Atrial fibrillation Wolff-Parkinson-White preexcitation syndromes

Resident Survival Guide

Sinus rhythm

Atrial fibrillation

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Anahita Deylamsalehi, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3]; Varun Kumar, M.B.B.S.

Overview[edit | edit source]

In up to one-third of patients with Wolff-Parkinson-White syndrome, paroxysmal atrial fibrillation develops. Studies have been demonstrated that Wolff-Parkinson-White syndrome with a left lateral bypass tract has even a higher incidence of atrial fibrillation. On the other hand Wolff-Parkinson-White syndrome patients with right free wall accessory pathway have a lower chance of atrial fibrillation development. Development of atrial fibrillation in a patient with Wolff-Parkinson-White syndrome can result in complications such as syncope, ventricular fibrillation and ultimately sudden death. There are some hypothesized mechanisms for development of paroxysmal atrial fibrillation in patients with Wolff-Parkinson-White syndrome, such as effects of accessory pathways on atrium, spontaneous deterioration of AV reentrant tachycardia (AVRT) into atrial fibrillation and atrial muscle's electrical abnormalities. In hemodynamically stable patients, intravenous procainamide may be administered to convert pre-exited atrial fibrillation to sinus rhythm. Atrial fibrillation associated with a rapid tachycardia due to an accessory pathway may be treated with flecainide that has shown to slower the ventricular rate by prolonging the shortest pre-excited cycle length during atrial fibrillation and hence terminate atrial fibrillation.

Atrial fibrillation in Wolff-Parkinson-White preexcitation syndromes[edit | edit source]

• The incidence of sudden cardiac death is between 0% and 0.6% in patients with Wolff-Parkinson-White syndrome, particularly those with short antegrade bypass tract refractory periods (less than 250 ms) and short R-R intervals during pre-excited atrial fibrillation (180 plus or minus 29 ms).^{[1][2][3][4][5][6]}
• In up to one-third of patients with Wolff-Parkinson-White syndrome, paroxysmal atrial fibrillation develops, nevertheless the mechanism for this elevated incidence is not completely understood.^[7]
• Studies have been demonstrated that Wolff-Parkinson-White syndrome with a left lateral bypass tract has even a higher incidence of double atrial potentials and induced atrial fibrillation. On the other hand Wolff-Parkinson-White syndrome patients with right free wall accessory pathway have a lower chance of atrial fibrillation development.^[8][9]
• Development of atrial fibrillation in a patient with Wolff-Parkinson-White syndrome can result in complications such as syncope, ventricular fibrillation and ultimately sudden death.^[10]
• The following are some of the hypothesized mechanisms for development of paroxysmal atrial fibrillation in patients with Wolff-Parkinson-White syndrome:^[7][11][12]
  • Spontaneous deterioration of AV reentrant tachycardia (AVRT) into atrial fibrillation
  • Effects of accessory pathways on atrium
    • Numerous studies have been reported a decreased incidence of atrial fibrillation in patients who undergone a successful ablation of accessory pathways.
  • Possible atrial muscle's electrical abnormalities and increased atrial vulnerability (which is independent of the role that accessory pathways play)
    • Since a fraction of patients experience atrial fibrillation even after a successful accessory pathway ablation, it can be concluded that there are other mechanisms independent of accessory pathways that cause atrial fibrillation in Wolff-Parkinson-White syndrome.
    • More evaluation with atrial endocardial mapping demonstrated the possibility of atrial diseases (such as intrinsic atrial muscle abnormalities) in patients with Wolff-Parkinson-White syndrome.
• Based on a study done on patients with Wolff-Parkinson-White syndrome with documented or induced atrial fibrillation, effective refractory period of the accessory pathway was correlated with the shortest RR interval and ventricular rate average.
• In hemodynamically stable patients, intravenous procainamide may be administered to convert pre-exited atrial fibrillation to sinus rhythm.^[13]
• AV nodal blocking agents such as digoxin, diltiazem, or verapamil are contra-indicated as they increase AV-node refractoriness which could encourage preferential conduction over the accessory pathway.^[14]
• Atrial fibrillation associated with a rapid tachycardia due to an accessory pathway may be treated with flecainide that has shown to slower the ventricular rate by prolonging the shortest pre-excited cycle length during atrial fibrillation and hence terminate atrial fibrillation.^{[15][16][17][18]}

2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation (DO NOT EDIT)^[19][edit | edit source]

Wolff-Parkinson-White and Pre-Excitation Syndromes[edit | edit source]

2011 ACCF/AHA/HRS Focused Updates Incorporated Into the ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation (DO NOT EDIT)^[20][edit | edit source]

Wolff-Parkinson-White (WPW) Preexcitation Syndromes (DO NOT EDIT) ^[20][edit | edit source]

Sources[edit | edit source]

• ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation ^[21]

• 2011 ACCF/AHA/HRS Focused Updates Incorporated Into the ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation ^[22]

• ACC/AHA/Physician Consortium 2008 clinical performance measures for adults with nonvalvular atrial fibrillation or atrial flutter ^[23]

References[edit | edit source]

CME Category::Cardiology