Quick View
Credits:Ermengol Valles
1,Francis E. Marchlinski
11University of Pennsylvania, Philadelphia, PA
Funding: None;
Disclosure : There areno relevant conflicts of interests for any of the authors involving the currentstudy topic;
Corresponding Author : Ermengol Valles MD,University of Pennsylvania, Philadelphia, PA. Email: Ermengol.Valles@uphs.upenn.edu
Submitted : 2008-03-12;Accepted : 2008-05-05
Copyright: Copyrightbelongs to Valles et.al., under Open Access License details available online at http://creativecommons.org
doi : 10.4022/jafib.v1i1.411
Atrial fibrillation (AF) is a supraventricular tachyarrhythmiacharacterized by uncoordinated atrial activation. On the ECG fibrillatory (f)waves (rapid oscillations with variable amplitude, shape and timing) replacenormal P waves. Ventricular response becomes irregular and rapid depending ofthe intrinsic electrophysiological properties of the AV node1and the balance between vagal and sympathetic tone1.
The presence of an irregularly pulse is a clinical signthat can be quickly and reliably identified in any healthcare situation and,indicates AF with a high sensitivity and specificity (95% and 75%,respectively). If the irregularity last for more than 20 seconds thespecificity reaches 98%2-4.Identification of AF can be done by using manual pulse palpation in thosepresenting with a variety of symptoms. It is desirable to check the bloodpressure and pulse in all patients who present with breathlessness, dyspnea,palpitations, syncope, dizziness or chest discomfort. Furthermore, manypatients presenting with an acute stroke are found to be in AF albeitasymptomatic with respect to non-neurologic complaints.
The finding of a sustained irregular wide QRS complextachycardia may be suspicious of AF conducted with bundle brunch aberrancy orover an accessory pathway, and in patients with A-V sequential pacemakers canreflect an inadequate configuration with ventricular tracking of sensed atrialactivity.
Although the pattern of AF can change over time, at themoment of diagnosis it may be helpful to characterize the arrhythmia. These arethe different patterns:
First-detected episode of AF. It can be self-limited or notand the symptoms can range from an ECG finding in absence of symptoms (up to30%5) to the development of heart failure orsyncope. In asymptomatic patients the uncertainty remains about the duration ofthe episode and the possibility of previous undetected episodes. Thepossibility of recurrent AF without significant symptoms must be taken intoaccount and ruled out.
Recurrent AF. After 2 or more episodes, AF is considered recurrent.When the arrhythmia terminates spontaneously, recurrent AF is designated paroxysmal; when sustained beyond 7 days, itis termed persistent. This last type includes those cases of long-standing AF, usuallyleading to permanent AF, in which cardioversion has failed to terminate AF.
It has been suggested that in most patients paroxysmal AFrepresents an earlier stage of the disease and that its natural history in theabsence of intervention is to progress to persistent/permanent types of AF.
Holter monitoring has shown that the majority of episodesof paroxysmal AF are triggered by atrial premature beats6,7 while a small number of episodes are preceded by typicalatrial flutter or another supraventricular tachycardia7.Ectopic foci are most often located near the PVs6,which is the most common origin of the AF triggers.
Atrial fibrillation in patients with cardiovasculardisease
AF isfrequently, but not uniformily, associated with underlying cardiovasculardisease or echocardiographic characteristic features. The most importantfactors that may contribute to AF in the setting of cardiovascular diseases areincluded in table 1.
 | Table 1 : Risk factors for AF in atients with cardiovascular disease |
Atrial Fibrillation in patients without cardiovasculardisease
Up to 25-30% of cases of AF occur in young patientswithout demonstrable underlying disease1. This isthe reason why this pattern of AF is usually called lone AF. Patients with lone AF oftenassociate certain triggers with episodes of AF22,and in up to 39% of them a family history of AF is present, suggesting thatinheritance may be of great importance in lone AF. Table 2 shows the mostimportant causes of AF in patients without known cardiovascular risk factors orstructural heart disease.
 | Table 2 : Risk factors for AF in patients without cardiovascular disease. |
AF can be related to temporary causes, including some ofthe conditions appearing in both tables above. In such cases, successfultreatment of underlying condition often eliminates AF. Some examples aredescribed below:
Several lines of evidence support a possible causalrelationship between OSA and AF. Observational studies have noted asignificantly larger proportion of patients with OSA between patients in AFundergoing cardioversion compared with controls without AF referred for generalcardiology evaluation (49% vs 32%)17. Thisobservation has been prospectively confirmed in patients undergoing coronaryartery bypass surgery, in whom preoperative sleep studies and postoperative AFincidence were assessed (39 % in OSA patients vs 18% in non-OSA patients)18.
The risk of cardiac arrhythmias with OSA appears to berelated to severity of the disease, such that the great majority of OSApatients presenting with significant arrhythmias have moderate or severe formsof the disease20. In a heart susceptible toatrial fibrillation, the presence of OSA would predispose to the subsequentdevelopment of atrial fibrillation. Furthermore, the frequent presence ofatrial fibrillation in OSA may contribute to the increased risk for stroke andheart failure in this patient population21. Ithas been speculated that factors directly related to OSA, such as repetitivehypoxemia, autonomic nervous system imbalance, systemic inflammation,fluctuations in intrathoracic hemodynamic, and diastolic dysfunction may serveas a trigger for atrial fibrillation and may favor the perpetuation of theatrial arrhythmia by altering the atrial substrate. Finally patients receivingtreatment with continuous positive pressure ventilation have a lower incidenceof AF recurrence at 12 months (42 vs 82%)19.
Patients with hyperthyroidism have an increased risk ofdeveloping AF28, and this risk is gender and age related.Thus AF due to hyperthyroidism is more likely to occur in men than in women(12,1 vs 7,6%) and in patients over age 60 (up to 10 to 20% of patients overage 60), while patients under age 40 have little or no increase in fold risk29. Even patients with subclinical hyperthyroidism(normal serum thyroid hormone –T4- concentrations and low serum thyroidstimulating hormone –TSH-) represent a population with increased risk ofAF, similar to patients with clinical hyperthyroidism30.
Increased beta-adrenergic tone may be in part responsiblefor the development of AF in these patients, and certainly contribute to arapid ventricular response. In addition, excess thyroid hormone increases thelikelihood of AF in experimental animals31. Ithas been hypothesized that ectopic beats initiating AF may be increased byenhanced automaticity or triggered activity32.
 | Figure 1 : Twelve-lead ECG showing an atrial fibrillation with rapid ventricular response in relation to an hyperthyroid state. |
Treatment consists of a beta-blocker to control theventricular rate, and correction of the hyperthyroid state. Spontaneousreversion to sinus rhythm occur within six weeks in patients under age 60 whoare rendered euthyroid28. Older patients show adecline in the frequency of spontaneous reversion. Cardioversion, eitherelectric or pharmacologic, is not indicated while the patient is thyrotoxic,since AF usually recurs28.
A detailed history and clinical examination will providehelpful information. Other tests, including thyroid function and complete bloodcount, are routine38. A serum TSH should bemeasured as part of the initial evaluation in all patient with AF, whetherthere are symptoms suggestive of thyrotoxicosis or not. A transthoracicechocardiogram may provide useful information, identifying the presence ofstructural heart disease and an increase risk of thromboembolism39(e.g. significant left ventricular dysfunction, severe valvular disease orsevere myocardial hypertrophy). Such information may influence subsequenttherapeutic management including the need for anticoagulation treatment. Insome of the patients transoesophageal echocardiography may be needed in orderto rule out the presence of left atrial appendage thrombus, especially in thosepatients considering cardioversion without an adequate period of oral anticoagulation.
Noninvasive ECG monitoring is used to detect AF40 and to identify its characteristic pattern duringthe initial diagnosis. Such monitor may be important to assess the control ofthe rhythm and rate during the follow up in patients under pharmacologicaltreatment or after an ablation procedure. Extended ECG monitoring will alsohelp document asymptomatic AF episodes and will held quantify the burden of AF.When symptoms are frequent a 24-h or 48-h Holter monitor may yield a diagnosisbut with less frequent episodes, a 7-days Holter or an event recorder, which iseither patient-triggered or auto-triggered, may be needed to document thearrhythmia. Implantable loop recorders and pacemakers can record continuousdata over prolonged periods. All monitoring modalities have limitations.Non-invasive ECG monitoring may provide useful information in only 10-40% ofcases, even with prolonged recordings41-43.
The current American College of Cardiology/American HeartAssociation (ACC/AHA) guidelines for the use of Ambulatory ECG Monitoringestablish the following indications for Holter monitoring in the setting of AF:
| Class I | To assess antiarrhythmic drug response in inpiduals in whom baseline frequency of arrhythmia has been well characterized as reproducible and of sufficient frequency to permit analysis. |
| Class IIA | To detect proarrhythmic response to antiarrhythmic therapy in high-risk patients. |
| Class IIB | To assess rate control during atrial fibrillation. To document recurrent symptomatic or asymptomatic non-sustained arrhythmias during therapy in the outpatient setting. |
Therefore in patients with suspected paroxysmal atrialfibrillation undetected by standard ECG, a 24–h ambulatory ECG monitorshould be used in those with suspected AF episodes less than 24 hours apart. Inpatients with symptomatic episodes more than 24 h apart an event-recorder ECGshould be used.
Monitoring can also help with embolism prevention. It isimportant to note that a 24 to 48-hour Holter monitoring identifies AF in 1 to5% of patients with previous stroke and undetected asymptomatic AF by initialbasal ECG assessment44. Increased duration ofmonitoring appears to be associated with increased rates of detection of AF.Certainly patients with risk factors for stroke with AF should undergo moreextensive monitoring to exclude the presence of asymptomatic AF. We routinelyencourage patient participation in monitoring with with frequent pulse takingto supplement ECG recording efforts.
1. Fuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC 2006 Guidelinesfor the Management of Patients with Atrial Fibrillation: a report of theAmerican College of Cardiology/American Heart Association Task Force onPractice Guidelines and the European Society of Cardiology Committee forPractice Guidelines (Writing Committee to Revise the 2001 Guidelines for theManagement of Patients With Atrial Fibrillation): developed in collaborationwith the European Heart Rhythm Association and the Heart Rhythm Society. Circulation.Aug 152006;114(7):e257-354.
2. Lip GY, Tean KN, Dunn FG. Treatment of atrial fibrillation in adistrict general hospital. Br Heart J. Jan 1994;71(1):92-95.
3. LokNS, Lau CP. Presentation and management of patients admitted with atrialfibrillation: a review of 291 cases in a regional hospital. Int J Cardiol. Mar 3 1995;48(3):271-278.
4. Zarifis J, Beevers G, Lip GY. Acute admissions with atrialfibrillation in a British multiracial hospital population. Br J Clin Pract. Mar 1997;51(2):91-96.
5. Dagres N, Nieuwlaat R, Vardas PE, et al. Gender-related differencesin presentation, treatment, and outcome of patients with atrial fibrillation inEurope: a report from the Euro Heart Survey on Atrial Fibrillation. J AmColl Cardiol. Feb6 2007;49(5):572-577.
6. Haissaguerre M, Jais P, Shah DC, et al. Spontaneous initiation ofatrial fibrillation by ectopic beats originating in the pulmonary veins. NEngl J Med. Sep 31998;339(10):659-666.
7. Kolb C, Nurnberger S, Ndrepepa G, et al. Modes of initiation ofparoxysmal atrial fibrillation from analysis of spontaneously occurringepisodes using a 12-lead Holter monitoring system. Am J Cardiol. Oct 15 2001;88(8):853-857.
8. Frost L, Hune LJ, Vestergaard P. Overweight and obesity as riskfactors for atrial fibrillation or flutter: the Danish Diet, Cancer, and HealthStudy. Am J Med. May2005;118(5):489-495.
9. Diker E, Aydogdu S, Ozdemir M, et al. Prevalence and predictors ofatrial fibrillation in rheumatic valvular heart disease. Am J Cardiol. Jan 1 1996;77(1):96-98.
10. Krahn AD, Manfreda J, Tate RB, et al. The natural history ofatrial fibrillation: incidence, risk factors, and prognosis in the ManitobaFollow-Up Study. Am J Med. May 1995;98(5):476-484.
11. Stevenson WG, Stevenson LW, Middlekauff HR, et al. Improvingsurvival for patients with atrial fibrillation and advanced heart failure. JAm Coll Cardiol. Nov15 1996;28(6):1458-1463.
12. Eldar M, Canetti M, Rotstein Z, et al. Significance of paroxysmalatrial fibrillation complicating acute myocardial infarction in thethrombolytic era. SPRINT and Thrombolytic Survey Groups. Circulation. Mar 17 1998;97(10):965-970.
13. Robinson K, Frenneaux MP, Stockins B, et al. Atrial fibrillationin hypertrophic cardiomyopathy: a longitudinal study. J Am Coll Cardiol. May 1990;15(6):1279-1285.
14. Berger F, Vogel M, Kramer A, et al. Incidence of atrialflutter/fibrillation in adults with atrial septal defect before and aftersurgery. Ann Thorac Surg. Jul 1999;68(1):75-78.
15. Levine HD. Myocardial fibrosis in constrictive pericarditis.Electrocardiographic and pathologic observations. Circulation. Dec 1973;48(6):1268-1281.
16. Grigioni F, Avierinos JF, Ling LH, et al. Atrial fibrillationcomplicating the course of degenerative mitral regurgitation: determinants andlong-term outcome. J Am Coll Cardiol. Jul 3 2002;40(1):84-92.
17. Gami AS, Pressman G, Caples SM, et al. Association of atrialfibrillation and obstructive sleep apnea. Circulation. Jul 27 2004;110(4):364-367.
18. Mooe T, Gullsby S, Rabben T, et al. Sleep-disordered breathing: anovel predictor of atrial fibrillation after coronary artery bypass surgery. CoronArtery Dis. Jun1996;7(6):475-478.
19. Kanagala R, Murali NS, Friedman PA, et al. Obstructive sleep apneaand the recurrence of atrial fibrillation. Circulation. May 27 2003;107(20):2589-2594.
20. Guilleminault C, Connolly SJ, Winkle RA. Cardiac arrhythmia andconduction disturbances during sleep in 400 patients with sleep apnea syndrome.Am J Cardiol. Sep1 1983;52(5):490-494.
21. Yaggi HK, Concato J, Kernan WN, et al. Obstructive sleep apnea asa risk factor for stroke and death. N Engl J Med. Nov 10 2005;353(19):2034-2041.
22. Patton KK, Zacks ES, Chang JY, et al. Clinical subtypes of loneatrial fibrillation. Pacing Clin Electrophysiol. Jul 2005;28(7):630-638.
23. Herweg B, Dalal P, Nagy B, et al. Power spectral analysis of heartperiod variability of preceding sinus rhythm before initiation of paroxysmalatrial fibrillation. Am J Cardiol. Oct 1 1998;82(7):869-874.
24. Fioranelli M, Piccoli M, Mileto GM, et al. Analysis of heart ratevariability five minutes before the onset of paroxysmal atrial fibrillation. PacingClin Electrophysiol. May1999;22(5):743-749.
25. Ettinger PO, Wu CF, De La Cruz C, Jr., et al. Arrhythmias and the"Holiday Heart": alcohol-associated cardiac rhythm disorders. AmHeart J. May1978;95(5):555-562.
26. Maisel WH, Rawn JD, Stevenson WG. Atrial fibrillation aftercardiac surgery. Ann Intern Med. Dec 18 2001;135(12):1061-1073.
27. Chung MK, Martin DO, Sprecher D, et al. C-reactive proteinelevation in patients with atrial arrhythmias: inflammatory mechanisms andpersistence of atrial fibrillation. Circulation. Dec 11 2001;104(24):2886-2891.
28. Woeber KA. Thyrotoxicosis and the heart. N Engl J Med. Jul 9 1992;327(2):94-98.
29. Frost L, Vestergaard P, Mosekilde L. Hyperthyroidism and risk ofatrial fibrillation or flutter: a population-based study. Arch Intern Med. Aug 9-23 2004;164(15):1675-1678.
30. Auer J, Scheibner P, Mische T, et al. Subclinical hyperthyroidismas a risk factor for atrial fibrillation. Am Heart J. Nov 2001;142(5):838-842.
31. Arnsdorf MF, Childers RW. Atrial electrophysiology in experimentalhyperthyroidism in rabbits. Circ Res. May 1970;26(5):575-581.
32. Chen YC, Chen SA, Chen YJ, et al. Effects of thyroid hormone onthe arrhythmogenic activity of pulmonary vein cardiomyocytes. J Am CollCardiol. Jan 162002;39(2):366-372.
33. Fox CS, Parise H, D'Agostino RB, Sr., et al. Parental atrialfibrillation as a risk factor for atrial fibrillation in offspring. Jama. Jun 16 2004;291(23):2851-2855.
34. Chen YH, Xu SJ, Bendahhou S, et al. KCNQ1 gain-of-functionmutation in familial atrial fibrillation. Science. Jan 10 2003;299(5604):251-254.
35. Olson TM, Michels VV, Ballew JD, et al. Sodium channel mutationsand susceptibility to heart failure and atrial fibrillation. Jama. Jan 26 2005;293(4):447-454.
36. Hsieh MH, Tai CT, Tsai CF, et al. Mechanism of spontaneoustransition from typical atrial flutter to atrial fibrillation: role of ectopicatrial fibrillation foci. Pacing Clin Electrophysiol. Jan 2001;24(1):46-52.
37. Hamer ME, Wilkinson WE, Clair WK, et al. Incidence of symptomaticatrial fibrillation in patients with paroxysmal supraventricular tachycardia. JAm Coll Cardiol. Apr1995;25(5):984-988.
38. Dewar RI, Lip GY. Identification, diagnosis and assessment ofatrial fibrillation. Heart. Jan 2007;93(1):25-28.
39. Echocardiographic predictors of stroke in patients with atrialfibrillation: a prospective study of 1066 patients from 3 clinical trials. ArchIntern Med. Jun22 1998;158(12):1316-1320.
40. Roche F, Gaspoz JM, Da Costa A, et al. Frequent and prolongedasymptomatic episodes of paroxysmal atrial fibrillation revealed by automaticlong-term event recorders in patients with a negative 24-hour Holter. PacingClin Electrophysiol. Nov2002;25(11):1587-1593.
41. Jabaudon D, Sztajzel J, Sievert K, et al. Usefulness of ambulatory7-day ECG monitoring for the detection of atrial fibrillation and flutter afteracute stroke and transient ischemic attack. Stroke. Jul 2004;35(7):1647-1651.
42. Plummer CJ, McComb JM. Detection of atrial fibrillation bypermanent pacemakers: observations from the STOP AF trial. CardElectrophysiol Rev. Dec2003;7(4):333-340.
43. Kinlay S, Leitch JW, Neil A, et al. Cardiac event recorders yieldmore diagnoses and are more cost-effective than 48-hour Holter monitoring inpatients with palpitations. A controlled clinical trial. Ann Intern Med. Jan 1 1996;124(1 Pt 1):16-20.
44. Bell C, Kapral M. Use of ambulatory electrocardiography for thedetection of paroxysmal atrial fibrillation in patients with stroke. CanadianTask Force on Preventive Health Care. Can J Neurol Sci. Feb 2000;27(1):25-31.
