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Premature Atrial Contractions
Introduction
Premature atrial contractions (PACs) are contractions of the atria that are triggered by the atrial myocardium but have not originated from the sinoatrial node (SA node). PACs are also commonly referred to as atrial premature complexes (APCs), premature supraventricular complexes, premature supraventricular beat, and premature atrial beat. This phenomenon can be caused by an assortment of medical diseases, structural abnormalities, pharmaceuticals, and non-regulated compounds.
Etiology
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Etiology
Triggers for PACs can be caused by a myriad of reasons and are commonly idiopathic. Idiopathic PACs, in the absence of structural cardiac disease, frequently originate from the pulmonary veins. Identifiable causes of premature atrial contractions can be stratified into structural, chemical, or as a sequela of other conditions.
Structural causes of PACs typically include coronary artery disease, hypertrophic cardiomyopathy, left atrial appendage aneurysms, left ventricular hypertrophy, valvular heart disease, septal defects, and congenital heart malformations.[1][2][3][4] At the biochemical level, sodium channel malformations and BMP2 mutations, a cause of pulmonary artery hypertension, may inadvertently predispose atrial arrhythmias.[5][6]
Chemical-based causes for PACs include beta-agonists, digoxin, chemotherapeutic agents, tricyclic antidepressants, sympathomimetics amines, and monoamine oxidase inhibitors.[7][8][9] Beta-blockers have also been associated with a higher incidence of PACs.[4]
A higher incidence of PACs is associated with many conditions and chronic states. Medical pathologies with associations for increased PACs include myocardial infarctions, congestive heart failure, hypertension, diabetes mellitus, a chronic obstructive pulmonary disorder, Coxsackie virus, and an overall higher CHA2DS2-VASC score.[4][10][11] Additional states such as anxiety, pregnancy, fatigue, and use of alcohol or tobacco have also predisposed for PACs.[12][13][14][15][16] Contrary to popular belief, caffeine has not been associated with an increased incidence of PACs.[17]
Epidemiology
PACs are prevalent amongst young and old patients, independent of many risk factors and previously known medical conditions.[18] Newborn infants, without associated risk factors, have been found to have variations typically considered pathologic.[19][20] Though still rare, elderly patients are more likely to present with abnormalities in their heart rhythm.[20] Nevertheless, an atypical rhythm is more likely to be found with continuous monitoring, such as a Holter monitor, than on a typical electrocardiogram strip.[21][22][23][24] This occurrence may be due in part to variations based on circadian rhythm.[25] As improvements in medical devices continue, amidst increased ubiquity of low-cost ambulatory and consumer options, the prevalence of arrhythmias may increase due to the detection of otherwise covert arrhythmias.[24][26][27][28][29]
Pathophysiology
The pathophysiology for premature atrial contractions has not been well established. This is due in part to the relatively benign nature of the condition and the unnecessary invasiveness of electrophysiologic studies on humans to find a cause. Common theoretic mechanisms for this condition are based around abnormal automaticity of the cardiac myocytes, increased eliciting events from chemical or physical instigators, and reentry of a retrograde impulse. For these causes, structural heart damage or chemical use may be found during the history and physical examination.
Genetic causes have also been studied, albeit in animals. Nevertheless, an LKB1 (cardiac-specific liver kinase B1) gene deletion has been associated with defects in ion channel formation of the atria. This has been shown to alter generation and conduction of action potentials, which predisposes the atria to remodeling, fibrosis, and ultimately atrial fibrillation.[30][31][32] Similar studies have also examined the formation of cytoskeletons, sarcomeres, desmosomes, and other ion channels for their role in automaticity.[33]
History and Physical
History findings can be occult and nonspecific for the identification of PACs. Many patients are asymptomatic, and PACs are often discovered incidentally during the workup for another disease or on routine examinations. In patients who do experience symptoms, most commonly, a skipping sensation or palpitations are noted. The patient may experience shortness of breath or anxiety, as well. If the PACs are consistent, however, patients may experience signs and symptoms of heart failure.[34]
Physical exam findings are also indiscriminate and lack sensitivity and specificity. The major contributor to this obscurity is the intermittent nature of PACs. When present, a clinician may palpate irregular pulses or visualize a canon a wave with jugular venous mapping. Auscultation may reveal early or additional heart sounds, as well as pauses in rhythm.
Evaluation
The use of an electrocardiogram is standard for identifying electrical variations within the heart. PACs typically have normal QRS complex and a normal, short, or longer PR interval than sinus rhythm. Sometimes, non conducted PACs occur in which there is no QRS complex following the PAC. PACs can be unifocal arising from one location (similar P waves in all PACs) or multifocal and arising from several locations (different P wave morphologies for PACs). The P wave of the PAC typically occurs earlier than the sinus P wave and has a different morphology and axis from the sinus P wave. It appears dissimilar from a standard sinus node generation, with variations in height, length, and shape of the P wave; furthermore, the P wave may be inverted or biphasic.
Depending on the location of the generating focus, the PR interval can be shorter (<120 milliseconds if originating from low right atrium near the AV node) or longer than usual. Examination of multiple leads may be required to differentiate subtle differences. A negative P wave in the inferior leads suggests a low atrial focus and a negative P wave in the lead I and aVL suggests a left atrial origin. PACs may also appear within the preceding T wave in accelerated heart rates. If the EKG does not reveal PACs on examination, a 24-hour Holter monitor may be useful for identifying intermittent complexes.[9][35]
Jugular venous pressure mappings may also play a role in the evaluation of PACs. Though the sensitivity of this test may be suboptimal, positive findings are useful for clinical correlation. Furthermore, being a simple physical exam finding to estimate central venous pressure, there is no added expensive or invasive method. Positive findings on this maneuver would be the visualization of the typical cannon 'a' wave, which is a sizeable venous pulse, causing a prominent bulge of the jugular veins. This occurs when the atrium contracts and blood is forced upon a close ventricle, cause a pressurized backflow into the central venous system. In the setting of PACs, if the premature contraction of the atrium occurs during systole when the tricuspid valve is closed, this sign may manifest. Electrophysiologic mapping studies are not indicated for the identification of PACs.
After the identification of PACs, echocardiography is useful in determining the functional status of the heart and identifying potential underlying structural abnormalities. Evaluation for structural heart disease should always be undertaken in patients with frequent PACs because of its prognostic important and treatment requirement. Laboratory testing can be done to identify electrolyte abnormalities.
Treatment / Management
Treatment of PACs depends on the symptomatology, triggers, and associated structural heart conditions. Typically, only patients with symptomatic PACs require treatment. After appropriate identification of triggers or underlying structural cardiac conditions, therapy starts by reassuring patients that PACs are typically benign and can be controlled by avoiding triggers. In patients with persistent symptoms despite avoidance of triggers, further therapy is indicated, starting with medications.
Pharmacologic management can be achieved using:
- Beta-adrenergic blockers at low doses are the relatively safe and first-line treatment in symptomatic patients if conservative measures fail. The role of calcium channel blockers to treat PACs is not well defined.
- Type IA, type IC, and type III antiarrhythmic agents can all suppress the PAC origin and are infrequently used only after careful consideration of their pro-arrhythmogenic nature.[36][37][38] (A1)
In patients with refractory symptoms despite medical therapy or those with cardiomyopathy and heart failure linked the frequent PACs, and in those patients in whom the PACs trigger atrial arrhythmias like atrial fibrillation, further interventional therapy is indicated. Some interventional options include atrial pacing, catheter ablation thoracoscopic ablation.[39] Of these, catheter ablation of the PAC origin is the most frequently used modality. Electrophysiologic mapping is used to identify the origin of PACs. If PACs are thought to be arising from the pulmonary veins, the pulmonary vein ostia are typically ablated to create pulmonary vein electrical isolation to prevent impulse entry into the left atrium.[40][41](A1)
Attempts should always be made to control with conservative non-pharmaceutical measures first. Primary healthcare providers may provide initial reassurance and medical treatment; however, refractory cases or use of antiarrhythmic medications should be referred to cardiologists. Percutaneous and surgical interventions are delegated to the appropriate specialists.[42][39][42](A1)
Differential Diagnosis
The differential diagnosis for PACs is broad due to its non-descript symptoms, physical exam, and imaging findings. Cardiac differentials can be categorized into arrhythmic and non-arrhythmic etiologies. Arrhythmic causes can include premature junctional contractions, premature ventricular contractions, and narrow or wide complex tachycardias. Accordingly, an EKG can be vital in the delineation of these causes. Non-arrhythmic cardiac etiologies include acute coronary syndrome, valvular disorders with a preponderance for mitral valve prolapse, pericarditis, heart failure, and pacemaker complications.
Non-cardiac causes may also mimic premature atrial contractions. A clinician should keep in mind psychiatric differentials such as panic attacks and anxiety. Alcohol, use of illicit drugs, and adverse effects of prescribed medications may cause or mimic PACs. Finally, other considerations should be given to pulmonary embolism, hyperthyroidism, and anemia.
Prognosis
Prognosis is dependent on the underlying cause of the PACs and the presence of structural cardiac disease. Many idiopathic PACs are relatively benign in the short term, although they can be associated with an increased risk of cardiac and all-cause mortality if they occur frequently.[43][44] Similarly, frequent PACs have also been shown to be associated with a greater risk of developing atrial fibrillation and atrial flutter.[45] Generally, underlying conditions play a more significant role in estimating prognosis.
Complications
The risk of complications from PACs should be explained in conjunction with underlying etiologies, should they exist. Complications from PACs, independent of other conditions, include:
- Atrial fibrillation[46][47][48][49]
- Ischemic stroke[50][51]
- Increased cardiac-related and all-cause mortality[43][44]
Isolated PACs (without premature ventricular complexes) are not associated with an increased risk of sudden cardiac death.[52]
Consultations
Many times, PACs have no adverse effect on a patient’s lifestyle or outcome and may be monitored by the primary care provider. Consultations for PACs should be made based on clinical suspicion for underlying morbid etiologies or when symptoms are obstructive and overwhelming. Referral to cardiology services can assist in diagnosing underlying structural or electrical conduction abnormalities and for initiation of anti-arrhythmic therapies when appropriate.
Deterrence and Patient Education
Education is essential in providing the most up to date guidance focused on evidence-based medicine. In particular, health care providers and patients should be educated on the benign nature of isolated PACs when not associated with underlying etiologies. Education regarding possible triggers should be provided and avoidance techniques can be taught. The psychological morbidity associate with PACs should be appropriate address and patients reassured.
Enhancing Healthcare Team Outcomes
Healthcare practitioners should be cautious in the diagnosis and treatment of PACs. Furthermore, incidental findings should not automatically warrant extended and invasive procedures when the patient is otherwise asymptomatic. When encountered, the provider should discuss treatment options with specific emphasis on the risks versus benefits. Consultations should be considered when appropriate situations are encountered. An interprofessional approach is essential in the evaluation of prognosis and management options.
Media
(Click Image to Enlarge)
A drawn image of premature atrial contraction (PAC) on II-lead ECG.
Contributed by Wikimedia Commons, Chikumaya (Public Domain-Self)
References
Lazzeroni E, Domenicucci S, Finardi A, Zoni A, Dodi C, Francescon P, Botti G. Severity of arrhythmias and extent of hypertrophy in hypertrophic cardiomyopathy. American heart journal. 1989 Oct:118(4):734-8 [PubMed PMID: 2529748]
Ramsdale DR, Arumugam N, Singh SS, Pearson J, Charles RG. Holter monitoring in patients with mitral stenosis and sinus rhythm. European heart journal. 1987 Feb:8(2):164-70 [PubMed PMID: 2436916]
Ergül Y, Öztürk E, Özgür S. Successful radiofrequency ablation of accessory pathway associated with left atrial appendage aneurysm in a low birthweight premature patient. The Turkish journal of pediatrics. 2019:61(1):142-146. doi: 10.24953/turkjped.2019.01.025. Epub [PubMed PMID: 31559738]
Durmaz E,Ikitimur B,Kilickiran Avci B,Atıcı A,Yurtseven E,Tokdil H,Ebren C,Polat F,Karaca O,Karadag B,Ongen Z, The clinical significance of premature atrial contractions: How frequent should they become predictive of new-onset atrial fibrillation. Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc. 2019 Oct 11; [PubMed PMID: 31603280]
Pascall E, Tulloh RM. Pulmonary hypertension in congenital heart disease. Future cardiology. 2018 Jul:14(4):343-353. doi: 10.2217/fca-2017-0065. Epub 2018 May 24 [PubMed PMID: 29792339]
Savio-Galimberti E, Argenziano M, Antzelevitch C. Cardiac Arrhythmias Related to Sodium Channel Dysfunction. Handbook of experimental pharmacology. 2018:246():331-354. doi: 10.1007/164_2017_43. Epub [PubMed PMID: 28965168]
Czaja AS, Ross ME, Liu W, Fiks AG, Localio R, Wasserman RC, Grundmeier RW, Adams WG, Comparative Effectiveness Research through Collaborative Electronic Reporting (CER2) Consortium. Electronic health record (EHR) based postmarketing surveillance of adverse events associated with pediatric off-label medication use: A case study of short-acting beta-2 agonists and arrhythmias. Pharmacoepidemiology and drug safety. 2018 Jul:27(7):815-822. doi: 10.1002/pds.4562. Epub 2018 May 27 [PubMed PMID: 29806185]
Level 3 (low-level) evidenceKamineni P, Prakasa K, Hasan SP, Akula R, Dawkins F. Cardiotoxicities of paclitaxel in African Americans. Journal of the National Medical Association. 2003 Oct:95(10):977-81 [PubMed PMID: 14620711]
Rae AP. Interpreting an ECG. Atrial premature complex. Geriatrics. 1984 Dec:39(12):43-5, 48, 50 [PubMed PMID: 6209190]
Holtzman D, Aronow WS, Mellana WM, Sharma M, Mehta N, Lim J, Chandy D. Electrocardiographic abnormalities in patients with severe versus mild or moderate chronic obstructive pulmonary disease followed in an academic outpatient pulmonary clinic. Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc. 2011 Jan:16(1):30-2. doi: 10.1111/j.1542-474X.2010.00404.x. Epub [PubMed PMID: 21251131]
Terasaki F, Kitaura Y, Hayashi T, Nakayama Y, Deguchi H, Kawamura K. Arrhythmias in Coxsackie B3 virus myocarditis. Continuous electrocardiography in conscious mice and histopathology of the heart with special reference to the conduction system. Heart and vessels. Supplement. 1990:5():45-50 [PubMed PMID: 1965542]
Level 3 (low-level) evidenceWang Z, Qin H, Chen G, Dai Y, Cai Y, Cheng X, Qian Y, Chu M, Lu X. Anxiety is associated with increased risk for atrial cardiopathy. Acta neurologica Belgica. 2020 Dec:120(6):1383-1388. doi: 10.1007/s13760-020-01335-0. Epub 2020 Mar 19 [PubMed PMID: 32193730]
Level 2 (mid-level) evidenceShotan A, Ostrzega E, Mehra A, Johnson JV, Elkayam U. Incidence of arrhythmias in normal pregnancy and relation to palpitations, dizziness, and syncope. The American journal of cardiology. 1997 Apr 15:79(8):1061-4 [PubMed PMID: 9114764]
Stamler JS, Goldman ME, Gomes J, Matza D, Horowitz SF. The effect of stress and fatigue on cardiac rhythm in medical interns. Journal of electrocardiology. 1992 Oct:25(4):333-8 [PubMed PMID: 1402519]
Day E, Rudd JHF. Alcohol use disorders and the heart. Addiction (Abingdon, England). 2019 Sep:114(9):1670-1678. doi: 10.1111/add.14703. Epub 2019 Jul 15 [PubMed PMID: 31309639]
Kamel H, Pearce LA, Ntaios G, Gladstone DJ, Perera K, Roine RO, Meseguer E, Shoamanesh A, Berkowitz SD, Mundl H, Sharma M, Connolly SJ, Hart RG, Healey JS. Atrial Cardiopathy and Nonstenosing Large Artery Plaque in Patients With Embolic Stroke of Undetermined Source. Stroke. 2020 Mar:51(3):938-943. doi: 10.1161/STROKEAHA.119.028154. Epub 2020 Jan 2 [PubMed PMID: 31893985]
Dixit S, Stein PK, Dewland TA, Dukes JW, Vittinghoff E, Heckbert SR, Marcus GM. Consumption of Caffeinated Products and Cardiac Ectopy. Journal of the American Heart Association. 2016 Jan 26:5(1):. doi: 10.1161/JAHA.115.002503. Epub 2016 Jan 26 [PubMed PMID: 26813889]
Conen D, Adam M, Roche F, Barthelemy JC, Felber Dietrich D, Imboden M, Künzli N, von Eckardstein A, Regenass S, Hornemann T, Rochat T, Gaspoz JM, Probst-Hensch N, Carballo D. Premature atrial contractions in the general population: frequency and risk factors. Circulation. 2012 Nov 6:126(19):2302-8. doi: 10.1161/CIRCULATIONAHA.112.112300. Epub 2012 Oct 9 [PubMed PMID: 23048073]
Level 2 (mid-level) evidenceSouthall DP, Richards J, Mitchell P, Brown DJ, Johnston PG, Shinebourne EA. Study of cardiac rhythm in healthy newborn infants. British heart journal. 1980 Jan:43(1):14-20 [PubMed PMID: 7356857]
Martin GR, Ruckman RN. Fetal echocardiography: a large clinical experience and follow-up. Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography. 1990 Jan-Feb:3(1):4-8 [PubMed PMID: 2310591]
Folarin VA, Fitzsimmons PJ, Kruyer WB. Holter monitor findings in asymptomatic male military aviators without structural heart disease. Aviation, space, and environmental medicine. 2001 Sep:72(9):836-8 [PubMed PMID: 11565820]
Level 2 (mid-level) evidenceSliwa K, Azibani F, Johnson MR, Viljoen C, Baard J, Osman A, Briton O, Ntsekhe M, Chin A. Effectiveness of Implanted Cardiac Rhythm Recorders With Electrocardiographic Monitoring for Detecting Arrhythmias in Pregnant Women With Symptomatic Arrhythmia and/or Structural Heart Disease: A Randomized Clinical Trial. JAMA cardiology. 2020 Apr 1:5(4):458-463. doi: 10.1001/jamacardio.2019.5963. Epub [PubMed PMID: 32074256]
Level 1 (high-level) evidenceTodo K, Iwata T, Doijiri R, Yamagami H, Morimoto M, Hashimoto T, Sonoda K, Yamazaki H, Koge J, Okazaki S, Sasaki T, Mochizuki H. Frequent Premature Atrial Contractions in Cryptogenic Stroke Predict Atrial Fibrillation Detection with Insertable Cardiac Monitoring. Cerebrovascular diseases (Basel, Switzerland). 2020:49(2):144-150. doi: 10.1159/000505958. Epub 2020 Feb 5 [PubMed PMID: 32023609]
Karunadas CP, Mathew C. Comparison of arrhythmia detection by conventional Holter and a novel ambulatory ECG system using patch and Android App, over 24 h period. Indian pacing and electrophysiology journal. 2020 Mar-Apr:20(2):49-53. doi: 10.1016/j.ipej.2019.12.013. Epub 2019 Dec 19 [PubMed PMID: 31866554]
Larsen BS, Kumarathurai P, Nielsen OW, Sajadieh A. The circadian variation of premature atrial contractions. Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology. 2016 Oct:18(10):1573-1580 [PubMed PMID: 26705556]
Lown M,Brown M,Brown C,Yue AM,Shah BN,Corbett SJ,Lewith G,Stuart B,Moore M,Little P, Machine learning detection of Atrial Fibrillation using wearable technology. PloS one. 2020; [PubMed PMID: 31978173]
Al-Alusi MA, Ding E, McManus DD, Lubitz SA. Wearing Your Heart on Your Sleeve: the Future of Cardiac Rhythm Monitoring. Current cardiology reports. 2019 Nov 25:21(12):158. doi: 10.1007/s11886-019-1223-8. Epub 2019 Nov 25 [PubMed PMID: 31768764]
Engdahl J, Svennberg E. [The core of the Apple Heart Study]. Lakartidningen. 2020 Feb 17:117():. pii: FYY6. Epub 2020 Feb 17 [PubMed PMID: 32068877]
Cho DJ. Editoral commentary: Beyond the early adopter: The smartwatch ECG goes mainstream. Trends in cardiovascular medicine. 2020 Oct:30(7):449-450. doi: 10.1016/j.tcm.2019.11.003. Epub 2019 Nov 20 [PubMed PMID: 31810859]
Kim GE, Ross JL, Xie C, Su KN, Zaha VG, Wu X, Palmeri M, Ashraf M, Akar JG, Russell KS, Akar FG, Young LH. LKB1 deletion causes early changes in atrial channel expression and electrophysiology prior to atrial fibrillation. Cardiovascular research. 2015 Oct 1:108(1):197-208. doi: 10.1093/cvr/cvv212. Epub [PubMed PMID: 26378152]
Ikeda Y, Sato K, Pimentel DR, Sam F, Shaw RJ, Dyck JR, Walsh K. Cardiac-specific deletion of LKB1 leads to hypertrophy and dysfunction. The Journal of biological chemistry. 2009 Dec 18:284(51):35839-49. doi: 10.1074/jbc.M109.057273. Epub [PubMed PMID: 19828446]
Level 3 (low-level) evidenceOzcan C, Battaglia E, Young R, Suzuki G. LKB1 knockout mouse develops spontaneous atrial fibrillation and provides mechanistic insights into human disease process. Journal of the American Heart Association. 2015 Mar 15:4(3):e001733. doi: 10.1161/JAHA.114.001733. Epub 2015 Mar 15 [PubMed PMID: 25773299]
Level 3 (low-level) evidenceChoy L, Yeo JM, Tse V, Chan SP, Tse G. Cardiac disease and arrhythmogenesis: Mechanistic insights from mouse models. International journal of cardiology. Heart & vasculature. 2016 Sep:12():1-10 [PubMed PMID: 27766308]
Vervueren PL,Delmas C,Berry M,Rollin A,Sadron M,Duparc A,Mondoly P,Honton B,Lairez O,Maury P, Reversal of Dilated Cardiomyopathy After Successful Radio-Frequency Ablation of Frequent Atrial Premature Beats, a New Cause for Arrhythmia-Induced Cardiomyopathy. Journal of atrial fibrillation. 2012 Dec; [PubMed PMID: 28496791]
Bagliani G, Della Rocca DG, De Ponti R, Capucci A, Padeletti M, Natale A. Ectopic Beats: Insights from Timing and Morphology. Cardiac electrophysiology clinics. 2018 Jun:10(2):257-275. doi: 10.1016/j.ccep.2018.02.013. Epub [PubMed PMID: 29784483]
Arif M, Laidlaw JC, Oshrain C, Willis PW 3rd, Nissen CH, McDermott DJ, Smith WS, Karim A, Wilson RR. A randomized, double-blind, parallel group comparison of disopyramide phosphate and quinidine in patients with cardiac arrhythmias. Angiology. 1983 Jun:34(6):393-400 [PubMed PMID: 6408949]
Level 1 (high-level) evidenceKimura E, Mashima S, Tanaka T. Clinical evaluation of antiarrhythmic effects of disopyramide by multiclinical controlled double-blind methods. International journal of clinical pharmacology, therapy, and toxicology. 1980:18(8):338-43 [PubMed PMID: 7409935]
Level 1 (high-level) evidenceMahtani AU, Nair DG. Supraventricular Tachycardia. The Medical clinics of North America. 2019 Sep:103(5):863-879. doi: 10.1016/j.mcna.2019.05.007. Epub [PubMed PMID: 31378331]
Sindby JE, Vadmann H, Lundbye-Christensen S, Riahi S, Hjortshøj S, Boersma LVA, Andreasen JJ. Percutaneous versus thoracoscopic ablation of symptomatic paroxysmal atrial fibrillation: a randomised controlled trial - the FAST II study. Journal of cardiothoracic surgery. 2018 Oct 3:13(1):101. doi: 10.1186/s13019-018-0792-8. Epub 2018 Oct 3 [PubMed PMID: 30285795]
Level 1 (high-level) evidenceWang X, Li Z, Mao J, He B. Electrophysiological features and catheter ablation of symptomatic frequent premature atrial contractions. Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology. 2017 Sep 1:19(9):1535-1541. doi: 10.1093/europace/euw152. Epub [PubMed PMID: 27702869]
Huang X, Chen Y, Xiao J, Zhao H, Chen Y, Liu S, He L, Huang Z, Zhou H, Xu D, Peng J. Electrophysiological characteristics and catheter ablation of symptomatic focal premature atrial contractions originating from pulmonary veins and non-pulmonary veins. Clinical cardiology. 2018 Jan:41(1):74-80. doi: 10.1002/clc.22853. Epub 2018 Jan 25 [PubMed PMID: 29369366]
Kliś M, Sławuta A, Gajek J. Antiarrhythmic properties of atrial pacing. Advances in clinical and experimental medicine : official organ Wroclaw Medical University. 2017 Mar-Apr:26(2):351-357. doi: 10.17219/acem/61429. Epub [PubMed PMID: 28791857]
Level 3 (low-level) evidenceQureshi W, Shah AJ, Salahuddin T, Soliman EZ. Long-term mortality risk in individuals with atrial or ventricular premature complexes (results from the Third National Health and Nutrition Examination Survey). The American journal of cardiology. 2014 Jul 1:114(1):59-64. doi: 10.1016/j.amjcard.2014.04.005. Epub 2014 Apr 16 [PubMed PMID: 24819898]
Level 3 (low-level) evidenceLin CY, Lin YJ, Chen YY, Chang SL, Lo LW, Chao TF, Chung FP, Hu YF, Chong E, Cheng HM, Tuan TC, Liao JN, Chiou CW, Huang JL, Chen SA. Prognostic Significance of Premature Atrial Complexes Burden in Prediction of Long-Term Outcome. Journal of the American Heart Association. 2015 Aug 27:4(9):e002192. doi: 10.1161/JAHA.115.002192. Epub 2015 Aug 27 [PubMed PMID: 26316525]
Prasitlumkum N, Rattanawong P, Limpruttidham N, Kanitsoraphan C, Sirinvaravong N, Suppakitjanusant P, Chongsathidkiet P, Chung EH. Frequent premature atrial complexes as a predictor of atrial fibrillation: Systematic review and meta-analysis. Journal of electrocardiology. 2018 Sep-Oct:51(5):760-767. doi: 10.1016/j.jelectrocard.2018.05.012. Epub 2018 May 23 [PubMed PMID: 30177309]
Level 1 (high-level) evidenceAlhede C, Lauridsen TK, Johannessen A, Dixen U, Jensen JS, Raatikainen P, Hindricks G, Walfridsson H, Kongstad O, Pehrson S, Englund A, Hartikainen J, Hansen PS, Nielsen JC, Jons C. The impact of supraventricular ectopic complexes in different age groups and risk of recurrent atrial fibrillation after antiarrhythmic medication or catheter ablation. International journal of cardiology. 2018 Jan 1:250():122-127. doi: 10.1016/j.ijcard.2017.09.208. Epub 2017 Oct 9 [PubMed PMID: 29050922]
Acharya T, Tringali S, Bhullar M, Nalbandyan M, Ilineni VK, Carbajal E, Deedwania P. Frequent Atrial Premature Complexes and Their Association With Risk of Atrial Fibrillation. The American journal of cardiology. 2015 Dec 15:116(12):1852-7. doi: 10.1016/j.amjcard.2015.09.025. Epub 2015 Oct 3 [PubMed PMID: 26611122]
Chong BH, Pong V, Lam KF, Liu S, Zuo ML, Lau YF, Lau CP, Tse HF, Siu CW. Frequent premature atrial complexes predict new occurrence of atrial fibrillation and adverse cardiovascular events. Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology. 2012 Jul:14(7):942-7. doi: 10.1093/europace/eur389. Epub 2011 Dec 19 [PubMed PMID: 22183750]
Dewland TA, Vittinghoff E, Mandyam MC, Heckbert SR, Siscovick DS, Stein PK, Psaty BM, Sotoodehnia N, Gottdiener JS, Marcus GM. Atrial ectopy as a predictor of incident atrial fibrillation: a cohort study. Annals of internal medicine. 2013 Dec 3:159(11):721-8. doi: 10.7326/0003-4819-159-11-201312030-00004. Epub [PubMed PMID: 24297188]
Huang BT, Huang FY, Peng Y, Liao YB, Chen F, Xia TL, Pu XB, Chen M. Relation of premature atrial complexes with stroke and death: Systematic review and meta-analysis. Clinical cardiology. 2017 Nov:40(11):962-969. doi: 10.1002/clc.22780. Epub 2017 Aug 28 [PubMed PMID: 28846809]
Level 1 (high-level) evidenceGladstone DJ, Dorian P, Spring M, Panzov V, Mamdani M, Healey JS, Thorpe KE, EMBRACE Steering Committee and Investigators. Atrial premature beats predict atrial fibrillation in cryptogenic stroke: results from the EMBRACE trial. Stroke. 2015 Apr:46(4):936-41. doi: 10.1161/STROKEAHA.115.008714. Epub 2015 Feb 19 [PubMed PMID: 25700289]
Level 1 (high-level) evidenceCheriyath P, He F, Peters I, Li X, Alagona P Jr, Wu C, Pu M, Cascio WE, Liao D. Relation of atrial and/or ventricular premature complexes on a two-minute rhythm strip to the risk of sudden cardiac death (the Atherosclerosis Risk in Communities [ARIC] study). The American journal of cardiology. 2011 Jan 15:107(2):151-5. doi: 10.1016/j.amjcard.2010.09.002. Epub [PubMed PMID: 21211594]