Version May 2024
INTRODUCTION — Supraventricular premature beats represent premature activation of the atria from a site other than the sinus node and can originate from the atria (premature atrial complexes [PACs]; also referred to as premature atrial beats, premature supraventricular complexes, or premature supraventricular beats) or the atrioventricular node (called junctional premature beats [JPBs]), though the vast majority are atrial in origin. PACs are triggered from the atrial myocardium in a variety of situations 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 manifestations, diagnosis, and treatment of PACs will be presented here. A discussion of premature ventricular complex/contraction (PVC; also referred to a premature ventricular beats or premature ventricular depolarizations) is presented separately. (See "Premature ventricular complexes: Clinical presentation and diagnostic evaluation".)
PREVALENCE — PACs are fairly ubiquitous, occurring commonly in both young and older adult subjects and in those with and without significant heart disease.
The prevalence of PACs is highly dependent upon the technique used for evaluation. PACs are less commonly seen on standard 10-second electrocardiogram (ECG) compared with 24-hour or longer duration Holter monitoring. In a cross-sectional analysis of 1742 Swiss adults (50 years of age or older) from the general population who underwent Holter monitoring for 24 hours, 99 percent had at least one PAC during the monitoring period [1]. In this Swiss cohort, the frequency of PACs steadily increased with age, with rates of 0.8, 1.4, and 2.6 PACs per hour among participants aged 50 to 55 years, 60 to 65 years, and 70 or more years, respectively [1]. Similar findings of greater PAC frequency with advancing age have been reported in other cohorts as well [2-4].
The presence and frequency of PACs is dependent upon the presence of structural heart disease. PACs are particularly frequent in patients with mitral valve disease and in those with left ventricular dysfunction regardless of etiology. However, the high prevalence of PACs in the normal population makes such associations uncertain. (See 'Etiology' below.)
The wide range in the reported prevalence of PACs in different populations may be related to the day-to-day variability in their prevalence and frequency. Circadian variation in the frequency of PACs may also occur, but there is significant interpatient variation. In the Copenhagen Holter Study cohort, in which 638 persons (ages 55 to 75 years) underwent up to 48-hour Holter recording and were followed for a median of 14 years, a circadian variation was observed in the group with frequent PACs (≥720/day; n = 66 persons), with the fewest PACs/h observed during the night with a nadir at 6 AM and then reaching a peak value in the afternoon at 3 PM. Runs of PACs in all subjects showed a similar circadian variation, while the risk of atrial fibrillation (AF) was equal in all time intervals throughout the day [5].
Junctional premature beats (JPBs) occur less commonly than both PACs and PVCs and are rarely seen in clinical practice. Their prevalence has not been well studied due in part to their scarcity as well as difficulty in making the correct diagnosis. In addition, many studies combine JPBs and PACs into one category of supraventricular premature beats.
MECHANISMS — Since invasive testing is rarely performed in patients with only simple PACs, there is little information about the mechanisms of PACs in humans. Although the mechanisms responsible for spontaneous PACs are not clear or well investigated, it seems likely that multiple mechanisms are responsible for PACs in different patients, depending upon the clinical situation. Possible mechanisms, which are discussed in greater detail elsewhere, include:
●Reentry within the atrium [6] (see "Reentry and the development of cardiac arrhythmias")
●Abnormal automaticity [7] (see "Enhanced cardiac automaticity")
●Triggered activity [8] (see "Premature ventricular complexes: Clinical presentation and diagnostic evaluation", section on 'Mechanisms for PVCs')
Although the mechanisms responsible for JPBs are not clear or well investigated, they are most likely due to abnormal automaticity. (See "Enhanced cardiac automaticity".)
ETIOLOGY
PACs — Because PACs occur frequently in subjects with normal hearts as well as in persons with known cardiovascular disease, it is difficult to establish a definite relationship to other disorders or to delineate the factors that predispose to these extra beats. Furthermore, the incidence of PACs is variable in different forms of structural heart disease.
●Idiopathic PACs – In patients without structural heart disease, PACs frequently originate from the pulmonary veins. PACs have long been observed to precede the degeneration of sinus rhythm into AF and are thus considered the main triggers of this common arrhythmia [9,10].
●Lifestyle risk factors – Smoking, alcohol, and coffee are widely considered as potential precipitants of PACs [11-13].
•Smoking and alcohol are known to increase sympathetic tone, which may affect the frequency of PACs [11,12].
•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 [14,15]. Caffeine has clear electrophysiologic effects on the atria, although the association with PACs is uncertain [13]. 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 PACs between users and non-users of caffeine [16]. Nevertheless, there are patients who may be more sensitive to caffeine and note a relationship of palpitations to caffeine intake. Theophylline, another methylxanthine compound, also may increase PAC frequency [17,18].
•Obesity and poor physical activity in midlife have been associated with a higher frequency of PACs in late life [19].
●Acute myocardial infarction – Patients with an acute myocardial infarction (MI) have an early increase in the frequency of PACs, with an incidence ranging from 25 to 81 percent [1,20,21]. One study noted a mean of 9 to 14 PACs per hour on day 1 post-MI, which decreased to one to two PACs per hour on day 10 post-MI [20]. Paroxysmal supraventricular tachycardia (PSVT) is discussed separately. (See "Supraventricular arrhythmias after myocardial infarction".)
●Coronary heart disease – Among patients with known or suspected coronary heart disease, PACs can be induced during exercise testing, but the prognostic importance of PACs during exercise testing remains unknown [22]. (See "Prognostic features of stress testing in patients with known or suspected coronary disease", section on 'Atrial arrhythmias'.)
●Other heart diseases – The frequency of PACs appears to be increased in mitral stenosis, hypertrophic cardiomyopathy, and any condition that results in an elevation in pressure or dilatation of the right or left atrium including cardiomyopathy and valvular heart disease [23,24].
Some studies have suggested the existence of an atrial myopathy as the underlying disease in patients with and without AF. The concept is that aging, atrial stretching, and/or inflammation may produce atrial remodeling, which may lead to left atrial thrombogenesis in some patients even in the absence of AF [25,26].
Apart from echocardiographic indices and possible biomarkers of inflammation, fibrosis, and endothelial dysfunction, recordings of frequent or excessive burden of PACs (≥30 PACs/h daily or ≥200 PACs/24 h, or any runs of ≥20 PACs) might constitute an ECG marker of such myopathy [26-29]. On the other hand, some investigators have suggested that frequent PACs impair left atrial contractile function and promote adverse atrial remodeling and may thus be responsible for the development of atrial myopathy [30].
In addition, cardiac amyloidosis, particularly atrial amyloidosis, a form of senile amyloidosis, may be another type of atrial myopathy causing frequent PACs that may lead to AF, mostly in older individuals [29]. (See "Cardiac amyloidosis: Epidemiology, clinical manifestations, and diagnosis".)
●Chronic obstructive pulmonary disease (COPD) – In patients with COPD, bronchodilator use has been identified as a significant risk factor for increased PACs [31].
JPBs — JPBs may occur in subjects with normal or abnormal hearts. Their presence may be increased by hypokalemia, digitalis toxicity, chronic lung disease, acute ischemia or myocardial infarction, excessive caffeine, nicotine or alcohol use, amphetamine use, stress, valvular heart disease, pericarditis, heart failure (HF), hyperthyroidism, or inflammatory changes in the AV junction following heart surgery.
CLINICAL MANIFESTATIONS — The presence of PACs is associated with several characteristic findings on history, physical examination, and ECG.
PACs may be asymptomatic or cause symptoms such as a sensation of "skipping" or palpitations. PACs are often single and isolated, but they may be frequent and may occur in a bigeminal pattern. Although PACs have a wide array of manifestations, they are not life-threatening by themselves. In predisposed individuals, PACs may initiate supraventricular and, less commonly, ventricular arrhythmias, with AF being the most common arrhythmia induced by PACs [32-35].
Symptoms — PACs produce few or no symptoms in the vast majority of patients (as is also the case in most persons with PVCs), although some individuals may experience palpitations or dizziness. PACs rarely cause true hemodynamic compromise, except when they are associated with an underlying bradycardia.
PACs may lead to palpitations (when there is a pause and increased left ventricular inotropy resulting from an increase in stroke volume) or the sensation of skipped beats which may be due to nonconducted PACs or ineffective contraction resulting from poor filling of the left ventricle during the premature beat. Atrial bigeminy with nonconducted PACs may lead to ventricular rates approaching 40 beats/min, possibly leading to symptoms (ie, lightheadedness, dizziness, presyncope) related to the bradyarrhythmia (waveform 1).
Frequent PACs have been associated with a reversible cardiomyopathy in animal models, with rare case reports in humans, wherein patients with incessant PACs may present with symptoms of HF [36]. This is discussed in more detail separately. (See "Arrhythmia-induced cardiomyopathy", section on 'Frequent atrial ectopy'.)
Most subjects with junctional premature beats (JPBs), like most subjects with PACs, are asymptomatic. However, JPBs may lead to symptoms of palpitations or the sensation of skipped beats. Concealed JPBs that lead to second degree AV block may be associated with symptoms of lightheadedness or near syncope, particularly if they occur in a bigeminal pattern.
Physical examination — The most characteristic finding on physical exam is the presence of an irregular pulse resulting from the presence of PACs or JPBs during the examination. Palpation of the peripheral pulse will demonstrate either premature pulse waves or pauses. Early PACs may lead to cannon A waves on the jugular venous pulsations as they may occur while the AV valves are still closed from the previous ventricular systole. This finding may be particularly helpful in differentiating early nonconducted PACs from sinus pauses. Auscultation of the heart may detect early heart sounds or pauses. PACs and JPBs may also lead to changes in the intensity or timing of a variety of cardiac murmurs (such as those due to mitral valve prolapse) due to the reduction in diastolic filling time and a reduction in ventricular volumes. These changes may be reversed with the post extrasystolic beat since there is an increase in ventricular volume due to the pause. (See "Auscultation of cardiac murmurs in adults".)
Electrocardiography — An ECG should be part of the standard evaluation for any patient with suspected PACs or JPBs.
ECG findings with APBs — PACs are observed on the surface ECG as a P wave that occurs relatively early in the cardiac cycle (ie, prematurely before the next sinus P wave should occur) and has a different morphology and axis from the sinus P wave. Often the PR interval is different from that during sinus rhythm; it may be longer or shorter, depending upon the site of origin of the PAC. With faster baseline heart rates, the abnormal P wave may be hidden within the preceding T wave, producing a "peaked" or "camel hump" type of T wave. If this is not apparent to the interpreting clinician, the PAC may be mistaken for a JPB. (See "ECG tutorial: Atrial and atrioventricular nodal (supraventricular) arrhythmias", section on 'Premature atrial complex'.)
PACs may have a variety of manifestations on the ECG (waveform 2), including:
●A normal QRS complex and a normal or short PR interval.
●A normal QRS complex and a prolonged PR interval.
●A conducted but aberrant (widened) QRS complex. In general, right bundle branch block aberrancy is more common than left bundle branch block aberrancy because of the longer refractory period of the right bundle branch [37].
●No QRS complex (nonconducted PAC) (waveform 3).
The site of origin of an PAC can affect its conduction through the AV node and its P wave morphology:
●An PAC originating in the low right atrium near the AV node may result in a short PR interval (<120 ms) and may even be mistaken for a junctional premature depolarization.
●A negative P wave in the inferior leads, particularly aVF, suggests a low atrial focus, while a negative P wave in lead I and aVL suggests a left atrial origin.
The AV nodal conduction time, and therefore the PR interval, may also differ depending on the input pathway to the AV node. PACs that originate from the left atrium typically have shorter conduction times than those originating from the right atrium [38].
An incomplete compensatory pause follows an PAC due to resetting of the sinus node by the PAC, with the subsequent sinus beat occurring slightly earlier than would be expected in sinus rhythm (less than twice the sinus P-P interval). This is in contrast to the fully compensatory pause which is observed after a ventricular premature beat. Rarely, one may encounter interpolated PACs without a compensatory pause [39].
A nonconducted PAC, especially one that may be obscured by the T wave, may give the false appearance of a sinus pause or sinoatrial exit block (waveform 3). Evaluation of multiple leads may be required to detect the PAC, since it may cause a discernible deflection, seen as a deformity of the normal T wave, in only one or a few ECG leads. (See "Sinoatrial nodal pause, arrest, and exit block".)
ECG findings with JPBs — JPBs may have a variety of manifestations on the surface ECG. They are most often detected when there is a premature beat with a normal QRS complex and:
●A P wave with a PR interval that is too short to be considered to be conducted through the AV node (waveform 4). Although the upper limits of the conduction times (PR interval) consistent with JPBs have not been defined, a premature complex with a PR interval less than 90 ms is unlikely to reflect a conducted PAC.
●No P wave. The absence of a P wave may be due to burial of the wave within the QRS complex or the lack of retrograde atrial activation.
●A P wave that occurs at the terminal portion of the QRS complex, within the ST segment, or on the T wave, depending upon the rate of retrograde conduction.
The location of the P wave relative to the QRS complex provides no definitive information regarding the site of origin within the AV junction; it is simply a manifestation of the relative anterograde and retrograde conduction velocities.
Like PACs, JPBs may conduct anterogradely with a functional or rate-related bundle branch block. In this setting, they may be indistinguishable on the ECG from premature ventricular depolarizations. In this setting, only intracardiac recording of His bundle activation will differentiate between these two possibilities. (See "Invasive diagnostic cardiac electrophysiology studies".)
JPBs may also conduct retrogradely to the atrium and demonstrate conduction block to the ventricles. In this setting, they are similar to PACs and are indistinguishable from nonconducted PACs on the surface ECG.
Ambulatory monitoring — Patients with palpitations or other symptoms suggesting PACs, but an unrevealing physical examination and ECG, should undergo ambulatory monitoring. In evaluating patients with suspected PACs, 24 to 48 hours of ambulatory ECG monitoring significantly increases the likelihood of making the diagnosis, given the sporadic nature of PACs in most patients. In addition, 24-hour Holter monitoring is also the best accepted approach to quantifying the frequency of PACs as a percentage of total heart beats. (See "Ambulatory ECG monitoring", section on 'Indications'.)
DIAGNOSIS — The diagnosis of an PAC is made when a P wave with a morphology different from that of the sinus P wave (inverted or biphasic) occurs earlier than the anticipated sinus P wave (waveform 5). If the ectopic focus is near the sinus node, the P wave may be similar to that of the sinus P. However, every lead should be examined as subtle differences in morphology may be present.
EVALUATION — The evaluation of patients with symptoms suggesting PACs (or JPBs) should focus on documenting their presence or absence with an ECG or some form of ambulatory cardiac monitoring. (See 'Electrocardiography' above.)
Once PACs (or JPBs) have been identified, an additional evaluation should be performed focusing on the presence or absence of underlying structural heart disease. For patients in whom PACs have been identified, the following evaluation should be performed:
●24-hour ambulatory (Holter) monitor to quantify the frequency of PACs and determine if they are monomorphic or multimorphic
●Echocardiography to assess cardiac structure and function
Further testing is indicated only when this initial evaluation identifies significant structural cardiac abnormalities that require further evaluation.
EP testing — There are no indications for performing electrophysiology (EP) studies in patients with PACs. JPBs generally do not require invasive electrophysiologic investigation unless there is a question of infra-His conduction disease, as in the patient with "pseudo AV block" who may possibly have Mobitz II second-degree AV block. (See "Second-degree atrioventricular block: Mobitz type II".)
However, when PACs occur in a patient undergoing EP study for another reason, EP findings include an atrial activation sequence that is different from the sinus activation sequence, and normal conduction through the AV node and His-Purkinje system (waveform 6). Additionally, functional bundle branch block may be seen, leading to HV interval prolongation. Nonconducted PACs typically demonstrate block at the AV node. (See "Invasive diagnostic cardiac electrophysiology studies".)
TREATMENT — In persons found to have frequent PACs or JPBs, further evaluation and management is based on the presence or absence of underlying structural heart disease and/or symptoms. The presence of frequent PACs should prompt a diagnostic evaluation for the possible presence of underlying structural heart disease, which has prognostic significance and may require specific therapy.
No therapy is required for PACs or JPBs in the asymptomatic individual. For patients with symptomatic PACs, simple reassurance regarding the benign nature of PACs is frequently adequate to alleviate symptoms. In addition, patients should be counselled to avoid or minimize potential PAC precipitants (ie, smoking, alcohol intake, stress, caffeine intake in patients whose symptoms are temporally related).
Options for therapy in patients with symptomatic PACs include medical therapy and, in patients with persistent symptoms, catheter ablation. However, there are few direct data to guide the choice of medical therapies, with most of the available data derived from case reports or small case series. Much of the rationale for the use of certain medications is drawn from their use in the treatment of other arrhythmias (eg, supraventricular tachyarrhythmias, PVCs). In addition, there are no studies that directly compare medical therapies with each other or with catheter ablation.
Due to their low frequency of JPBs and even rarer incidence of significant symptoms, the appropriate treatment of symptomatic JPBs has not been evaluated. Reassurance of the benign nature of this rhythm abnormality may alleviate symptoms. For patients with persistent, limiting symptoms due to JPBs, therapy is similar to that for PACs, with beta blockers as the primary option.
Medical therapy — For patients with ongoing symptomatic PACs following efforts to minimize potential PAC precipitants (ie, smoking, caffeine intake, alcohol intake, stress), medical therapy with a beta blocker is recommended if no contraindication exists for its use (eg, oral metoprolol 25 mg twice daily with uptitration as needed for effect). Beta blockers can reduce the symptoms related to PACs and may reduce their frequency, particularly if they are due to enhanced automaticity related to enhanced sympathetic output. Beta blockers do not suppress PACs but may be useful to reduce symptoms by reducing the increased inotropy seen with the post extrasystolic beat (ie, post extrasystolic potentiation). The response to beta blockers is inconsistent and variable, with some patients having complete or near complete symptom resolution and others showing minimal benefit.
A cohort study examined whether beta blockers at low doses may improve long-term outcomes in individuals with PACs, stratified into high-burden (≥100 PACs/24 h) and low-burden (<100 PACs/24 h) subcohorts [40]. In the high-burden subcohort, after propensity score matching, the treatment group (n = 208) had significantly lower mortality rates during mean follow-up of about three years than the nontreatment group (n = 832; hazard ratio [HR] 0.52, 95% CI 0.294-0.923), but rates of new stroke and of new AF were similar in the two groups. Similarly, in the low-burden subcohort, the treatment group (n = 614) had a 40 percent mortality reduction (HR 0.60, 95% CI 0.396-0.913) compared with the nontreatment group (n = 1228), but rates of new stroke and new AF were similar in the two groups. These findings suggest that beta blockers may decrease the mortality rate in patients with high or low burden of PACs, but this effect was not related to the risk of new stroke or new AF.
Type IA, type IC, and type III antiarrhythmic agents (table 1) can diminish the frequency of PACs in the symptomatic patient. These drugs may also suppress PACs that precipitate or trigger other supraventricular arrhythmias including AF, atrial flutter, atrioventricular nodal reentrant tachycardia, or atrioventricular reentrant tachycardia. Although controlled studies have not been performed with many of these agents, several reports describe their successful use [41-43]. However, administration of these agents must be balanced with the risk of proarrhythmia. (See "Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation: Clinical trials" and "Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation: Recommendations", section on 'Proarrhythmia' and "Major side effects of class I antiarrhythmic drugs".)
By comparison, digoxin, calcium channel blockers, and type IB antiarrhythmic agents have not been clearly shown to be beneficial in patients with symptomatic PACs.
Catheter ablation — When PACs are symptomatic and documented to trigger AF, they may be a target for catheter ablation, particularly in patients with concern for cardiomyopathy due to frequent PACs or those with persistent PACs and symptoms in spite of medical therapy. (See "Atrial fibrillation: Catheter ablation".)
PACs arising from the pulmonary veins may be treated by pulmonary vein isolation. PACs of non-pulmonary vein origin may also be managed by ablation guided by electroanatomic mapping techniques [44-47]. Successful pulmonary vein isolation procedures in patients with paroxysmal AF and high trigger burden (approximately 500 PACs/h) not only reduce the trigger burden but also increase the PAC coupling interval, suggesting that shorter coupled PACs originate preferentially from the pulmonary veins, which has been considered a reflection of the pulmonary veins' abbreviated refractoriness in patients with AF [48-50].
PROGNOSIS — The prognosis related to PACs depends on the presence of any underlying cardiovascular pathology. However, the presence of PACs in populations of apparently healthy persons appears to be associated with a greater risk of cardiovascular morbidity and mortality.
●Cardiovascular mortality – Frequent PACs have been associated with greater risk of cardiovascular mortality [51-55].
•Among 7692 healthy participants with no history of myocardial infarction, stroke, AF, or atrial flutter enrolled in the prospective Japanese NIPPON DATA 90 cohort and followed for an average of 14 years, only 64 persons (0.8 percent) had one or more PACs on a screening 12-lead ECG at enrollment [53]. However, the presence of PACs was an independent predictor for cardiovascular (CV) deaths (hazard ratio [HR] 2.03, 95% CI 1.12-3.66).
•Among 7504 healthy participants in the NHANES study without known CVD who were followed for up to 18 years, 89 persons (1.2 percent) had one or more PACs on a screening 12-lead ECG [54]. As seen in the Japanese study, the presence of PACs was associated with higher CV mortality (HR 1.78, 95% CI 1.26-2.44) as well as higher total mortality (HR 1.41, 95% CI 1.08-1.80).
•Among 5371 consecutive Taiwanese patients without AF or a permanent pacemaker (PPM) at baseline who underwent 24-hour Holter monitoring, an PAC burden >76 beats per day was an independent predictor of mortality (HR 1.4, 95% CI 1.2-1.6), cardiovascular hospitalization (HR 1.3; 95% CI 1.1-1.5), new-onset AF (HR 1.8, 95% CI 1.4-2.2), and PPM implantation (HR 2.8, 95% CI 1.9-4.2) over a mean follow-up of 10 years [55].
•A cohort study examined the distribution of PAC burden and its relationship to all-cause mortality and CV death in 15,893 persons [56]. PAC burden increased with age with no apparent sex difference. Multivariate analysis found that PAC burden was associated with the risk of all-cause mortality (4th versus 1st quartile, adjusted HR 1.67) and CV death (HR 1.12 per ln PAC increase). In subgroup analyses, the risk of high PAC burden (≥100 PACs/24 h) was consistent across the overall cohort and prespecified subgroups.
Similar findings, though with a less magnitude of risk, have been seen in other smaller cohorts of patients who were evaluated with 24-hour Holter monitoring and who were stratified based on total numbers of PACs in 24 hours [51,52].
●AF – Frequent PACs or increased PAC burden may predict new or undiagnosed AF and adverse cardiovascular events [51,52,55,57-65]. As examples:
•In a single-center cohort of 428 patients without AF or structural heart disease who were referred for 24-hour Holter monitoring to evaluate palpitations, dizziness, or syncope, 107 (25 percent) had frequent PACs (number of PACs at the top quartile, ie, >100 PACs/day) [51]. After a mean of 6.1 years of follow-up, significantly more patients with frequent PACs developed AF (31 patients [29 percent] compared with 29 patients [9 percent] with less frequent PACs).
•In a subset of the prospective Cardiovascular Health Study, 1260 adults without prevalent AF who enrolled between 1989 and 1990 underwent 24-hour Holter monitoring and were followed for 15 years. Using the Framingham AF risk algorithm, doubling of the hourly PAC count was associated with a significant increase in AF risk (HR 1.17, 95% CI 1.13-1.22) [52].
•In a Japanese cohort of 63,197 persons without known CVD at baseline who were followed for an average of 14 years, the presence of PACs on baseline ECG was associated with a significantly higher likelihood of developing AF in both men (HR 4.9, 95% CI 3.6-6.6) and women (HR 3.9, 95% CI 2.7-5.6) [59].
•In a retrospective cohort, which analyzed Holter recordings from 1357 veterans free of AF at baseline (mean age 64 years; 93 percent men), with a median follow-up of 7.5 years, AF was significantly more common in patients with frequent (≥100/day) PACs compared with patients with infrequent (<100/day) PACs (22 versus 6 percent, adjusted HR 3.0, 95% CI 1.9-4.8) [60].
•In the STROKESTOP I mass-screening study for AF in 75- and 76-year-old persons in Sweden, over a median follow-up of 4.2 years, of the 6100 participants, 15 percent (n = 894) had arrhythmia, with frequent PACs being the most common (11.6 percent; n = 709) and irregular supraventricular tachycardias being more common than regular [66]. Persons with the most AF-similar supraventricular tachycardias, irregular and lacking p waves (1.6 percent; n = 97), had the highest risk of developing AF (HR 4.3) and an increased risk of death (HR 2.0). Thus, progression of atrial arrhythmias from PACs to more AF-like episodes was associated with development of AF, suggesting a possible role for screening for AF in individuals with frequent supraventricular activity.
•Frequent PACs during exercise (>5 beats per stage) provided prognostic information with a higher incidence (5.5 percent) of new-onset AF/atrial flutter at follow-up (approximately one year) in 128 patients compared with 870 patients with no frequent PACs (0.6 percent AF/atrial flutter incidence) [67]. Treadmill-induced frequent PACs, chronotropic incompetence, and palpitation as a reason for treadmill testing were independent risk factors that predicted new-onset AF/atrial flutter.
•Higher numbers of PACs have also been shown to be a predictor of subclinical AF in patients with cryptogenic stroke as well as a predictor of late AF recurrence following pulmonary vein isolation for AF [62,63]. (See "Cryptogenic stroke and embolic stroke of undetermined source (ESUS)" and "Atrial fibrillation: Catheter ablation".)
-In a meta-analysis of 12 studies with a total of 109,689 subjects with frequent (n = 9217) and non-frequent (n = 100,472) PACs, patients with frequent PACs, however variably defined, had an increased risk of new onset AF (pooled risk ratio 2.8, 95% CI 2.1-3.7) [68].
-In a study of 4331 participants with hypertension and receiving treatment, AF risk associated with PACs could potentially be decreased by treatment with angiotensin-II receptor blockers (ARBs) and statins, along with lowering blood pressure and managing diabetes [69].
●Stroke – There are mixed data on the risk of stroke in patients with PACs, with some studies suggesting a higher risk of stroke in patients with frequent PACs [27,28,70,71] while others have found no such increase in risk [72]. Because not all of the studies presented data on the development of AF during follow-up, and AF is definitively associated with an increased risk of stroke, the impact of frequent PACs on stroke risk remains uncertain. However, in patients with acute stroke, the presence of numerous PACs and short runs of supraventricular tachycardia have been associated with a greater risk for subsequently developing AF, which might potentially explain the etiology of the stroke [73-75]. Furthermore, the concept that atrial myopathy might play a role and be responsible for a stroke in some patients independently from AF has also been advanced, and frequent or an excessive burden of PACs (≥30 PACs/h daily or any runs of ≥20 PACs) might constitute an ECG marker for such a myopathy [26,27].
A meta-analysis of 12 studies examining whether PACs can predict AF in 2340 ischemic stroke patients (mean age 66 years) indicated that PACs were highly associated with AF occurrence in stroke (pooled odds ratio [OR] 4.16, 95% CI 3.06-5.65) and cryptogenic stroke patients (pooled OR 3.72, 95% CI 2.66-5.20) [76]. Subgroup analysis showed that PAC presence (pooled OR 3.72, 95% 1.65-8.36) and frequent PACs (pooled OR 5.12, 95% CI 3.12-8.41) were correlated with stroke in AF patients. Frequent PACs were identified as the risks for asymptomatic AF (OR 6.18, 95% CI 3.23-11.83) and future AF occurrence (OR 3.71, 95% CI 2.62-5.26) in stroke patients.
●Sudden cardiac death – Isolated PACs have not been associated with sudden death (SCD). Among 14,574 patients in the ARIC study who had a 12-lead ECG and a two-minute 3-lead rhythm strip at baseline, there was no significant increase in the risk of SCD among persons with PACs (HR 1.15, 95% CI 0.56-2.39), although when PACs occur concurrently in individuals with VPBs, the risk of SCD was higher (HR 6.39 compared with patients with neither PACs nor VPBs; 95% CI 2.58-15.84) [77].
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: Catheter ablation of arrhythmias" and "Society guideline links: Supraventricular arrhythmias".)
SUMMARY AND RECOMMENDATIONS
●Definition – Supraventricular premature beats represent premature activation of the atria from a site other than the sinus node. The vast majority originate from the atria (premature atrial complexes [PACs]) though some originate from the atrioventricular node (called junctional premature beats [JPBs]). (See 'Introduction' above.)
●Prevalence – PACs are fairly ubiquitous, occurring commonly in both young and older adult subjects and in those with and without significant heart disease. JPBs occur less commonly than both PACs and premature ventricular complexes/contractions (PVCs) and are rarely seen in clinical practice. (See 'Prevalence' above.)
●Symptoms and signs – PACs and JPBs are asymptomatic in the vast majority of patients but can cause symptoms such as a sensation of "skipping" or palpitations. The most characteristic physical exam finding is an irregular pulse. (See 'Clinical manifestations' above.)
●Diagnostic evaluation – The evaluation of patients with suspected PACs (or JPBs) should focus on documenting their presence or absence with an ECG or ambulatory cardiac monitoring.
•PACs – These are observed on the surface ECG as a P wave that occurs earlier than the anticipated next sinus P wave and has a different morphology (eg, inverted or biphasic) from the sinus P wave (waveform 1 and waveform 2 and waveform 3 and waveform 5). Every lead should be examined as subtle differences in morphology may be present. Often the PR interval is different from that during sinus rhythm. (See 'ECG findings with APBs' above.)
•JPBs – These are observed on the ECG as a QRS complex with no preceding P wave or with a P wave occurring too soon before the QRS to be considered to be conducted through the AV node (waveform 4). (See 'ECG findings with JPBs' above.)
Once PACs (or JPBs (waveform 4)) have been identified, additional evaluation should be performed to identify any underlying structural heart disease. (See 'Evaluation' above.)
●Management – In persons with frequent PACs or JPBs, management is based on the presence or absence of symptoms and/or underlying structural heart disease. (See 'Treatment' above.)
•Asymptomatic PACs or JPBs – No therapy is required for PACs or JPBs in the asymptomatic individual.
•Symptomatic PACs – For patients with symptomatic PACs, reassurance regarding the benign nature of PACs is frequently adequate to alleviate symptoms. In addition, patients should be counseled to avoid or minimize potential PAC precipitants (eg, smoking, alcohol intake, stress, caffeine intake, obesity, poor physical activity).
For patients with persistent symptomatic PACs despite efforts to minimize potential PAC precipitants we suggest a trial of medical therapy with a beta blocker (eg, oral metoprolol 25 mg twice daily with uptitration as needed for effect) (Grade 2C).
When PACs are symptomatic and documented to trigger atrial fibrillation (AF) or persist despite medical therapy, they may be a target for catheter ablation, particularly in patients with concern for cardiomyopathy due to frequent PACs. (See 'Catheter ablation' above.)
•Symptomatic JPBs – Reassurance of the benign nature of this rhythm abnormality may alleviate symptoms. For patients with persistent, limiting symptoms due to JPBs, therapy is similar to that for PACs, with beta blockers as the primary option.
ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges Philip Podrid, MD, FACC, and Bernard Gersh, MB, ChB, DPhil, FRCP, MACC, who contributed to earlier versions of this topic review.
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