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Wolff-Parkinson-White syndrome

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3]; Alonso Alvarado, M.D.

Synonyms and keywords: WPW syndrome, WPW pattern

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Sara Zand, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3]

Overview

Wolff-Parkinson-White (WPW) syndrome is the most common cause of ventricular pre-excitation and the second common cause of supraventricular tachycardia. There is a muscle fiber that bridges the atrioventricular groove providing electrical continuity between the atrium and ventricle in parallel to the atrioventricular node-His-Purkinje axis. The atrial impulse activates the entire or part of the ventricle or the ventricular impulse activates the entire atrium or part of it, earlier than normally be expected. Patients with WPW syndrome may present with abrupt palpitation, presyncope, syncope, or sudden cardiac death (SCD). In some patients, SCD is the first presentation of WPW syndrome, especially in the setting of atrial fibrillation with a rapid ventricular response. Wolff-Parkinson-White syndrome is named after the cardiologists Louis Wolff, John Parkinson, and Paul Dudley White who gave a definitive description of the conduction disorder of the heart in 1930. The term Wolff-Parkinson-White syndrome was coined in 1940. Bundle of Kent was first discovered by Albert Frank Stanley Kent, a British physiologist following finding the lateral branch in the atrioventricular groove of the monkey heart. Wolff-Parkinson-White (WPW) syndrome is the occurrence of arrhythmia in the presence of an accessory pathway. WPW can be classified according to the site of origin, location in the mitral or tricuspid annulus, type of conduction (antegrade vs retrograde), and characteristics of the conduction (decremental vs nondecremental). In addition, WPW can be classified based on the type of atrioventricular reciprocating tachycardia (AVRT) it causes, which can be either orthodromic (~95% of the cases) or antidromic.In normal individuals, electrical activity in the heart is initiated in the sinoatrial (SA) node (located in the right atrium), propagates to the atrioventricular (AV) node, and then through the bundle of His to the ventricles of the heart. Individuals with Wolf-Parkinson-White syndrome (WPW) have an accessory pathway, known as the bundle of Kent, that communicates between the atria and the ventricles. The conduction through the accessory pathway can be bidirectional (most commonly), only retrogarde (less common), or only antegrade (least common). The most common type of tachycardia associated with WPW is atrioventricular reciprocating tachycardia (AVRT). The accessory pathway does not share the rate-slowing properties of the AV node; therefore, the combination of an accessory pathway and cardiac arrhythmia can trigger ventricular fibrillation, a leading cause of sudden cardiac death. The prevalence of WPW syndrome is approximately 100-300 per 100000 individuals worldwide. The incidence of tachyarrhythmia was estimated to be 1000 cases per 100000 individuals in the year in patients with WPW pattern. The incidence of sudden cardiac death in patients with Wolff-Parkinson-White syndrome was estimated to be 70-450 per 100000 patient-years. WPW syndrome is more commonly observed among young patients. In one study WPW syndrome was observed in 7% of individuals over 60-year-old. Men are more commonly affected with WPW syndrome than women. The men to women ratio is approximately 2 to 1. There is no racial predilection for WPW syndrome. High-risk criteria for sudden cardiac death in Wolff-Parkinson-White syndrome during electrophysiology study include the presence of multiple accessory pathways, R-R interval <250 milliseconds in antegrade conduction of accessory pathway during inducing atrial fibrillation, sustained atrial fibrillation induced by AV re-entry tachycardia, presence of Structural heart disease such as ebstein anomaly or hypertrophic cardiomyopathy. Patients with WPW pattern can remain asymptomatic throughout all their lives, nearly 65% of adolescents and 40% of adults present ECG changes but remain asymptomatic. Common complications of tachyarrhythmia associated WPW disease include reduced blood pressure and syncope, tachycaria induced cardiomyopathy, cardiac arrest, ventricular fibrillation, sudden cardiac death, complications of ablation, side effects of medications. SCD may occur in WPW syndrome due to rapid conduction of atrial fibrillation with heart rate >240/min to the ventricles via the accessory bypass tract leading ventricular fibrillation. Prognosis is generally excellent in asymptomatic WPW pattern. Catheter ablation (radiofrequency ablation) has a success rate between 95 – 98%, which varies depending on the location and number of accessory pathways. Successful ablation prevents future supraventricular tachyarrhythmia. The risk of lethal arrhythmia in asymptomatic children is higher than in adults. Long-term rates of atrial fibrillation in adult patients that present with WPW remains high despite ablation. Increased risk of atrial fibrillation in ablated WPW patients may be related to atrial fibrillation genesis. The diagnose of WPW pattern is commonly made by an incidental ECG finding in an asymptomatic individuals. The characteristic EKG finding is a delta wave, which represents the pre-excitation of the ventricles through the accessory pathway. This phenomenon presents because the AV node has the property of slowing the impulses, therefore the conduction through the accessory pathway is faster and the ventricles are excited through two different pathways. The delta wave is an upstroke in the R wave of the QRS complex that is associated with a short PR interval. Delta waves are only present when the patient is in sinus rhythm, whentachycardia starts the delta wave is no longer present. Patients with WPW syndrome and episodes of atrial fibrillation may present rapid irregular wide-complex tachycardia on EKG. The combination of atrial fibrillation and WPW may increase the risk of very rapid antidromic AVRT and occurrence of ventricular fibrillation. AV node blocking agents are contraindicated in these patients because of enhancement of the conduction through the accessory pathway. Patients with Ebstein anomaly and WPW may exhibit more than one accessory pathway. The most common combination of accessory pathways in Ebstein anomaly are the right posteroseptal and right free wall pathway. Wolff-Parkinson-White syndrome is sometimes associated with Leber’s hereditary optic neuropathy (LHON), a form of mitochondrial disease. Symptoms of WPW syndrome may include Palpitation, chest pain or chest tightness, diziness, light-headedness, Brief loss of consciousness, shortness of breath, exercise intolerance, anxiety. WPW syndrome, uncommonly presents as cardiac arrest or sudden cardiac death.The accessory pathway of WPW syndrome is present since birth. The age of presentation of tachyarrhythmia varies from patient to patient. Infants may develop heart failure if the tachyarrhythmia keeps without treatment. Symptoms of tachycardia related WPW syndrome in infants may include lethargy, breathlessness, loss of appetite. Atrial fibrillation in a patient with WPW should be suspected when there is ECG findings of an irregularly irregular rhythm and absent P waves suggestive of atrial fibrillation in the context of a heart rate higher than 240 beats per minute. The electrophysiologic study is used for determining the location and number of accessory pathways, determining the mechanism of tachycardia, establishing the diagnosis in those patients with questionable resting EKG. Treatment is based on the risk stratification of the individual. Risk stratification is performed to determine which individuals with WPW syndrome are at risk for sudden cardiac death (SCD). Sudden cardiac death in these individuals is due to the propagation of an atrial arrhythmia to the ventricles at a very high rate. Noninvasive tests have a 70% positive predictive value and 30% negative predictive value for identifying pathways with life-threatening properties.Electrophysiologic studies are useful for evaluation of patients’ symptoms. Wolff-Parkinson-White syndrome patients who are hemodynamically unstable, as reflected by the presence of hypotension, cold extremities, mottling or peripheral cyanosis, or those who present with ischemic chest pain or decompensated heart failure must undergo cardioversion urgently. The medical therapy of hemodynamically stable patients with WPW syndrome depends on the type of the tachycardia. When the ECG findings suggest orthodromic AVRT, the patient should be managed similar to AVNRT, and administration of adenosine, beta-blocker verapamil, and procainamide is recommended. Among patients with antidromic AVRT, AV nodal blocking agents should be avoided and patients should be treated with either procainamide, ibutilide. The long term treatment of patients with WPW syndrome depends on the presence or absence of symptoms and their severity. Patients who have poorly tolerated symptomatic WPW syndrome should undergo [[catheter ablation. Effective medication for prevention of tachyarrhythmia AVRT in patients without preexcitation in resting ECG include oral beta-blocker, diltiazem, and verapamil. Oral flecainide and propaphenone for prevention of tachyarrhythmia is recommended in patients with preexcitation in resting ECG that are not candidates for catheter ablation and do not have structural or ischemic heart disease.

Historical Perspective

Wolff-Parkinson-White syndrome is named after the cardiologists Louis Wolff, John Parkinson, and Paul Dudley White who gave a definitive description of the conduction disorder of the heart in 1930. The term Wolff-Parkinson-White syndrome was coined in 1940. Bundle of Kent was first discovered by Albert Frank Stanley Kent, a British physiologist following finding the lateral branch in the atrioventricular groove of the monkey heart.

Classification

Wolff-Parkinson-White (WPW) syndrome is the occurrence of arrhythmia in the presence of an accessory pathway. WPW can be classified according to the site of origin, location in the mitral or tricuspid annulus, type of conduction (antegrade vs retrograde), and characteristics of the conduction (decremental vs nondecremental). In addition, WPW can be classified based on the type of atrioventricular reciprocating tachycardia (AVRT) it causes, which can be either orthodromic (~95% of the cases) or antidromic.

Pathophysiology

In normal individuals, electrical activity in the heart is initiated in the sinoatrial (SA) node (located in the right atrium), propagates to the atrioventricular (AV) node, and then through the bundle of His to the ventricles of the heart. Individuals with Wolf-parkinson-White (WPW) have an accessory pathway, known as the bundle of Kent, that communicates between the atria and the ventricles. The conduction through the accessory pathway can be bidirectional (most commonly), only retrogarde (less common), or only antegrade (least common). The most common type of tachycardia associated with WPW is atrioventricular reciprocating tachycardia (AVRT). The accessory pathway does not share the rate-slowing properties of the AV node; therefore, the combination of an accessory pathway and cardiac arrhythmia can trigger ventricular fibrillation, a leading cause of sudden cardiac death.

Differentiating WPW syndrome from Other Diseases

WPW syndrome should be differentiated from other causes of narrow QRS tachycardia such as AVNRT, PJRT,[[AT],SNRT.

Epidemiology and Demographics

The prevalence of WPW syndrome is approximately 100-300 per 100000 individuals worldwide. The incidence of tachyarrhythmia was estimated to be 1000 cases per 100000 individuals in the year in patients with WPW pattern. The incidence of sudden cardiac death in patients with Wolff-Parkinson-White syndrome was estimated to be 70-450 per 100000 patient-years. WPW syndrome is more commonly observed among young patients. In one study WPW syndrome was observed in 7% of individuals over 60-year-old. Men are more commonly affected with WPW syndrome than women. The men to women ratio is approximately 2 to 1. There is no racial predilection for WPW syndrome.


Risk Factors

High-risk criteria for sudden cardiac death in Wolff-Parkinson-White syndrome during electrophysiology study include the presence of multiple accessory pathways, R-R interval <250 milliseconds in antegrade conduction of accessory pathway during inducing atrial fibrillation, sustained atrial fibrillation induced by AV re-entry tachycardia, precence of Structural heart disease such as ebstein anomaly or hypertrophic cardiomyopathy.

Natural History, Complications, and Prognosis

Patients with WPW pattern can remain asymptomatic through all their lives, nearly 65% of adolescents and 40% of adults present ECG changes but remain asymptomatic. Complications Wolff-Parkinson-White syndrome is a consequence of symptomatic tachycardias and can occur at any age. Common complications of tachyarrhythmia associated WPW disease include reduced blood pressure and syncope, tachycaria induced cardiomyopathy, cardiac arrest, ventricular fibrillation, usdden cardiac death, complications of ablation, side effects of medications. SCD may occur in WPW syndrome due to rapid conduction of atrial fibrillation with heart rate >240/min to the ventricles via the accessory bypass tract leading ventricular fibrillation. Prognosis is generally excellent in asymptomatic WPW pattern.Catheter ablation (radiofrequency ablation) has a success rate between 95 – 98%, which varies depending on the location and number of accessory pathways. Successful ablation prevents future supraventricular tachyarrhythmia. The risk of lethal arrhythmia in asymptomatic children is higher than in adults. Long-term rates of atrial fibrillation in adult patients that present with WPW remains high despite ablation. Increased risk of atrial fibrillation in ablated WPW patients may be related atrial fibrillation genesis.

Diagnosis

Diagnostic Study of Choice

The diagnose of WPW pattern is commonly made by an incidental ECG finding in an asymptomatic individuals. The characteristic EKG finding is a delta wave, which represents the pre-excitation of the ventricles through the accessory pathway. This phenomenon presents because the AV node has the property of slowing the impulses, therefore the conduction through the accessory pathway is faster, therefore the ventricles are excited through two different pathways. The delta wave is an upstroke in the R wave of the QRS complex that is associated with a short PR interval. Delta waves are only present when the patient is in sinus rhythm, whentachycardia starts the delta wave is no longer present. Patients WPW syndrome with episodes of atrial fibrillation will present ECG with rapid irregular wide-complex tachycardia. The combination of atrial fibrillation and WPW may increase the risk of very rapid antidromic AVRT and occurrence of ventricular fibrillation. AV node blocking agents are contraindicated in these patients because it will enhance the conduction through the accessory pathway. Patients with WPW may exhibit more than one accessory pathway which is common in patients with Ebstein’s anomaly. The most common combination of accessory pathways in Ebstein anomaly was the right posteroseptal and right free wall pathway. Wolff-Parkinson-White syndrome is sometimes associated with Leber’s hereditary optic neuropathy (LHON), a form of mitochondrial disease.

History and Symptoms

Symptoms of WPW syndrome may include Palpitation, Chest pain or chest tightness, Dizziness, Light-headedness, Brief loss of consciousness, Shortness of breath, Exercise intolerance, Anxiety. The most common arrhythmias associated with Wolff-Parkinson-White syndrome is AV reentry tachycardia. WPW syndrome, uncommonly presents as cardiac arrest or sudden cardiac death.The accessory pathway of WPW syndrome is present since birth. The age of presentation of tachyarrhythmia varies from patient to patient. Infants may develop heart failure if not treated immediately. Symptoms of tachycardia related WPW syndrome in infants may include Lethargy, Breathlessness, Loss of appetite.

Physical Examination

Laboratory Findings

There is no laboratory finding related to WPW syndrome.

Electrocardiogram

Wolff-Parkinson-White (WPW) pattern is characterized by ECG findings such as a short PR interval and a delta wave and wide QRS complex.WPW syndrome is the occurrence of tachycardia with or without associated symptoms in a subject with existing WPW pattern. WPW syndrome can present as an orthodromic or antidromic AVRT during which the delta wave no longer appears. Atrial fibrillation in a patient with WPW should be suspected when there is ECG findings of an irregularly irregular rhythm and absent P waves suggestive of atrial fibrillation in the context of a heart rate higher than 240 beats per minute.

Other Diagnostic Studies

.The electrophysiologic study is used for determining the location and number of accessory pathways, determining the mechanism of tachycardia, establishing the diagnosis in those patients with questionable resting EKG.

Treatment

Risk stratification

Treatment is based on the risk stratification of the individual. Risk stratification is performed to determine which individuals with WPW syndrome are at risk for sudden cardiac death (SCD). Sudden cardiac death in these individuals is due to the propagation of an atrial arrhythmia to the ventricles at a very high rate. Noninvasive tests have a 70% positive predictive value and 30% negative predictive value for identifying pathways with life-threatening properties.Electrophysiologic studies are useful for evaluation of patients’ symptoms.

Cardioversion

Wolff-Parkinson-White syndrome patients who are hemodynamically unstable, as reflected by the presence of hypotension, cold extremities, mottling or peripheral cyanosis, or those who present with ischemic chest pain or decompensated heart failure must undergo cardioversion urgently.

Medical Therapy

The medical therapy of hemodynamically stable patients with WPW syndrome depends on the type of the tachycardia. When the ECG findings suggest orthodromic AVRT, the patient should be managed similarly to patients with supreventricular tachycardia followed by the sequential administration of adenosine, verapamil and procainamide in case of failure to improve. Among patients with antidromic AVRT, AV nodal blocking agents should be avoided and patients should be treated with either procainamide, ibutilide or flecainide. The long term treatment of patients with WPW syndrome depends on the presence or absence of symptoms and their severity. Patients who have poorly tolerated symptomatic WPW syndrome should undergo catheter ablation.

Drug prophylaxia

Oral beta-blocker, diltiazem, and verapamil for prevention of AVRT in patients without preexcitation in resting ECG. Oral flecainide and propaphenone in patients with preexcitation in resting ECG that are not candidates for catheter ablation and do not have structural or ischemic heart disease.

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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Sara Zand, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3]

Overview

Wolff-Parkinson-White syndrome is named after the cardiologists Louis Wolff, John Parkinson, and Paul Dudley White who gave a definitive description of the conduction disorder of the heart in 1930. The term Wolff-Parkinson-White syndrome was coined in 1940. Bundle of Kent was first discovered by Albert Frank Stanley Kent, a British physiologist following finding the lateral branch in the atrioventricular groove of the monkey heart.

Historical Perspective



Louis Wolff, Sir John Parkinson and Paul Dudley, who discovered the phenomenon that later would be called the WPW syndrome

References

  1. ↑ Wilson FN (1915). (abstract) “A case in which the vagus influenced the form of the ventricular complex of the electrocardiogram” Check |url= value (help). Archives of Internal Medicine. 16 (6): 1008–27. doi:10.1001/archinte.1915.00080060120009.
  2. ↑ L. Wolff, J. Parkinson, P. D. White. Bundle-branch block with short P-R interval in healthy young people prone to paroxysmal tachycardia. American Heart Journal, St. Louis, 1930, 5: 685.
  3. ↑ Kent AFS (1893). “Researches on the structure and function of the mammalian heart”. Journal of Physiology. 14 (4–5): 233–54. PMC 1514401. PMID 16992052.
  4. ↑ Kent AFS (1914). “A conducting path between the right auricle and the external wall of the right ventricle in the heart of the mammal”. Journal of Physiology. 48: 57.

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Classification

Classification

EKG Classification | WPW Variants

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Sara Zand, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3]; Rim Halaby, M.D. [4]

Overview

Wolff-Parkinson-White (WPW) syndrome is the occurrence of arrhythmia in the presence of an accessory pathway. WPW can be classified according to the site of origin, location in the mitral or tricuspid annulus except at the aortomitral continuity (left anteroseptal region), type of conduction (antegrade vs retrograde), and characteristics of the conduction (decremental vs nondecremental). In addition, WPW can be classified based on the type of atrioventricular reciprocating tachycardia (AVRT) it causes, which can be either orthodromic (~95% of the cases) or antidromic.[1]

Classification

The accessory pathway may be localized on ECG during preexcitation based on the delta wave axis and P-wave axis.

Delta-wave axis

  • Negative delta in V1 indicates a left-sided accessory pathway[4][5]
  • Negative delta in lead 1 and avl or 2,3,avf indicates left free wall or left posterior accessory pathway
  • rsR` or QR complexes in V1 in the absent of incomplete RBBB, indicates left-sided septal accessory pathway
  • Negative delta in lead 2, the positive delta in Avr ,deep s wave in V6 indicates postroseptal accessory pathway within the coronary sinus
  • LBBB pattern, transitioning zone before V4, the positive delta in 2,3,avf indicates an anteroseptal accessory pathway

P-wave axis

  • Positive P wave in AVR, negative P wave in AVL indicates left-sided accessory pathway[6]
  • Positive P wave in AVL, negative P wave in AVR indicates right-sided accessory pathway
  • Superior axis in P waves indicates a posteroseptal accessory pathway
  • Inferior axis in P waves indicates the anteroseptal accessory pathway

Classification Based on the Type of Conduction

The accessory pathway in WPW may be classified into:[1]

  • Antegrade conduction: also known as manifest, responsible for the “pre-excitation” finding on ECG
  • Retrograde conduction: also known as concealed

Most commonly, the accessory pathways conduct in both directions. Isolated retrograde conduction is less common. Isolated antegrade conduction is the least common and is usually associated with accessory pathways in the right side of the heart.

Classification Based on the Characteristics of Conduction

  • Decremental conduction (8% of the cases)
    • Decremental conduction is the progressive delay in the conduction through the accessory pathway following an increase in the paced rates.
  • Non-decremental conduction (92% of the cases)[1]

Classification Based on the Type of AVRT

The most common arrhythmia in WPW syndrome is atrioventricular reciprocating tachycardia (AVRT). AVRT in WPW can be classified into:[1]

Variants of WPW

Lown-Ganong-Levine Syndrome (LGL)

Mahaim Type Preexcitation

Pattern of preexcitation:

References

  1. ↑ 1.0 1.1 1.2 1.3 Blomström-Lundqvist C, Scheinman MM, Aliot EM, Alpert JS, Calkins H, Camm AJ; et al. (2003). “ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias–executive summary. a report of the American college of cardiology/American heart association task force on practice guidelines and the European society of cardiology committee for practice guidelines (writing committee to develop guidelines for the management of patients with supraventricular arrhythmias) developed in collaboration with NASPE-Heart Rhythm Society”. J Am Coll Cardiol. 42 (8): 1493–531. PMID 14563598.
  2. ↑ Cain, Michael E.; Luke, Robert A.; Lindsay, Bruce D. (1992). “Diagnosis and Localization of Accessory Pathways”. Pacing and Clinical Electrophysiology. 15 (5): 801–824. doi:10.1111/j.1540-8159.1992.tb06847.x. ISSN 0147-8389.
  3. ↑ Goldreyer, Bruce N.; Damato, Anthony N. (1971). “The Essential Role of Atrioventricular Conduction Delay in the Initiation of Paroxysmal Supraventricular Tachycardia”. Circulation. 43 (5): 679–687. doi:10.1161/01.CIR.43.5.679. ISSN 0009-7322.
  4. ↑ Cain ME, Luke RA, Lindsay BD (May 1992). “Diagnosis and localization of accessory pathways”. Pacing Clin Electrophysiol. 15 (5): 801–24. doi:10.1111/j.1540-8159.1992.tb06847.x. PMID 1382283.
  5. ↑ Szabo, Tibor S.; Klein, George J.; Guiraudon, Gerard M.; Yee, Raymond; Sharma, Arjun D. (1989). “Localization of Accessory Pathways in the Wolff-Parkinson-White Syndrome”. Pacing and Clinical Electrophysiology. 12 (10): 1691–1705. doi:10.1111/j.1540-8159.1989.tb01848.x. ISSN 0147-8389.
  6. ↑ Tai CT, Chen SA, Chiang CE, Lee SH, Chang MS (March 1996). “Electrocardiographic and electrophysiologic characteristics of anteroseptal, midseptal, and para-Hisian accessory pathways. Implication for radiofrequency catheter ablation”. Chest. 109 (3): 730–40. doi:10.1378/chest.109.3.730. PMID 8617084.
  7. ↑ Katritsis DG, Wellens HJ, Josephson ME (April 2017). “Mahaim Accessory Pathways”. Arrhythm Electrophysiol Rev. 6 (1): 29–32. doi:10.15420/aer.2016:35:1. PMC 5430943. PMID 28507744.

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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3]

Overview

In normal individuals, electrical activity in the heart is initiated in the sinoatrial (SA) node (located in the right atrium), propagates to the atrioventricular (AV) node, and then through the bundle of His to the ventricles of the heart. Individuals with Wolf-parkinson-White (WPW) have an accessory pathway, known as the bundle of Kent, that communicates between the atria and the ventricles. The conduction through the accessory pathway can be bidirectional (most commonly), only retrogarde (less common), or only antegrade (least common). The most common type of tachycardia associated with WPW is atrioventricular reciprocating tachycardia (AVRT). The accessory pathway does not share the rate-slowing properties of the AV node; therefore, the combination of an accessory pathway and cardiac arrhythmia can trigger ventricular fibrillation, a leading cause of sudden cardiac death.

Pathophysiology

Accessory Pathway

The accessory pathway is characterized by:[4]

  • Conducting electrical stimulus faster than the AV node
  • Longer refractory period compared to the AV node
  • A non-decremental conduction in response to an increased paced rates

Electrical Activity

Normal Electrical Activity

Shown below is an image depicting the conduction system in the normal heart.

The conduction system in the normal heart
The conduction system in the normal heart
  • The AV node serves an important function as a “gatekeeper”, limiting the electrical activity that reaches the ventricles.
  • In situations where the atria generate excessively rapid electrical activity (such as atrial fibrillation or atrial flutter), the AV node limits the number of signals conducted to the ventricles.
  • For example, if the atria are electrically activated at 300 beats per minute, half those electrical impulses may be blocked by the AV node, so that the ventricles are stimulated at only 150 beats per minute—resulting in a pulse of 150 beats per minute.


  • Another important property of the AV node is that it slows down individual electrical impulses.
  • This is manifested on the electrocardiogram as the PR interval (the time from electrical activation of the atria to electrical activation of theventricles), which is usually shortened to less than 120 milliseconds in duration.

Electrical Activity in WPW

Shown below is an image depicting the normal conduction of electrical signals in the heart versus that in the presence of an accessory pathway.

[[File: Abnormal electrical pathway in WPW.jpeg|center| The normal conduction of electrical signals in the normalheart versus that in the presence of an accessory pathway

  • The conduction through the accessory pathway can be:
  • Bidirectional (most commonly): retrogarde (also known as concealed) as well as antegrade (also known as manifest, responsible for the ECG findings of delta wave and short PR interval)
  • Only retrogarde (less common)
  • Only antegrade (least common)


Associated Conditions

WPW syndrome is associated with the following disorders:

References

  1. ↑ Sorbo MD, Buja GF, Miorelli M, Nistri S, Perrone C, Manca S, Grasso F, Giordano GM, Nava A (1995). “The prevalence of the Wolff–Parkinson–White syndrome in a population of 116,542 young males”. Giornale Italiano di Cardiologia (in Italian). 25 (6): 681–7. PMID 7649416.
  2. ↑ Munger TM, Packer DL, Hammill SC, Feldman BJ, Bailey KR, Ballard DJ, Holmes DR Jr, Gersh BJ (1993). “A population study of the natural history of Wolff–Parkinson–White syndrome in Olmsted County, Minnesota, 1953–1989”. Circulation. 87 (3): 866–73. doi:10.1161/01.CIR.87.3.866. PMID 8443907.
  3. ↑ americanheart.org Atrial and Ventricular Depolarization Changes Last updated 11/24/2008.
  4. ↑ Obel OA, Camm AJ (1998). “Accessory pathway reciprocating tachycardia”. Eur Heart J. 19 Suppl E: E13–24, E50–1. PMID 9717020.
  5. ↑ Sidhu J, Roberts R (October 2003). “Genetic basis and pathogenesis of familial WPW syndrome”. Indian Pacing Electrophysiol J. 3 (4): 197–201. PMC 1502052. PMID 16943919.
  6. ↑ Rao MP, Panduranga P, Al-Mukhaini M, Al-Jufaili M (2012). “Ebstein anomaly in an adult presenting with wide QRS tachycardia: diagnostic and therapeutic dilemmas”. Am J Emerg Med. 30 (5): 834.e1–4. doi:10.1016/j.ajem.2011.03.001. PMID 21570234. Unknown parameter |month= ignored (help)
  7. ↑ Bayar N, Canbay A, Uçar O, Aydoğdu S, Diker E (2010). “[Association of Gerbode-type defect and Wolff-Parkinson-White syndrome with Ebstein’s anomaly]”. Anadolu Kardiyol Derg (in Turkish). 10 (1): 88–90. PMID 20150013. Unknown parameter |month= ignored (help)
  8. ↑ Legius B, Van De Bruaene A, Van Deyk K; et al. (2010). “Behavior of Ebstein’s anomaly: single-center experience and midterm follow-up”. Cardiology. 117 (2): 90–5. doi:10.1159/000318041. PMID 20924185.
  9. ↑ Savini E, Capone PL (1994). “[Wolff-Parkinson-White, a study on the prevalence of the site of accessory pathways: relations between stability of pre-excitation, symptoms, cardiac arrhythmias and association of mitral valve prolapse with localization of pre-excitation]”. Minerva Cardioangiol (in Italian). 42 (7–8): 339–43. PMID 7970027.
  10. ↑ Kruchina TK, Vasichkina ES, Egorov DF, Tatarskiĭ BA (2012). “[Asymptomatic ventricular pre-excitation in children: a 17 year follow-up study]”. Kardiologiia (in Russian). 52 (5): 30–6. PMID 22839583.
  11. ↑ 11.0 11.1 11.2 “Wolff-Parkinson-White syndrome – Genetics Home Reference”. Retrieved 15 April 2014.

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Differentiating Wolff-Parkinson-White syndrome from other Diseases

Differentiating Wolff-Parkinson-White syndrome from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Syed Hassan A. Kazmi BSc, MD [3] Cafer Zorkun, M.D., Ph.D. [4]

Overview

Differentiating Tachycardia Associated Wolf-Parkinson-White syndrome from other Diseases

Abbreviations: VT: Ventricular tachycardia; VF: Ventricular fibrillation; AF: Atrial fibrillation ; AVNRT: Atrionodal reentrant tachycardia; AV node: Atrioventricular node; AVRT: Atrioventricular reentrant tachycardia; AT: Arial tachycardia; PJRT: Permanent junctional reciprocating tachycardi; SNRT: Sinus nodal reentrant tachycardia.
[1]


Regular Narrow complex tachycardia (QRS≤ 120ms) Irregular Narrow complex tachycardia (QRS≤ 120ms) Regular wide QRS tachycardia(QRS>120ms) Irregular wide QRS tachycardia (QRS>120ms)
Physiologic sinus tachycardia Atrial fibrillation (AF) Ventricular tachycardia/flutter AF or atrial flutter or focal atrial tachycardia with varying block conducted with abrerration
Inappropriate sinus tachycardia Focal atrial tachycardia or atrial flutter with varying AV block Antidromic AV re-entrant tachycardia [[Antidromic AV reentrant tachycardia]] due to nodo-ventricular/fascicular accessory pathway with variable VA conduction
Sinus nodal re-entrant tachycardia Multifocal atrial tachycardia Supraventricular tachycardia with aberration/bunddle branch block (preexcisting or rate-dependent tachycardia pre-excited AF
Focal atrial tachycardia Atrial or junction tachycardia with preexcitation/bystander accessory pathway Polymorphic VT
AV nodal re-entrant tachycardia Supraventricular tachycardia with QRS widening due to electrolyte disturbance or antiarrhythmic drug Torsade-de pointed
Orthodromic AV re-entrant tachycardia Ventricular pace rhythm Ventricular fibrillation
Junctional ectopic tachycardia
Ideopathic VT (high septal VT)


Arrhythmia Rhythm Rate P wave PR Interval QRS Complex Response to Maneuvers Epidemiology Co-existing Conditions
Atrial Fibrillation (AFib)[2][3]
  • Irregularly irregular
  • Absent
  • Fibrillatory waves
  • Absent
  • Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
  • 2.7–6.1 million people in the United States have AFib
  • 2% of people younger than age 65 have AFib, while about 9% of people aged 65 years or older have AFib
Atrial Flutter[4]
  • Regular or Irregular
  • 75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) beats per minute (bpm), but 150 is more common
  • Sawtooth pattern of P waves at 250 to 350 bpm
  • Biphasic deflection in V1
  • Varies depending upon the magnitude of the block, but is short
  • Less than 0.12 seconds, consistent, and normal in morphology
  • Conduction may vary in response to drugs and maneuvers dropping the rate from 150 to 100 or to 75 bpm
Atrioventricular nodal reentry tachycardia (AVNRT)[5][6][7][8]
  • Regular
  • 140-280 bpm
  • Slow-Fast AVNRT:
    • Pseudo-S wave in leads II, III, and AVF
    • Pseudo-R’ in lead V1.
  • Fast-Slow AVNRT
  • Slow-Slow AVNRT
  • Inverted, superimposed on or buried within the QRS complex (pseudo R prime in V1/pseudo S wave in inferior leads)
  • Absent (P wave can appear after the QRS complex and before the T wave, and in atypical AVNRT, the P wave can appear just before the QRS complex)
  • Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
  • QRS alternans may be present
Multifocal Atrial Tachycardia[9][10]
  • Irregular
  • Atrial rate is > 100 beats per minute
  • Varying morphology from at least three different foci
  • Absence of one dominant atrial pacemaker, can be mistaken for atrial fibrillation if the P waves are of low amplitude
  • Less than 0.12 seconds, consistent, and normal in morphology
Paroxysmal Supraventricular Tachycardia
  • Regular
  • 150 and 240 bpm
  • Absent
  • Hidden in QRS
  • Absent
  • Narrow complexes (< 0.12 s)
Wolff-Parkinson-White Syndrome[11][12]
  • Regular
  • Atrial rate is nearly 300 bpm and ventricular rate is at 150 bpm
  • Less than 0.12 seconds
  • A delta wave and evidence of ventricular pre-excitation if there is conduction to the ventricle via ante-grade conduction down an accessory pathway
  • A delta wave and pre-excitation may not be present because bypass tracts do not conduct ante-grade.
Ventricular Fibrillation (VF)[13][14][15]
  • Irregular
  • 150 to 500 bpm
  • Absent
  • Absent
  • Absent (R on T phenomenon in the setting of ischemia)
  • Initial rhythm in 23% of out of hospital cardiac arrest
Ventricular Tachycardia[16][17]
  • Regular
  • > 100 bpm (150-200 bpm common)
  • Absent
  • Absent
  • Initial R wave in V1, initial r > 40 ms in V1/V2, notched S in V1, initial R in aVR, lead II R wave peak time ≥50 ms, no RS in V1-V6, and atrioventricular dissociation
  • Wide complex, QRS duration > 120 milliseconds
  • 5-10% of patients presenting with AMI

References

  1. ↑ Zaza, Antonio; Suwalski, Piotr; Sarquella-Brugada, Georgia; Sacher, Frederic; Lambiase, Pier David; Kuck, Karl-Heinz; Kaski, Juan-Carlos; Ho, Siew Yen; Grace, Andrew; Gorenek, Bulent; Gomez-Doblas, Juan J; Diller, Gerhard-Paul; Deftereos, Spyridon G; Corrado, Domenico; Calkins, Hugh; Blomström-Lundqvist, Carina; Bax, Jeroen J; Arribas, Fernando; Arbelo, Elena; Katritsis, Demosthenes G; Brugada, Josep; De Potter, Tom; Sticherling, Christian; Aboyans, Victor; Basso, Cristina; Bocchiardo, Mario; Budts, Werner; Delgado, Victoria; Dobrev, Dobromir; Fitzsimons, Donna; Gevaert, Sofie; Heidbuchel, Hein; Hindricks, Gerhard; Hlivak, Peter; Kanagaratnam, Prapa; Katus, Hugo; Kautzner, Josef; Kriebel, Thomas; Lancellotti, Patrizio; Landmesser, Ulf; Leclercq, Christophe; Lewis, Basil; Lopatin, Yury; Merkely, Béla; Paul, Thomas; Pavlović, Nikola; Petersen, Steffen; Petronio, Anna Sonia; Potpara, Tatjana; Roffi, Marco; Scherr, Daniel; Shlyakhto, Evgeny; Simpson, Iain A; Zeppenfeld, Katja; Arbelo, Elena; Arribas, Fernando; Bax, Jeroen J; Blomström-Lundqvist, Carina; Calkins, Hugh; Deftereos, Spyridon G; Diller, Gerhard-Paul; Gomez-Doblas, Juan J; Gorenek, Bulent; Grace, Andrew; Ho, Siew Yen; Kaski, Juan-Carlos; Kuck, Karl-Heinz; Lambiase, Pier David; Sacher, Frederic; Sarquella-Brugada, Georgia; Suwalski, Piotr; Zaza, Antonio; Windecker, Stephan; Aboyans, Victor; Baigent, Colin; Collet, Jean-Philippe; Dean, Veronica; Delgado, Victoria; Fitzsimons, Donna; Gale, Chris P; Grobbee, Diederick; Halvorsen, Sigrun; Hindricks, Gerhard; Iung, Bernard; Jüni, Peter; Katus, Hugo A; Landmesser, Ulf; Leclercq, Christophe; Lettino, Maddalena; Lewis, Basil S; Merkely, Bela; Mueller, Christian; Petersen, Steffen E; Petronio, Anna Sonia; Richter, Dimitrios J; Roffi, Marco; Shlyakhto, Evgeny; Simpson, Iain A; Sousa-Uva, Miguel; Touyz, Rhian M; Amara, Walid; Grigoryan, Svetlana; Podczeck-Schweighofer, Andrea; Chasnoits, Alexandr; Vandekerckhove, Yves; Sokolovich, Sekib; Traykov, Vassil; Skoric, Bosko; Papasavvas, Elias; Kautzner, Josef; Riahi, Sam; Kampus, Priit; Parikka, Hannu; Piot, Olivier; Etsadashvili, Kakhaber; Stellbrink, Christoph; Manolis, Antonis S; Csanádi, Zoltán; Gudmundsson, Kristjan; Erwin, John; Barsheshet, Alon; De Ponti, Roberto; Abdrakhmanov, Ayan; Jashari, Haki; Lunegova, Olga; Jubele, Kristine; Refaat, Marwan M; Puodziukynas, Aras; Groben, Laurent; Grosu, Aurel; Pavlovic, Nikola; Ibtissam, Fellat; Trines, Serge A; Poposka, Lidija; Haugaa, Kristina H; Kowalski, Oskar; Cavaco, Diogo; Dobreanu, Dan; Mikhaylov, Evgeny N; Zavatta, Marco; Nebojša, Mujović; Hlivak, Peter; Ferreira-Gonzalez, Ignacio; Juhlin, Tord; Reichlin, Tobias; Haouala, Habib; Akgun, Taylan; Gupta, Dhiraj (2020). “2019 ESC Guidelines for the management of patients with supraventricular tachycardiaThe Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC)”. European Heart Journal. 41 (5): 655–720. doi:10.1093/eurheartj/ehz467. ISSN 0195-668X.
  2. ↑ Lankveld TA, Zeemering S, Crijns HJ, Schotten U (July 2014). “The ECG as a tool to determine atrial fibrillation complexity”. Heart. 100 (14): 1077–84. doi:10.1136/heartjnl-2013-305149. PMID 24837984.
  3. ↑ Harris K, Edwards D, Mant J (2012). “How can we best detect atrial fibrillation?”. J R Coll Physicians Edinb. 42 Suppl 18: 5–22. doi:10.4997/JRCPE.2012.S02. PMID 22518390.
  4. ↑ Cosío FG (June 2017). “Atrial Flutter, Typical and Atypical: A Review”. Arrhythm Electrophysiol Rev. 6 (2): 55–62. doi:10.15420/aer.2017.5.2. PMC 5522718. PMID 28835836.
  5. ↑ Katritsis DG, Josephson ME (August 2016). “Classification, Electrophysiological Features and Therapy of Atrioventricular Nodal Reentrant Tachycardia”. Arrhythm Electrophysiol Rev. 5 (2): 130–5. doi:10.15420/AER.2016.18.2. PMC 5013176. PMID 27617092.
  6. ↑ Letsas KP, Weber R, Siklody CH, Mihas CC, Stockinger J, Blum T, Kalusche D, Arentz T (April 2010). “Electrocardiographic differentiation of common type atrioventricular nodal reentrant tachycardia from atrioventricular reciprocating tachycardia via a concealed accessory pathway”. Acta Cardiol. 65 (2): 171–6. doi:10.2143/AC.65.2.2047050. PMID 20458824.
  7. ↑ “Atrioventricular Nodal Reentry Tachycardia (AVNRT) – StatPearls – NCBI Bookshelf”.
  8. ↑ Schernthaner C, Danmayr F, Strohmer B (2014). “Coexistence of atrioventricular nodal reentrant tachycardia with other forms of arrhythmias”. Med Princ Pract. 23 (6): 543–50. doi:10.1159/000365418. PMC 5586929. PMID 25196716.
  9. ↑ Scher DL, Arsura EL (September 1989). “Multifocal atrial tachycardia: mechanisms, clinical correlates, and treatment”. Am. Heart J. 118 (3): 574–80. doi:10.1016/0002-8703(89)90275-5. PMID 2570520.
  10. ↑ Goodacre S, Irons R (March 2002). “ABC of clinical electrocardiography: Atrial arrhythmias”. BMJ. 324 (7337): 594–7. doi:10.1136/bmj.324.7337.594. PMC 1122515. PMID 11884328.
  11. ↑ Rao AL, Salerno JC, Asif IM, Drezner JA (July 2014). “Evaluation and management of wolff-Parkinson-white in athletes”. Sports Health. 6 (4): 326–32. doi:10.1177/1941738113509059. PMC 4065555. PMID 24982705.
  12. ↑ Rosner MH, Brady WJ, Kefer MP, Martin ML (November 1999). “Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and initial therapeutic issues”. Am J Emerg Med. 17 (7): 705–14. doi:10.1016/s0735-6757(99)90167-5. PMID 10597097.
  13. ↑ Glinge C, Sattler S, Jabbari R, Tfelt-Hansen J (September 2016). “Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction”. J Geriatr Cardiol. 13 (9): 789–797. doi:10.11909/j.issn.1671-5411.2016.09.006. PMC 5122505. PMID 27899944.
  14. ↑ Samie FH, Jalife J (May 2001). “Mechanisms underlying ventricular tachycardia and its transition to ventricular fibrillation in the structurally normal heart”. Cardiovasc. Res. 50 (2): 242–50. doi:10.1016/s0008-6363(00)00289-3. PMID 11334828.
  15. ↑ Adabag AS, Luepker RV, Roger VL, Gersh BJ (April 2010). “Sudden cardiac death: epidemiology and risk factors”. Nat Rev Cardiol. 7 (4): 216–25. doi:10.1038/nrcardio.2010.3. PMC 5014372. PMID 20142817.
  16. ↑ Koplan BA, Stevenson WG (March 2009). “Ventricular tachycardia and sudden cardiac death”. Mayo Clin. Proc. 84 (3): 289–97. doi:10.1016/S0025-6196(11)61149-X. PMC 2664600. PMID 19252119.
  17. ↑ Levis JT (2011). “ECG Diagnosis: Monomorphic Ventricular Tachycardia”. Perm J. 15 (1): 65. doi:10.7812/tpp/10-130. PMC 3048638. PMID 21505622.

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Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3]

Overview

The prevalence of WPW syndrome is approximately 100-300 per 100000 individuals worldwide. The incidence of tachyarrhythmia was estimated to be 1000 cases per 100000 individuals in the year in patients with WPW pattern. The incidence of sudden cardiac death in patients with Wolff-Parkinson-White syndrome was estimated to be 70-450 per 100000 patient-years. WPW syndrome is more commonly observed among young patients. In one study WPW syndrome was observed in 7% of individuals over 60-year-old. Men are more commonly affected with WPW syndrome than women. The men to women ratio is approximately 2 to 1. There is no racial predilection for WPW syndrome.

Epidemiology and Demographics











  • Estimated prevalence of WPW syndrome is 1 – 3 per 1000 people in the entire world.[1]
  • Prevalence increases in first degree relatives in which it can get as high as 5-6 per 1000 people.[1]
  • The incidence of tachyarrhythmias is not well established in patients who present WPW pattern. It has been reported that the incidence of tachyarrhytmias is approximately 1% per year in patients with WPW pattern.[2]
  • The incidence of sudden cardiac death in patients with Wolff-Parkinson-White pattern is not high. A serious of studies have been performed and found a that this events appear in a range of 0.7 tp 4.5 per 1000 patient-years.[1][7][4]
  • Incidence of WPW is higher in men than in women in a ratio of approximately 2:1. Also, atrial fibrillation and ventricular fibrillation are more common in men than in women with WPW.[8]
  • Incidence of Orthodromic AVRT is more common in women than in men.[9]
  • The presentation of symptoms in patients without heart structural abnormalities has been found to be age dependent.[1]
  • The frequency of Supraventricular tachycardias (SVT) usually decrease during the first year in more than 90% of the patients.[1]
  • In 30% of the patients, tachycardias recur during childhood at a mean age of 7 to 8 years of age.[1]
  • When patients with WPW present persistent symptomatic tachycardias over 5 years of age, they usually continue presenting SVT episodes for more than a decade later in 75% of the cases.[1]
  • The occurrence of atrial fibrillation in patients with WPW ha been estimated in between 10% to 30%.[10][11]
* There is no racial predilection for WPW syndrome.

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 Pediatric and Congenital Electrophysiology Society (PACES). Heart Rhythm Society (HRS). American College of Cardiology Foundation (ACCF). American Heart Association (AHA). American Academy of Pediatrics (AAP). Canadian Heart Rhythm Society (CHRS); et al. (2012). “PACES/HRS expert consensus statement on the management of the asymptomatic young patient with a Wolff-Parkinson-White (WPW, ventricular preexcitation) electrocardiographic pattern: developed in partnership between the Pediatric and Congenital Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS). Endorsed by the governing bodies of PACES, HRS, the American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), the American Academy of Pediatrics (AAP), and the Canadian Heart Rhythm Society (CHRS)”. Heart Rhythm. 9 (6): 1006–24. doi:10.1016/j.hrthm.2012.03.050. PMID 22579340.
  2. ↑ 2.0 2.1 Fitzsimmons, PJ.; McWhirter, PD.; Peterson, DW.; Kruyer, WB. (2001). “The natural history of Wolff-Parkinson-White syndrome in 228 military aviators: a long-term follow-up of 22 years”. Am Heart J. 142 (3): 530–6. doi:10.1067/mhj.2001.117779. PMID 11526369. Unknown parameter |month= ignored (help)
  3. ↑ Obeyesekere, MN.; Leong-Sit, P.; Massel, D.; Manlucu, J.; Modi, S.; Krahn, AD.; Skanes, AC.; Yee, R.; Gula, LJ. (2012). “Risk of arrhythmia and sudden death in patients with asymptomatic preexcitation: a meta-analysis”. Circulation. 125 (19): 2308–15. doi:10.1161/CIRCULATIONAHA.111.055350. PMID 22532593. Unknown parameter |month= ignored (help)
  4. ↑ 4.0 4.1 Obeyesekere MN, Leong-Sit P, Massel D, Manlucu J, Modi S, Krahn AD; et al. (2012). “Risk of arrhythmia and sudden death in patients with asymptomatic preexcitation: a meta-analysis”. Circulation. 125 (19): 2308–15. doi:10.1161/CIRCULATIONAHA.111.055350. PMID 22532593.
  5. ↑ Brembilla-Perrot, B.; Yangni N’Da, O.; Huttin, O.; Chometon, F.; Groben, L.; Christophe, C.; Benzaghou, N.; Luporsi, J.D.; Tatar, C.; Bertrand, J.; Ammar, S.; Cedano, G.; Zhang, N.; Beurrier, D. (2008). “Wolff-Parkinson-White syndrome in the elderly: clinical and electrophysiological findings”. Archives of Cardiovascular Diseases. 101 (1): 18–22. doi:10.1016/S1875-2136(08)70250-X. ISSN 1875-2136.
  6. ↑ “http://www.cardiology.sk/casopis/606/pdf/04.pdf” (PDF). Retrieved 11 April 2014. External link in |title= (help)
  7. ↑ Obeyesekere, MN.; Leong-Sit, P.; Massel, D.; Manlucu, J.; Modi, S.; Krahn, AD.; Skanes, AC.; Yee, R.; Gula, LJ. (2012). “Risk of arrhythmia and sudden death in patients with asymptomatic preexcitation: a meta-analysis”. Circulation. 125 (19): 2308–15. doi:10.1161/CIRCULATIONAHA.111.055350. PMID 22532593. Unknown parameter |month= ignored (help)
  8. ↑ “http://www.cardiology.sk/casopis/606/pdf/04.pdf” (PDF). Retrieved 11 April 2014. External link in |title= (help)
  9. ↑ “http://www.cardiology.sk/casopis/606/pdf/04.pdf” (PDF). Retrieved 11 April 2014. External link in |title= (help)
  10. ↑ Campbell, RW.; Smith, RA.; Gallagher, JJ.; Pritchett, EL.; Wallace, AG. (1977). “Atrial fibrillation in the preexcitation syndrome”. Am J Cardiol. 40 (4): 514–20. PMID 910715. Unknown parameter |month= ignored (help)
  11. ↑ Sharma, AD.; Klein, GJ.; Guiraudon, GM.; Milstein, S. (1985). “Atrial fibrillation in patients with Wolff-Parkinson-White syndrome: incidence after surgical ablation of the accessory pathway”. Circulation. 72 (1): 161–9. PMID 4006127. Unknown parameter |month= ignored (help)

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Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Raviteja Guddeti, M.B.B.S. [3]

Overview

High-risk criteria for sudden cardiac death in Wolff-Parkinson-White syndrome during electrophysiology study include the presence of multiple accessory pathways, R-R interval <250 milliseconds in antegrade conduction of accessory pathway during inducing atrial fibrillation, sustained atrial fibrillation induced by AV re-entry tachycardia, precence of Structural heart disease such as ebstein anomaly or hypertrophic cardiomyopathy.

Risk Factors

High risk criteria for sudden cardiac death in Wolff-Parkinson-White syndrome during electrophysiology study include:[1][2][3]

References

  1. ↑ Cohen MI, Triedman JK, Cannon BC, Davis AM, Drago F, Janousek J, Klein GJ, Law IH, Morady FJ, Paul T, Perry JC, Sanatani S, Tanel RE (June 2012). “PACES/HRS expert consensus statement on the management of the asymptomatic young patient with a Wolff-Parkinson-White (WPW, ventricular preexcitation) electrocardiographic pattern: developed in partnership between the Pediatric and Congenital Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS). Endorsed by the governing bodies of PACES, HRS, the American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), the American Academy of Pediatrics (AAP), and the Canadian Heart Rhythm Society (CHRS)”. Heart Rhythm. 9 (6): 1006–24. doi:10.1016/j.hrthm.2012.03.050. PMID 22579340.
  2. ↑ Klein GJ, Bashore TM, Sellers TD, Pritchett EL, Smith WM, Gallagher JJ (November 1979). “Ventricular fibrillation in the Wolff-Parkinson-White syndrome”. N. Engl. J. Med. 301 (20): 1080–5. doi:10.1056/NEJM197911153012003. PMID 492252.
  3. ↑ Pappone C, Vicedomini G, Manguso F, Baldi M, Pappone A, Petretta A, Vitale R, Saviano M, Ciaccio C, Giannelli L, Calovic Z, Tavazzi L, Santinelli V (February 2012). “Risk of malignant arrhythmias in initially symptomatic patients with Wolff-Parkinson-White syndrome: results of a prospective long-term electrophysiological follow-up study”. Circulation. 125 (5): 661–8. doi:10.1161/CIRCULATIONAHA.111.065722. PMID 22215859.

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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Raviteja Guddeti, M.B.B.S. [3]

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Overview

Patients with WPW pattern can remain asymptomatic through all their lives, nearly 65% of adolescents and 40% of adults present ECG changes but remain asymptomatic. Complications Wolff-Parkinson-White syndrome is a consequence of symptomatic tachycardias and can occur at any age. Common complications of tachyarrhythmia associated WPW disease include reduced blood pressure and syncope, tachycaria induced cardiomyopathy, cardiac arrest, ventricular fibrillation, usdden cardiac death, complications of ablation, side effects of medications. SCD may occur in WPW syndrome due to rapid conduction of atrial fibrillation with heart rate >240/min to the ventricles via the accessory bypass tract leading ventricular fibrillation. Prognosis is generally excellent in asymptomatic WPW pattern.

Natural History

Wolff-Parkinson-White syndrome can be either asymptomatic or symptomatic. As it is difficult to evaluate asymptomatic patients, most information about the natural history of these patients has been taken from symptomatic patients.[1] Patients with WPW pattern can remain asymptomatic through all their lives, nearly 65% of adolescents and 40% of adults present ECG changes but remain asymptomatic.[2]

Complications

  • Complications Wolff-Parkinson-White syndrome is a consequence of symptomatic tachycardias and can occur at any age.
  • Most patients with this condition never experience symptoms associated with the accessory pathway.

Common complications of tachyarrhythmia associated WPW disease include:

Prognosis

  • Prognosis is generally excellent in asymptomatic WPW pattern.
  • Catheter ablation (radiofrequency ablation) has a success rate between 95 – 98%, which varies depending on the location and number of accessory pathways.
  • Successful ablation prevents future supraventricular tachyarrhythmia.
  • Even patients with worse prognosis regain a good prognosis with treatment using radio-frequency ablation.
  • The overall risk of death in patients with WPW syndrome reaches 0.15% every year.
  • Patients with WPW pattern can remain asymptomatic through all their lives, nearly 65% of adolescents and 40% of adults present ECG changes but remain asymptomatic.[2]
  • The risk of lethal arrhythmia in asymptomatic children is higher than adults.[3]
  • Long-term mortality in adult patients with WPW syndrome is low and similar to control patients without WPW.[4]
  • Long-term rates of atrial fibrillation in adult patients that present with WPW remains high despite ablation.[4]
  • Increased risk of atrial fibrillation in ablated WPW patients may be related atrial fibrillation genesis.[4]

References

  1. ↑ Pediatric and Congenital Electrophysiology Society (PACES). Heart Rhythm Society (HRS). American College of Cardiology Foundation (ACCF). American Heart Association (AHA). American Academy of Pediatrics (AAP). Canadian Heart Rhythm Society (CHRS); et al. (2012). “PACES/HRS expert consensus statement on the management of the asymptomatic young patient with a Wolff-Parkinson-White (WPW, ventricular preexcitation) electrocardiographic pattern: developed in partnership between the Pediatric and Congenital Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS). Endorsed by the governing bodies of PACES, HRS, the American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), the American Academy of Pediatrics (AAP), and the Canadian Heart Rhythm Society (CHRS)”. Heart Rhythm. 9 (6): 1006–24. doi:10.1016/j.hrthm.2012.03.050. PMID 22579340.
  2. ↑ 2.0 2.1 Obeyesekere MN, Leong-Sit P, Massel D, Manlucu J, Modi S, Krahn AD; et al. (2012). “Risk of arrhythmia and sudden death in patients with asymptomatic preexcitation: a meta-analysis”. Circulation. 125 (19): 2308–15. doi:10.1161/CIRCULATIONAHA.111.055350. PMID 22532593.
  3. ↑ Rao AL, Salerno JC, Asif IM, Drezner JA (July 2014). “Evaluation and management of wolff-Parkinson-white in athletes”. Sports Health. 6 (4): 326–32. doi:10.1177/1941738113509059. PMC 4065555. PMID 24982705.
  4. ↑ 4.0 4.1 4.2 Bunch, T. Jared; May, Heidi T.; Bair, Tami L.; Anderson, Jeffrey L.; Crandall, Brian G.; Cutler, Michael J.; Jacobs, Victoria; Mallender, Charles; Muhlestein, Joseph B.; Osborn, Jeffrey S.; Weiss, J. Peter; Day, John D. (2015). “Long-Term Natural History of Adult Wolff–Parkinson–White Syndrome Patients Treated With and Without Catheter Ablation”. Circulation: Arrhythmia and Electrophysiology. 8 (6): 1465–1471. doi:10.1161/CIRCEP.115.003013. ISSN 1941-3149.

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Diagnosis

Diagnosis

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Treatment

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