the main QRS vector.

●Compensatory pause – Most PVCs are followed by a fully compensatory pause, which means that the P-P interval surrounding the PVC is twice the sinus P-P interval. The pause occurs because the sinus node fires on time, but the impulse is not conducted through the ventricles, which are refractory after the PVC. Less frequently, the PVC is “interpolated” (waveform 3), meaning the P-P interval surrounding the PVC is equal to the sinus P-P interval; this occurs if the ventricles are not refractory when the sinus impulse arrives. On occasion, a PVC can reset the sinus node due to retrograde conduction through the atrioventricular (AV) node, creating a noncompensatory pause.

●Lack of premature P wave preceding the QRS complex – While most premature atrial complexes (PACs) have a narrow QRS complex, those with aberrant conduction may be mistaken for PVCs. The key to distinguishing between a PVC and a PAC with aberrant conduction is to determine whether the QRS complex is preceded by a premature P wave; if this is present, the beat is a PAC, not a PVC. If the complex is preceded by a normal sinus P wave, the beat is a PVC with a long coupling interval, not a PAC.

●Other characteristics – It can be helpful to describe additional PVC characteristics that may impact the patient’s prognosis and treatment. These include the following:

•Pattern – In some cases, frequent PVCs may occur in a repeating manner. We describe the pattern as follows:

-“Ventricular bigeminy” refers to alternating normal and premature beats (ie, every other QRS complex is a PVC) (waveform 4).

-“Ventricular trigeminy” refers to two normal beats followed by a PVC.

-“Ventricular quadrigeminy” refers to three normal beats followed by a PVC (waveform 5).

•Unifocal versus multifocal/polymorphic – Most patients have unifocal PVCs, which originate from a single ventricular focus and have a consistent appearance on ECG. Multifocal/polymorphic PVCs are typically seen in patients with structural heart disease and can be identified when the PVCs do not all have the same morphology. Multifocal PVCs may originate from more than one site, from one site with multiple exit points into the ventricular myocardium, or from changes in the pattern or direction of myocardial activation due to variables in ventricular electrophysiologic properties.

•Site of origin – The morphology of PVCs is a clue to the site of their origin, which may impact suitability for catheter ablation.

-Right ventricular outflow tract (RVOT) PVCs can be seen in patients with or without structural heart disease. On ECG, these PVCs have a negative QRS in aVL and aVR, a positive QRS in the inferior leads, and an LBBB morphology (waveform 1).

-Left ventricular outflow tract (LVOT) PVCs can be seen in patients with or without structural heart disease. On ECG, these PVCs have a negative QRS in aVL and aVR, a positive QRS in the inferior leads, and an RBBB morphology (waveform 2).

-PVCs can originate in many other regions of the right or left ventricle. The identification of other sites of origin based on the ECG is beyond the scope of this discussion [6].

•Coupling interval – The coupling interval refers to the interval between the previous QRS complex and the PVC. Most unifocal PVCs exhibit fixed coupling intervals with the preceding beats because they have a reentrant mechanism. PVCs can be described as short- or long-coupled, depending on the interval between the PVC and the preceding beat. Less commonly, PVCs may have a variable coupling interval but a constant interval between two successive PVCs; this phenomenon, which is called ventricular parasystole, suggests that automaticity is the mechanism (waveform 6). Ventricular parasystole, which is suggestive of structural heart disease, is discussed in detail elsewhere. (See "ECG tutorial: Ventricular arrhythmias", section on 'Ventricular parasystole'.)

•R-on-T phenomenon – The term "R-on-T phenomenon" is used when the PVC occurs at or near the T wave apex, otherwise known as the vulnerable period. While it has little prognostic importance in most clinical situations [29-31], it may be of importance in subsets of patients at risk for polymorphic ventricular tachycardia (VT) or ventricular fibrillation (VF), such as those with acute myocardial ischemia, the Brugada syndrome, the malignant form of early repolarization, and idiopathic VF [32-34]. (See "Early repolarization" and "Brugada syndrome: Clinical presentation, diagnosis, and evaluation".)

The ECG tutorial on ventricular arrhythmias provides further discussion about PVCs. (See "ECG tutorial: Ventricular arrhythmias", section on 'Premature ventricular contractions'.)

High-risk PVC characteristics — PVCs are described as high-risk when their presence increases the likelihood of left ventricular dysfunction (either underlying or PVC-induced), heart failure, malignant arrhythmias, or death. The following PVC characteristics, which are discussed above (see 'Describing PVCs' above), have been identified as high-risk [6,35-49]:

●Frequent PVCs (eg, PVC burden >10 to 15 percent)

●Long QRS duration (eg, >140 ms) (waveform 7)

●Superiorly directed QRS axis

●Interpolated PVCs (waveform 3) (discussed in “compensatory pause” bullet)

●Complex PVCs (eg, multifocal, pairs, or R-on-T) (waveform 8)

●Ventricular parasystole (waveform 6) (discussed in “coupling interval” bullet)

●Highly variable coupling intervals (eg, >60 ms difference between intervals) or, in some circumstances, short or long coupling intervals

PVCs originating in the LVOT or RVOT (waveform 1 and waveform 2) are not considered to be high-risk, although they are not always benign [50-52].

A systematic review of 25 observational studies comprising 4863 persons indicated that three independent risk factors were associated with PVC-induced cardiomyopathy: lack of symptoms, interpolation, and epicardial origin of the arrhythmia [49].

FURTHER EVALUATION FOR SELECTED PATIENTS

Selecting patients for further evaluation — Further evaluation with laboratory testing, echocardiography, and ambulatory electrocardiography (ECG) monitoring is indicated for most patients with premature ventricular complexes (PVCs). Exercise testing and cardiac magnetic resonance (CMR) are indicated for a minority of patients. There are three purposes of performing further evaluation: to diagnose underlying structural heart disease that may require treatment, to quantify PVCs (because frequent PVCs can lead to cardiomyopathy), and to identify other arrhythmias that may be responsible for a patient’s symptoms.

We perform further evaluation in patients with any of the following:

●Symptoms (eg, palpitations, syncope).

●Concerning historical features (eg, history of myocardial infarction, family history of sudden cardiac death).

●Suspected high frequency of PVCs (eg, >1 PVC on an ECG).

●High-risk PVC features. (See 'High-risk PVC characteristics' above.)

Components of further evaluation — For all patients with PVCs (except for those at low risk) (see 'Selecting patients for further evaluation' above), we perform further testing, including laboratory tests, echocardiography, and ambulatory ECG monitoring. In addition, we perform exercise testing for patients with exertional palpitations. CMR imaging is reserved for select patients.

Laboratory tests — For all patients for whom further evaluation is indicated, we perform the following laboratory tests to look for conditions that cause or exacerbate PVCs:

●Serum electrolytes to rule out hypokalemia and hypomagnesemia

●Complete blood count to rule out anemia

●Serum digoxin level (for patients taking that medication)

●Thyroid function testing (for patients with symptoms or signs of hyper- or hypothyroidism)

We treat any underlying conditions that are found.

Echocardiography — For all patients for whom further evaluation is indicated, we perform a transthoracic echocardiogram (TTE) to determine whether there are any cardiac conditions (eg, cardiomyopathy, left ventricular hypertrophy) known to be associated with PVCs, because these conditions may require treatment. (See 'Associated conditions' above.)

If the TTE shows evidence of structural heart disease (eg, dilated cardiomyopathy, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy), further workup may be indicated. As an example, if the TTE revealed a left ventricular ejection fraction (LVEF) of 25 percent, further testing to elucidate the etiology of the diminished LVEF might include coronary angiography and/or CMR imaging.

Ambulatory ECG monitoring — For all patients for whom further evaluation is indicated, we perform 24- to 48-hour ambulatory ECG monitoring to quantify the PVC burden, which is the percentage of the total QRS complexes that are PVCs. PVC burden is classified as follows:

●Low: <1 percent or 1000 PVCs/day

●Intermediate: >1 to <15 percent PVCs/ day

●High: >15 percent or 15,000 PVCs/day

A high PVC burden may cause a reversible cardiomyopathy. The risk of PVC-induced cardiomyopathy is highest for patients with PVCs that have a longer QRS duration, superiorly directed axis, long coupling interval, or interpolated PVCs [39-41,53-55] (see "Arrhythmia-induced cardiomyopathy"). An intermediate to high PVC burden also appears to be associated with an increased risk of new-onset atrial fibrillation (AF) [56].

Exercise testing (for exertional symptoms only) — For patients with documented PVCs who experience palpitations primarily with activity, an exercise stress test is appropriate to determine whether PVCs or other arrhythmias can be provoked with exercise. Exercise-induced PVCs, particularly those during the recovery phase, are associated with increased mortality [57-60]. The prognostic significance of exercise-induced PVCs is discussed in detail elsewhere. (See "Prognostic features of stress testing in patients with known or suspected coronary disease", section on 'Premature ventricular complexes'.)

Cardiac magnetic resonance (for select patients) — A small subset of patients with normal echocardiograms may benefit from CMR, including patients with certain high-risk PVC characteristics (see 'High-risk PVC characteristics' above) and family history of cardiomyopathy. In a study of 64 athletes with PVCs of left ventricular origin who underwent CMR, 56 percent were found to have nonischemic left ventricular scar [61]. A family history of cardiomyopathy and several ECG variables (eg, low QRS voltages in limb leads) were associated with the presence of scar. Myocardial scar may increase the likelihood of clinically significant ventricular arrhythmias.

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Ventricular arrhythmias".)

INFORMATION FOR PATIENTS — 

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Ventricular premature beats (The Basics)")

SUMMARY AND RECOMMENDATIONS

●General principles – Premature ventricular complexes (PVCs) are early beats arising from the ventricular myocardium that commonly occur in individuals with or without structural heart disease (SHD). Benign PVCs (ie, PVCs occurring in individuals without SHD) usually originate in the right or left ventricular outflow tract (LVOT). (See 'Prevalence and pathophysiology' above.)

●Associated conditions – Many cardiac and noncardiac conditions are associated with increased prevalence and frequency of PVCs. (See 'Associated conditions' above.)

●Clinical presentation – Most individuals with PVCs are asymptomatic, but some experience palpitations, lightheadedness, or other symptoms. (See 'Clinical presentation' above.)

●Initial evaluation of all patients

•The initial evaluation of all patients includes a history, physical examination, and 12-lead electrocardiogram (ECG). (See 'Initial evaluation of all patients' above.)

•Most PVCs have the following ECG characteristics: QRS duration ≥120 ms, atypical QRS morphology, T wave vector in the opposite direction from the main QRS vector, compensatory pause, and lack of premature P wave preceding the QRS complex. (See 'Describing PVCs' above.)

•Certain ECG characteristics (eg, frequent, interpolated, complex) are associated with an increased risk of left ventricular dysfunction, heart failure, malignant arrhythmias, or death. (See 'High-risk PVC characteristics' above.)

●Further evaluation for most patients

•We perform further diagnostic testing for most patients with PVCs, including those who have symptoms, concerning historical features (eg, family history of sudden death), suspected high frequency of PVCs, or high-risk PVC characteristics. (See 'Selecting patients for further evaluation' above.)

•For all patients in whom further evaluation is indicated, we perform laboratory tests (eg, electrolytes, complete blood count, thyroid function studies, digoxin if appropriate), echocardiography, and ambulatory ECG monitoring. (See 'Laboratory tests' above and 'Echocardiography' above and 'Ambulatory ECG monitoring' above.)

•We perform exercise stress testing for patients with documented PVCs who experience palpitations with exercise. (See 'Exercise testing (for exertional symptoms only)' above.)

•Cardiac magnetic resonance (CMR) imaging is indicated for select patients, such as those with high-risk ECG characteristics and a family history of cardiomyopathy. (See 'Cardiac magnetic resonance (for select patients)' above.)

ACKNOWLEDGMENT — 

The authors and UpToDate thank Dr. Philip Podrid, Dr. Brian Olshansky, and Dr. Bernard Gersh, who contributed to earlier versions of this topic review.