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 https://www.uptodate.com/contents/supraventricular-premature-beats/print 13/30 7/6/23, 1:51 PM Supraventricular premature beats - UpToDate 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.) https://www.uptodate.com/contents/supraventricular-premature-beats/print 14/30 7/6/23, 1:51 PM Supraventricular premature beats - UpToDate 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 https://www.uptodate.com/contents/supraventricular-premature-beats/print 15/30 7/6/23, 1:51 PM Supraventricular premature beats - UpToDate 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. 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Am J Cardiol 2011; 107:151. Topic 932 Version 36.0 https://www.uptodate.com/contents/supraventricular-premature-beats/print 21/30 7/6/23, 1:51 PM Supraventricular premature beats - UpToDate GRAPHICS Single-lead electrocardiogram (ECG) showing atrial bigeminy and blocked atrial premature beats (APBs) The single channel electrocardiographic recording shows a sinus P wave (P) followed by an atrial premature beat (P') in a repeating pattern, termed atrial bigeminy. The P' does not result in ventricular activation since conduction is blocked within the atrioventricular node (blocked atrial premature beat). Graphic 72122 Version 3.0 https://www.uptodate.com/contents/supraventricular-premature-beats/print 22/30 7/6/23, 1:51 PM Supraventricular premature beats - UpToDate Electrocardiogram (ECG) showing atrial premature beats (APBs) that are norma conducted and aberrantly conducted APBs may be normally (asterisk) or aberrantly conducted (double asterisk; usually RBBB aberrancy), and may different P wave morphology and axis and variable PR intervals. APBs: atrial premature beats; RBBB: right bundle branch block. Graphic 96438 Version 2.0 https://www.uptodate.com/contents/supraventricular-premature-beats/print 23/30 7/6/23, 1:51 PM Supraventricular premature beats - UpToDate Electrocardiogram (ECG) strips showing a blocked atrial premature beat (APB) Simultaneous electrocardiographic leads V1, II, and V5 show an atrial premature beat (red arrow) that is blocked within the atrioventricular node and not conducted to the ventricle. The P wave of the atrial premature beats alters the terminal portion of preceding T wave, seen in leads V1 and II, but not in lead V5. Graphic 77154 Version 3.0 https://www.uptodate.com/contents/supraventricular-premature-beats/print 24/30 7/6/23, 1:51 PM Supraventricular premature beats - UpToDate Electrocardiogram (ECG) strips showing junctional premature beats Three simultaneous electrocardiographic surface leads V1, II, and V5 show a junctional premature beat (asterisk). In panel A, there is a sinus P wave seen in lead II just prior to the junctional premature beat, which alters its initial deflection (arrow). The junctional premature beat has a QRS morphology that is identical to that of the sinus beat. In panel B, a sinus P wave is seen immediately after the junctional premature beat in lead II (arrow). The junctional premature beat has a QRS morphology which is slightly different from the sinus QRS complex. Graphic 62336 Version 3.0 https://www.uptodate.com/contents/supraventricular-premature-beats/print 25/30 7/6/23, 1:51 PM Supraventricular premature beats - UpToDate Electrocardiogram strips showing an atrial premature beat, followed by a noncompensatory pause Simultaneous electrocardiographic recording from surface leads V1, II, and V5 shows an atrial premature beat (P'), which is conducted with aberration. The P wave is different from that of the sinus beat and the PR interval is longer,due to delayed conduction in the atrioventricular node. A noncompensatory pause is present (ie, the interval measured from the sinus beat before and after the atrial premature beat is less than 2 sinus RR intervals). Graphic 66489 Version 5.0 https://www.uptodate.com/contents/supraventricular-premature-beats/print 26/30 7/6/23, 1:51 PM Supraventricular premature beats - UpToDate Electrophysiology (EP) study showing surface and intracardiac electrocardiogram tracings of an atrial premature beat (APB) Simultaneous surface electrocardiographic leads I, II, V1 and intracardiac recordings from the high right atrium (HRA), His bundle (HBE), proximal (CSp) and distal (CSd) coronary sinus, and right ventricular apex (RVA). During sinus rhythm, the impulse originates in the HRA and is then conducted through the HBE, CSp, CSd, and ultimately the RVA (blue line 1). An atrial premature beat (APB), denoted by the red asterisk, originates in the CSp (blue line 2) and is conducted retrogradely to the HRA and antegradely to the CSd and RVA. The APB has a longer AH interval compared with sinus rhythm and is associated with a full compensatory pause. Graphic 70505 Version 4.0 https://www.uptodate.com/contents/supraventricular-premature-beats/print 27/30 7/6/23, 1:51 PM Supraventricular premature beats - UpToDate Revised (2018) Vaughan Williams classification of antiarrhythmic drugs abridged table Class 0 (HCN channel blockers) Ivabradine Class I (voltage-gated Na+ channel blockers) Class Ia (intermediate dissociation): Quinidine, ajmaline, disopyramide, procainamide Class Ib (rapid dissociation): Lidocaine, mexilitine Class Ic (slow dissociation): Propafenone, flecainide Class Id (late current): Ranolazine Class II (autonomic inhibitors and activators) Class IIa (beta blockers): Nonselective: carvedilol, propranolol, nadolol Selective: atenolol, bisoprolol, betaxolol, celiprolol, esmolol, metoprolol Class IIb (nonselective beta agonists): Isoproterenol Class IIc (muscarinic M2 receptor inhibitors): Atropine, anisodamine, hyoscine, scopolamine Class IId (muscarinic M2 receptor activators): Carbachol, pilocarpine, methacholine, digoxin Class IIe (adenosine A1 receptor activators): Adenosine Class III (K+ channel blockers and openers) Class IIIa (voltage dependent K+ channel blockers): Ambasilide, amiodarone, dronedarone, dofetilide, ibutilide, sotalol, vernakalant Class IIIb (metabolically dependent K+ channel openers): https://www.uptodate.com/contents/supraventricular-premature-beats/print 28/30 7/6/23, 1:51 PM Supraventricular premature beats - UpToDate Nicorandil, pinacidil Class IV (Ca++ handling modulators) Class IVa (surface membrane Ca++ channel blockers): Bepridil, diltiazem, verapamil Class IVb (intracellular Ca++ channel blockers): Flecainide, propafenone Class V (mechanosensitive channel blockers): No approved medications Class VI (gap junction channel blockers) No approved medications Class VII (upstream target modulators) Angiotensin converting enzyme inhibitors Angiotensin receptor blockers Omega-3 fatty acids Statins HCN: hyperpolarization-activated cyclic nucleotide-gated; Na: sodium; K: potassium; Ca: calcium. Graphic 120433 Version 3.0 https://www.uptodate.com/contents/supraventricular-premature-beats/print 29/30 7/6/23, 1:51 PM Supraventricular premature beats - UpToDate Contributor Disclosures Antonis S Manolis, MD No relevant financial relationship(s) with ineligible companies to disclose. Hugh Calkins, MD Grant/Research/Clinical Trial Support: Adagio Medical [Atrial fibrillation]; Boston Scientific [ARVC]; Farapulse [Atrial fibrillation]; Medtronic [Atrial fibrillation]. Consultant/Advisory Boards: Abbott [Atrial fibrillation]; Atricure [Atrial fibrillation]; Biosense Webster [Catheter ablation]; Boston Scientific [ARVC and atrial fibrillation]; Medtronic [Atrial fibrillation]; Sanofi [Atrial fibrillation]. Other Financial Interest: Atricure [Lecture honoraria]; Biosense Webster [Lecture honoraria]; Boston Scientific [Lecture honoraria]; Medtronic [Lecture honoraria]. All of the relevant financial relationships listed have been mitigated. Susan B Yeon, MD, JD, FACC No relevant financial relationship(s) with ineligible companies to disclose. Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence. Conflict of interest policy https://www.uptodate.com/contents/supraventricular-premature-beats/print 30/30