Version May 2024
INTRODUCTION — Premature ventricular complexes/contractions (PVCs; also referred to as premature ventricular beats, premature ventricular depolarizations, or ventricular extrasystoles) are triggered 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, mechanisms, clinical presentation, and approach to diagnostic testing for patients with known or suspected PVCs will be presented here. Discussion of the treatment and prognosis related to PVCs, as well as review of supraventricular premature beats, are presented separately. (See "Premature ventricular complexes: Treatment and prognosis" and "Supraventricular premature beats".)
PREVALENCE — The prevalence of PVCs is directly related to the study population, the detection method, and the duration of observation. PVCs are more likely to be detected in older patients, patients with more comorbidities, and patients who are monitored for longer durations of time [1].
In patients with no known heart disease, PVCs have been seen in approximately 1 percent of routine 12-lead electrocardiograms (ECG) of 30 to 60 seconds duration and up to 6 percent of ECGs of two minutes duration [2-4]. By comparison, when 24-hour ambulatory monitoring is used, up to 80 percent of apparently healthy people have occasional PVCs [5,6]. The occurrence of frequent PVCs accounting for more than 20 percent of overall heart beats is rare, seen in less than 2 percent of patients [7].
There is an age-related increase in the prevalence of PVCs in normal individuals and those with underlying heart disease [2,4,6,8]. The prevalence of PVCs increase with age and in the presence of other factors, such as faster sinus rate, hypokalemia, hypomagnesemia, and hypertension [4].
It is generally considered that a "normal number" of PVCs in an adult is <500 per 24 hours [9].
MECHANISMS FOR PVCS — Since invasive testing is rarely performed in patients with only simple PVCs, there is little information about the mechanisms of PVCs in humans. Mechanisms by which PVCs are generated include [1]:
●Reentry — Reentry is one potential mechanism for PVCs, particularly in patients with structural heart disease such as in the post-myocardial infarction (MI) setting. Reentrant PVCs occur with conduction delay and unidirectional block, settings that are characteristically seen in patients with a healed MI or evidence of myocardial fibrosis of any etiology. A wave front may then perpetuate under the correct set of circumstances, such as the administration of a drug that prolongs conduction. (See "Reentry and the development of cardiac arrhythmias".)
●Abnormal automaticity — Abnormal automaticity is most probable with electrolyte abnormalities or acute ischemia and is enhanced by catecholamines. 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. (See "Enhanced cardiac automaticity".)
●Triggered activity — Early (phase 3 of the action potential) or late (phase 4) afterdepolarizations may occur in Purkinje cells or in the ventricular myocardium; such electrical activity may arise because of a number of conditions, including hypokalemia, ischemia, infarction, cardiomyopathy, excess calcium, and 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.
CLASSIFICATION — PVCs can be classified in a variety of manners:
●The absence (idiopathic) or presence of underlying structural heart disease (SHD)
●Clinical presentation (symptomatic or asymptomatic)
●ECG morphology (LBBB) (waveform 1) or RBBB (waveform 2); unifocal with single morphology or multifocal with >1 morphologies; interpolated when interposed within two sinus beats without a compensatory pause) (waveform 3)
●Relationship (or not) to exercise (ie, exercise-induced or not)
●Frequency of occurrence (PVC burden)
●Prognosis (potentially "malignant," eg, frequent PVCs in patients with SHD, or short-coupled "idiopathic" PVCs)
Idiopathic PVCs most commonly originate from the right ventricular outflow tract, the left ventricular outflow tract, and the paravalvular aortic cusps. (See 'Electrocardiography' below.)
CLINICAL PRESENTATION AND ECG FINDINGS — The presence of PVCs is associated with several characteristic findings on history, physical examination, and ECG. The identification of PVCs in an otherwise healthy person is usually a benign and incidental finding, but PVCs may also be seen in a variety of inherited and acquired forms of heart disease.
Symptoms — The vast majority of patients with PVCs experience no symptoms. When patients experience symptoms, palpitations are the most frequent symptom, with dizziness occurring infrequently. PVCs rarely cause true hemodynamic compromise, except when they occur frequently in a patient with severely depressed left ventricular (LV) function or when they are associated with an underlying bradycardia. Though less commonly seen, associated symptoms of syncope, (especially with no prodrome, preceded by palpitations), chest pain, or dyspnea could signal associated underlying cardiac structural or electrical conduction system disease.
The most common symptoms resulting from PVCs are palpitations. Palpitations result from the hypercontractility of a post-PVC beat or a feeling that the heart has stopped secondary to a post-PVC pause. Less often, frequent PVCs can result in a pounding sensation in the neck, lightheadedness, or near syncope.
There is great variability as to when the symptoms are most prominent, although a quiet environment, such as at night while lying in bed, may make patients more aware of their ectopy. They are more frequently appreciated when subjects are lying on their left side and the heart is closer to the chest wall.
Correctable causes or triggers should be sought by clinical history (inquiring about possible underlying cardiovascular diseases, but also about use of alcohol or caffeine-containing beverages, or illicit drugs, etc) and/or laboratory testing (electrolyte levels, thyroid stimulating hormone [TSH]). (See 'Laboratory studies' below.)
Physical examination — Unless the patient is actively experiencing PVCs at the time of evaluation, there are no sensitive or specific findings from the physical examination. When PVCs are actively occurring, the following may be seen:
●Irregular pulse – The most characteristic finding on physical exam is the presence of an irregular pulse resulting from the presence of PVCs during the examination.
●Atrioventricular dissociation – If present, this will result in variable intensity of the first heart sound (secondary to a changing PR interval) and in cannon "A" waves (due to almost simultaneous retrograde atrial and antegrade ventricular activation and subsequent contraction).
●The splitting of the second heart sound (S2) – This will also vary, depending upon whether the PVC has a right or left bundle branch morphology; a widely split S2 due to a delayed P2 may be appreciated if a right bundle branch block PVC occurs. (See "Auscultation of heart sounds".)
●Compensatory pause – An auscultated fully compensatory pause is present with most PVCs and is identified by the prolonged pause following the premature beat.
Electrocardiography — An ECG should be part of the standard evaluation for any patient with suspected PVCs (waveform 4) [1]. PVCs have the following ECG characteristics (see "ECG tutorial: Ventricular arrhythmias"):
●QRS duration – A PVC has a duration of more than 120 milliseconds.
●QRS morphology – A PVC morphology is different from usual aberration (ie, a typical right bundle branch block [RBBB] or left bundle branch block [LBBB]), although RBBB-like and LBBB-like morphologies may also be seen.
●T wave – In a PVC this is in the opposite direction from the main QRS vector.
●A fully compensatory pause – This is defined as a PP interval surrounding the PVC that is twice the sinus PP interval; less frequently, the PVC is interpolated and does not alter the baseline sinus interval (ie, the PP interval surrounding the PVC is equal to the sinus PP interval). The pause results from retrograde block in the atrioventricular (AV) node and hence an inability of the ventricular impulse to penetrate the atrium and affect the sinus node. The sinus node fires on time, but the impulse it generates is unable to conduct to the ventricle.
●Multifocal PVCs – These may originate from various sites, 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.
●Specific PVC pattern – Several specific PVC patterns have been described. One pattern, ventricular bigeminy, refers to a persistent alternation of normal and premature beats (ie, every other QRS complex is a PVC) (waveform 5). Ventricular trigeminy (two normal beats followed by a PVC) and quadrigeminy (three normal beats followed by a PVC) have also been described (waveform 6). They rarely cause severe symptoms and have no known independent prognostic importance.
There are notable exceptions to these characteristic findings, including:
●A less wide QRS complex – This can result from a PVC originating from the contralateral ventricle in a patient with a preexisting bundle branch block.
●A relatively narrow QRS complex (<130 milliseconds) with an RBBB morphology – This is seen in fascicular PVCs displaying a left axis deviation (left anterior fascicular block) when originating in the left posterior fascicle or a right axis deviation (left posterior fascicular block) when originating in the anterior fascicle of the left bundle [10]. Very rarely, a PVC may originate from the left bundle branch itself and resemble a sinus beat, indistinguishable from an PAC on surface ECG [11].
●A pseudonormalized T wave – This is seen in PVCs in a patient with a prior myocardial infarction.
●Noncompensatory pause – A PVC that resets the sinus node and thereby creates a noncompensatory pause.
●An interpolated PVC – This is interposed between two sinus beats without a compensatory pause (waveform 3). Interpolated PVCs have also been reported to be associated with PVC-induced cardiomyopathy [12]. (See "ECG tutorial: Ventricular arrhythmias", section on 'Premature ventricular contractions'.)
Classically, unifocal PVCs have fixed coupling intervals with the preceding beat since the most frequent mechanism is localized reentry. By comparison, unifocal PVCs with variable coupling suggests a parasystolic focus due to ectopic tissue that exhibits autonomy.
Ventricular parasystole represents an independent ectopic ventricular rhythm that competes with the sinus rhythm. It appears on the ECG as unifocal PVCs with a variable coupling interval (the interval between the prior sinus beat and the premature beat varies) (waveform 7). There is entrance block into this focus, and thus it continues to fire at its own rate. There is also exit block from this focus (ie, it will result in ventricular depolarization and a ventricular complex only when the ventricular myocardium is capable of being stimulated). (See "ECG tutorial: Ventricular arrhythmias", section on 'Ventricular parasystole'.)
R-on-T phenomenon — The term "R-on-T phenomenon" (ie, when the PVC occurs at or near the T wave apex, otherwise known as the vulnerable period), has little prognostic importance in most clinical situations [13-15]. During the performance of an electrophysiology study, PVCs are applied at the vulnerable period of the cardiac cycle, without producing malignant ventricular arrhythmias in normal hearts. However, the R-on-T phenomenon 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 [16-18]. (See "Early repolarization" and "Brugada syndrome: Clinical presentation, diagnosis, and evaluation".)
Short- versus long-coupled PVCs/variable PVC coupling interval — Short-coupled PVCs are potentially malignant as they can induce the short-coupled variant of torsade de pointes that may degenerate into VF [19,20].
Long-coupled fascicular PVCs are traditionally considered benign; however, in a subgroup of patients, they can also be associated with idiopathic VF, particularly if they are left-sided in origin [21].
Importantly, variability in PVC coupling interval, rather than fixed short- or long-coupling interval, seems to be more important, as it has been suggested to increase the risk of cardiomyopathy and sudden death [22].
Associated conditions — While PVCs can and do occur sporadically at some point in nearly all persons, certain conditions, both cardiac and non-cardiac, are associated with more frequent PVCs. Examples of cardiac conditions in which PVCs are frequently seen include [23-30]:
●Hypertension with LV hypertrophy (the presence of LVH has been associated with a higher prevalence of PVCs in patients with hypertension; LVH has been linked to higher morbidity and mortality) [31].
●Acute MI
●HF
●Myocarditis
●Arrhythmogenic right ventricular cardiomyopathy
●Hypertrophic cardiomyopathy
●Congenital heart disease
●Idiopathic ventricular tachycardia
Non-cardiac conditions in which PVCs may arise include [32-35]:
●Chronic obstructive pulmonary disease
●Sleep apnea syndromes
●Pulmonary hypertension
●Endocrinopathies (thyroid, adrenal, or gonadal abnormalities) can all be associated with PVCs
●Nicotine, alcohol, or stimulants use, including sympathomimetic medications (eg, beta-agonists, decongestants, antihistamines) or illicit drugs (eg, cocaine, amphetamines)
Although there is a widespread belief that caffeine, particularly at high doses, is associated with palpitations and a number of arrhythmias, there is no evidence that it is proarrhythmic [36-38]. In a study of 1388 participants in the Cardiovascular Health Study, in which caffeine consumption was self-reported and patients underwent 24-hour ambulatory monitoring, there was no significant differences in the frequency of PVCs between users and non-users of caffeine [39]. Additionally, more frequent consumption of caffeine in this study was not associated with more ectopy. Nevertheless, there are patients who may be more sensitive to caffeine and note a relationship of palpitations to caffeine intake.
A greater discussion of the relevance of PVCs in various clinical conditions can be found in the specific topics.
PVC-induced cardiomyopathy — Frequent PVCs are associated with a reversible cardiomyopathy, even in the absence of sustained ventricular arrhythmias or symptoms [40]. Risk factors for PVC-induced cardiomyopathy are a greater PVC burden and epicardial origin of PVCs [41], as well as longer PVC QRS duration [42], superiorly directed PVC axis (odds ratio [OR] 2.7), high PVC burden of 10 to 20 percent (OR 3.5) or >20 percent (OR 4.4), PVC coupling interval >500 ms (OR 4.7), nonsustained ventricular tachycardia (OR 5.3) [43], duration of ectopic (PVC) activity, male sex, lack of diurnal variation, and interpolated PVCs [44]. PVCs with longer coupling intervals but not PVC location were shown to be associated with pronounced LV dyssynchrony and more severe cardiomyopathy [45]. PVC burden has been found to be the most consistent parameter for the risk of development of PVC cardiomyopathy [46].
Data on the time course of PVC cardiomyopathy are limited. Some studies suggest PVC cardiomyopathy develops slowly and may take as long as four years, even in persons with a high PVC (>20 percent) burden [47]. However, animal studies have suggested that left ventricular dysfunction may develop as early as two to four weeks, dependent on pattern (eg, bigeminal), coupling interval, PVC burden, degree of asynchrony, and individual-related characteristics [47].
Elimination of PVCs using catheter ablation or medications often leads to normalization of cardiac function. This is discussed in more detail separately. (See "Arrhythmia-induced cardiomyopathy", section on 'Frequent ventricular ectopy'.)
PVC-related cardiomyopathy should be suspected in individuals who present with an unexplained cardiomyopathy and very frequent unifocal PVCs (typically >15 percent of all beats). It should be noted that some patients with high PVC burdens can maintain normal cardiac function, and PVC-induced cardiomyopathy has also been reported in patients with PVC burdens as low as 4 to 5 percent.
One large population study suggested that PVC-induced cardiomyopathy may be underdiagnosed or mistaken for idiopathic cardiomyopathy. In this database study of 16.8 million patients, those with PVCs were more likely to develop systolic heart failure compared with those who did not have VCs (62.8 versus 6.1 per 1000 patient-years; hazard ratio [HR] 1.8, 95% CI 1.8-1.9) [28]. The effect of PVCs on the incidence of systolic heart failure is even greater in younger patients (<65 years of age) without comorbidities, suggesting that PVCs may be an important cause of "idiopathic" HF (HR 6.5, 95% CI 5.5-7.7).
PVC-induced atrial fibrillation — Recent data indicate that increased (moderate to high) PVC burden is associated with a higher risk of new-onset AF [48].
ADDITIONAL TESTING — Once PVCs are suspected or definitively identified, the need for additional testing is based on the suspected presence or absence of associated cardiac disease and possibly if PVCs with high-risk features are present. This is discussed separately. (See "Premature ventricular complexes: Treatment and prognosis", section on 'Underlying or associated cardiac disease' and "Premature ventricular complexes: Treatment and prognosis", section on 'Risk assessment'.)
Laboratory studies — Although there is no routine approach to laboratory testing in patients with PVCs, patient history and physical examination can guide appropriate testing for PVC triggers (table 1).
Ambulatory monitoring — Ambulatory ECG monitoring should be performed for diagnostic or prognostic purposes in many and/or most patients with PVCs. Ambulatory monitoring is especially valuable in the following settings:
●Unclear etiology – Patients with palpitations of unclear etiology with significant symptoms, in whom therapeutic decisions will differ depending upon the etiology of palpitations
●Management decisions – Patients in whom PVCs have been identified when therapeutic or prognostic decisions may vary based on the quantity and morphology of PVCs. Examples include patients with cardiomyopathy that may be PVC related in whom catheter ablation is being considered, underlying heart disease in whom PVCs may contribute to prognosis and therapeutic decisions (eg, for an implantable cardioverter-defibrillator in patients with hypertrophic cardiomyopathy, etc) or any patient with arrhythmogenic right ventricular cardiomyopathy.
When ambulatory ECG monitoring is indicated, a monitoring period of 24 to 48 hours is typically sufficient to identify PVCs and quantify the overall PVC burden. A variety of ambulatory ECG monitoring techniques are available, but for most patients Holter monitoring or patch monitoring will be the preferred approach. (See "Ambulatory ECG monitoring".)
Echocardiogram — An echocardiogram should be performed if there are high-risk symptoms, frequent PVCs, or if there is any suspicion of underlying or new structural heart disease (including PVC LV cardiomyopathy) and/or high-risk information from other risk assessments such as abnormal 12-lead ECG or family history of heart disease and especially of sudden cardiac death. Most commonly, transthoracic echocardiography is the initial test (and test of choice) for the evaluation of underlying cardiac structure, function, and noninvasive hemodynamic measurements. In addition to LV cardiomyopathy, frequent PVCs can also cause a right ventricular cardiomyopathy that is reversible after successful PVC ablation [49].
Further testing in selected patients — In selected patients with PVCs, exercise testing, cardiac magnetic resonance imaging, and electrophysiologic testing are indicated. These tests and their indications are described separately. (See "Premature ventricular complexes: Treatment and prognosis", section on 'Further testing in selected patients'.)
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 5th to 6th 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 10th to 12th 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
●Background – Premature ventricular complexes/contractions (PVCs; also referred to as premature ventricular beats, premature ventricular depolarizations, or ventricular extrasystoles) are common and occur in a broad spectrum of the population, including patients with and without structural heart disease. (See 'Introduction' above.)
●Prevalence – The prevalence of PVCs is directly related to the study population, the detection method, and the duration of observation. PVCs are more likely to be detected in older patients, patients with more comorbidities, and patients who are monitored for longer durations of time. (See 'Prevalence' above.)
●Clinical presentation – The vast majority of patients with PVCs experience no symptoms. When patients experience symptoms, palpitations are the most frequent symptom, and dizziness is less common. PVCs rarely cause true hemodynamic compromise, except when they occur frequently in a patient with severely depressed left ventricular (LV) function or when they are associated with an underlying bradycardia. (See 'Symptoms' above.)
●PVC-induced cardiomyopathy – Frequent PVCs have been associated with a reversible cardiomyopathy, even in the absence of sustained ventricular arrhythmias or symptoms. (See 'PVC-induced cardiomyopathy' above and "Arrhythmia-induced cardiomyopathy", section on 'Frequent ventricular ectopy'.)
●Diagnostic evaluation
•Electrocardiogram – This should be part of the standard evaluation for any patient with suspected PVCs. Typical electrocardiographic (ECG) findings of PVCs include QRS duration >120 milliseconds, QRS morphology that is different from usual aberration, T wave in the opposite direction from the main QRS vector, and a fully compensatory pause (ie, the PP interval surrounding the PVC is twice the sinus PP interval). (See 'Electrocardiography' above.)
•Laboratory studies – Although there is no routine approach to laboratory testing in patients with PVCs, patient history and physical examination can guide appropriate testing for PVC triggers (table 1). (See 'Laboratory studies' above.)
•Ambulatory monitoring – Ambulatory ECG monitoring is performed for diagnostic or prognostic purposes in many and/or most patients with PVCs. (See 'Ambulatory monitoring' above.)
•Echocardiogram – This should be performed if there are high-risk symptoms, frequent PVCs, suspicion of underlying or new structural heart disease, and/or high-risk information from other risk assessments; these include abnormal 12-lead ECG, family history of sudden cardiac death, or other cardiac disease. (See 'Echocardiogram' above.)
•Further testing – In selected patients with PVCs, exercise testing, cardiac magnetic resonance imaging, and electrophysiologic testing are indicated. (See "Premature ventricular complexes: Treatment and prognosis", section on 'Further testing in selected patients'.)
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.
آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟
