Wolff-Parkinson-White syndrome overview: Difference between revisions
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==Overview== | ==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 of 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 node|sinoatrial]] (SA) node (located in the [[right atrium]]), propagates to the [[atrioventricular node|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]]. 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 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. | [[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 of 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 node|sinoatrial]] (SA) node (located in the [[right atrium]]), propagates to the [[atrioventricular node|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]]. 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 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. | ||
==Historical Perspective== | ==Historical Perspective== | ||
Revision as of 20:21, 9 November 2020
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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 of 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 (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 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.
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.
Causes
Differentiating Xyz from Other Diseases
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.
Screening
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.