Preexcitation was defined by Durrer et al in 1970 when they wrote, "Preexcitation exists, if in relation to atrial events, the whole or some part of the ventricular muscle is activated earlier by the impulse originating from the atrium than would be expected if the impulse reached the ventricles by way of the normal specific conduction system only." Wolff-Parkinson-White (WPW) syndrome is a congenital abnormality involving the presence of abnormal conductive tissue between the atria and the ventricles that is often in association with supraventricular tachycardia (SVT). It involves activation of the ventricles that occurs earlier than anticipated (preexcitation), which occurs because of conduction of an atrial impulse not by means of the normal conduction system, but via an extra atrioventricular (AV) muscular connection, termed an accessory pathway, that bypasses the AV node.1
Classic electrocardiographic (ECG) findings that are associated with WPW syndrome include the following:
Presence of a short PR interval (<120 ms)
A wide QRS complex of longer than 120 milliseconds with a slurred onset of the QRS waveform producing a delta wave in the early part of QRS
Secondary ST-T wave changes
Patients with WPW syndrome are potentially at an increased risk of dangerous ventricular arrhythmias due to extremely fast conduction across the bypass tract if they develop fast supraventricular arrhythmias, such as atrial flutter or fibrillation.
Patients with a concealed bypass tract are also discussed in this article. While they have an accessory AV connection, it lacks antegrade conduction, and accordingly they do not have the classical abnormalities of the surface ECG.
Only a small number of patients with WPW syndrome are at risk for sudden death. In these patients, cardiac electrophysiologic (EP) studies and radiofrequency (RF) catheter ablation may be curative. Other presentations include symptomatic SVT, which can also be cured by catheter ablation. Asymptomatic patients, who form the majority, may merely need periodic observation.
This review discusses the pathogenesis, clinical presentation, evaluation, and treatment of patients with WPW syndrome.
Patients with preexcitation are at risk of developing supraventricular tachycardia (SVT) generally due to a reentrant mechanism, of which the accessory connections often play an essential role. The genesis of reentrant SVT involves the presence of dual conducting pathways between the atria and the ventricles.2 These pathways are as follows:
The natural AV nodal His-Purkinje tract
An AV accessory tract (ie, AV connection or bypass tract, Kent fibers, Mahaim fibers)
These 2 pathways usually exhibit 2 different conduction properties and refractory periods that facilitate reentry. The effective refractory period (ERP) of the accessory tract is usually longer than that of the normal AV nodal His-Purkinje tract. Several types of SVT have been described, including orthodromic tachycardias, orthodromic tachycardia with a concealed accessory pathway, and antidromic tachycardia.
When a premature ectopic atrial impulse begins to traverse down towards the ventricle, it may block at the accessory tract but conduct in antegrade fashion down the normal pathway, which includes the AV node. The impulse then reenters the accessory tract in retrograde fashion to perpetuate a circus movement of the impulse. Such reentrant tachycardia is described as orthodromic. Premature ventricular contractions (PVCs) can also initiate orthodromic tachycardia.
In orthodromic tachycardia, the normal pathway is used for ventricular depolarization and the accessory tract is used for the retrograde conduction essential for reentry. On ECG findings, the delta wave is absent, QRS complex is normal, and P waves are inverted in the inferior and lateral leads.
Orthodromic tachycardia with a concealed accessory pathway
Some accessory (bypass) tracts are unable to conduct in the antegrade fashion. These are called concealed accessory pathways (ie, concealed WPW syndrome). Although no evidence of the pathway is present during sinus rhythm (ie, no preexcitation), orthodromic tachycardias can occur. Orthodromic tachycardia may also occur when there are 2 or more accessory connections, and, in that case, the retrograde conduction may occur either through the AV node and/or one of the accessory connections.
Differentiation between this type of SVT and usual AV nodal reentrant tachycardia (AVNRT) may be difficult on the standard surface ECG. Nonetheless, if the heart rate is higher than 200 beats per minute and a retrograde P wave is visible following the QRS complex, a concealed accessory pathway may be the diagnosis.
Less commonly, a shorter refractory period in the accessory tract may cause block of an ectopic atrial impulse in the normal pathway, with antegrade conduction down the accessory tract and then retrograde reentry of the normal pathway. This type of tachycardia produced is called antidromic tachycardia.
On ECG findings, the QRS is wide, which is an exaggeration of the delta wave during sinus rhythm (ie, wide-QRS tachycardia). Such tachycardias are difficult to differentiate from ventricular tachycardia.
Thus, the mechanism underlying the majority of the tachycardias in patients with WPW syndrome is macroreentry caused by antegrade conduction over the AV node His bundle pathway and retrograde conduction over an accessory pathway (orthodromic). Less common in patients with WPW syndrome is antidromic tachycardia. Even when the accessory pathway conducts only in retrograde fashion, it can still participate in the reentrant circuit and produce an orthodromic AV reciprocating tachycardia.
The prevalence of ventricular preexcitation is thought to be 0.1-0.3% in the general population. Estimates of arrhythmia incidence in patients with preexcitation vary widely, ranging from 12-80% in several surveys.
Incidence of preexcitation and WPW syndrome varies from 0.1-3 cases per thousand population (average of 1.5 cases per thousand population) in otherwise healthy persons.
In a review of ECG findings from 22,500 healthy aviation personnel, 0.25% exhibited findings consistent with the WPW pattern, with 1.8% incidence of tachycardia.
The location of the accessory pathways, in descending order of frequency, is (1) the left free wall, (2) posteroseptal, (3) right free wall, and (4) anteroseptal.
The presence of concealed accessory pathways accounts for approximately 30% of patients with apparent SVT referred for EP evaluation.
Approximately 80% of patients with WPW syndrome have a reciprocating tachycardia, 15-30% have atrial fibrillation, and 5% have atrial flutter. Ventricular tachycardia is uncommon.
Incidence and prevalence of WPW syndrome worldwide parallels that in the United States.
Patients with WPW syndrome have a very small risk of sudden arrhythmic death. Medical therapy with agents such as digoxin may increase this risk. The risk in asymptomatic patients is extremely low.
Overall, sudden death occurs rarely, with an estimated frequency rate of 0.1%.
Other factors that appear to influence risk are the presence of multiple bypass tracts and a family history of premature sudden death. Sudden cardiac death is unusual without preceding symptoms.
Morbidity may be related to rapid near syncopal or syncopal arrhythmias. Even when syncope is absent, the arrhythmia episodes may be highly symptomatic. The potential for syncope, hemodynamically compromising rhythms, or sudden death may prevent patients with WPW from participating in competitive sports or hazardous occupations until the substrate is definitively addressed in an ablative procedure.
No clear racial predilection appears to exist.
Prevalence may be higher in males.
Certain factors exist regarding age and the prevalence of preexcitation and WPW syndrome.
WPW syndrome is found in persons of all ages, from those in fetal and neonatal age groups to elderly individuals.
Prevalence decreases with age because of loss of preexcitation. Cases have been described in which electrocardiographic evidence of preexcitation disappears.
In patients with abnormal ECG findings indicative of WPW syndrome, the frequency of SVT paroxysms increases from 10% in people aged 20-39 years to 36% in people older than 60 years.3
WPW syndrome can result in SVT that uses an AV accessory (bypass) tract. The accessory pathway may also act as an innocent bystander and allow conduction during other supraventricular arrhythmias, such as atrial fibrillation or flutter. The possibility of a concealed bypass tract as a mechanism underlying certain types of SVT should be considered because treatment options may vary. Paradoxically, the use of digoxin and perhaps other AV nodal blocking agents may accelerate conduction through the bypass tract, causing potentially lethal ventricular arrhythmias or hemodynamic instability during atrial fibrillation.
SVT in WPW syndrome may begin in childhood or may not appear clinically until the patient reaches middle age. In some patients in whom it first presents during childhood, it may then cease for some time, only to recur. In fact, the probability is 75% that the tachycardia will persist if it is still present in patients older than 5 years.
In asymptomatic patients, the probability of losing the capacity for antegrade conduction across the accessory pathway increases with advancing age. This probably results from fibrotic changes at the site of insertion of the accessory bypass tract.
In patients with WPW syndrome, the tachycardia that produces symptoms may be an SVT, atrial fibrillation, or atrial flutter. In a series of 212 patients with tachyarrhythmias and WPW syndrome, SVT alone occurred in 64%, atrial fibrillation alone in 20%, and both occurred in 16% of patients.
Light-headedness and near syncope appear to occur more commonly in persons with WPW syndrome who have paroxysmal SVT (PSVT) or atrial fibrillation than in those with AV nodal reentry.
Syncope can occur because of inadequate cerebral circulation due to a rapid ventricular rate or because the tachyarrhythmia is depressing the sinus pacemaker, causing a period of asystole at the point of tachycardia termination.
PSVT can be followed after termination by polyuria, which is due to atrial dilatation and release of atrial natriuretic factor.
During SVT, the rhythm is unvarying and regular, with constant intensity of the first heart sound.
The jugular venous pressure can be elevated, but the waveform generally remains constant.
Clinical features of associated cardiac defects may be present, such as the following:
Ebstein anomaly: Patients with right-sided accessory pathways should be screened for the Ebstein anomaly.
Hypertrophic cardiomyopathy (AMPK mutation)
The abnormal QRS complexes of WPW syndrome, when present, may appear similar to those observed in acute myocardial infarction (MI). Repolarization abnormalities are common in patients with WPW syndrome.
In patients with WPW syndrome, the underlying cardiac structural abnormality consists of accessory conduction tissue that bypasses the normal AV node His-Purkinje system pathway. Such pathways are generally believed to be congenital in nature.
The causes of WPW syndrome can be summarized as follows:
Congenital or hereditary
An accessory pathway is quite likely to be congenital, although its manifestations can be detected in later years and it may appear to be acquired.
Relatives of patients with preexcitation, particularly those with multiple pathways, have an increased prevalence of preexcitation, suggesting a hereditary mode of acquisition.
Associated with congenital cardiac defects
Patients with the Ebstein anomaly may develop WPW syndrome. Patients with the Ebstein anomaly frequently have multiple accessory bypass tracts, mostly right-sided, in the posterior part of the septum or the posterolateral wall. Preexcitation generally occupies the atrialized ventricle. The orthodromic reciprocating tachycardia in such patients exhibits right bundle-branch block (RBBB) and a long ventriculoatrial (VA) interval.
Hypertrophic cardiomyopathy may include idiopathic hypertrophic subaortic stenosis or asymmetric septal hypertrophy.
Associated with other acquired cardiac defects - Cardiomyopathies
Abu Zubair meriwayatkan dari Jabir bin Abdullah bahwa Nabi Muhammad SAW bersabda:
"Setiap penyakit ada obatnya. Jika obat yang tepat diberikan dengan izin Allah, penyakit itu akan sembuh".
(HR. Muslim, Ahmad dan Hakim).
Kamis, 24 Desember 2009
Diposting oleh FX di 07.29
The Holy Al-Qur'an (English version)
- Surah 1 - Al Fatiha THE OPENING
- Surah 2 - Al Baqarah THE HEIFER
- Surah 3 - Ali 'Imran - THE FAMILY OF 'IMRAN
- Surah 4 - Al-Nisa' THE WOMEN
- Surah 5 - Al Ma'idah THE REPAST
- Surah 6 - Al An'am THE CATTLE
- Surah 7 - Al A'raf THE HEIGHTS
- Surah 8 - Al Anfal THE SPOILS OF WAR
- Surah 9 - Al Tawbah THE REPENTANCE
- Surah 10 - Yunus JONAH
- Surah 11 - Hud THE PROPHET HUD
- Surah 12 - Yusuf JOSEPH
- Surah 13 - Al Ra'd THE THUNDER
- Surah 14 - Ibrahim ABRAHAM
- Surah 15 - Al Hijr THE ROCKY TRACT
- Surah 16 - Al Nahl BEES
- Surah 17 - Al Isra' THE NIGHT JOURNEY
- Surah 18 - Al Kahf THE CAVE
- Surah 19 - Maryam MARY
- Surah 20 - TA HA
- Surah 21 - Al Anbiya THE PROPHETS
- Surah 22 - Al Hajj THE PILGRIMAGE
- Surah 23 - Al Mu'minun THE BELIEVERS
- Surah 24 - Al Nur THE LIGHT
- Surah 25 - Al Furqan THE CRITERION
- Surah 26 - Al Shu'ara' THE POETS
- Surah 27 - Al Naml THE ANTS
- Surah 28 - Al Qasas THE NARRATIONS
- Surah 29 - Al 'Ankabut THE SPIDER
- Surah 30 - Al Rum THE ROMANS
- Surah 31 - Luqman LUQMAN
- Surah 32 - Al Sajdah THE PROSTRATION
- Surah 33 - Al Ahzab THE CONFEDERATES
- Surah 34 - Saba' SHEBA
- Surah 35 - Fatir THE ORIGINATOR OF CREATION
- Surah 36 - Ya Sin YA SIN
- Surah 37 - Al Saffat THOSE RANGED IN RANKS
- Surah 38 - Sad SAD
- Surah 39 - Al Zumar CROWDS
- Surah 40 - Ghafir FORGIVER
- Surah 41 - Fussilat EXPOUNDED
- Surah 42 - Al Shura CONSULTATION
- Surah 43 - Al Zukhruf THE GOLD ADORNMENTS
- Surah 44 - Al Dukhan THE SMOKE
- Surah 45 - Al Jathiyah THE KNEELING DOWN
- Surah 46 - Al Ahqaf WINDING SAND-TRACTS
- Surah 47 - Muhammad MUHAMMAD
- Surah 48 - Al Fath THE VICTORY
- Surah 49 - Al Hujurat THE CHAMBERS
- Surah 50 - Qaf QAF
- Surah 51 - Al Dhariyat THE WINDS THAT SCATTER
- Surah 52 - Al Tur THE MOUNT
- Surah 53 - Al Najm THE STAR
- Surah 54 - Al Qamar THE MOON
- Surah 55 - Al Rahman THE MOST GRACIOUS
- Surah 56 - Al Waq'iah THE INEVITABLE
- Surah 57 - Al Hadid IRON
- Surah 58 - Al Mujadilah THE WOMAN WHO PLEADS
- Surah 59 - Al Hashr THE MUSTERING
- Surah 60 - Al Mumtahinah THAT WHICH EXAMINES
- Surah 61 - Al Saff THE BATTLE ARRAY
- Surah 62 - Al Jumu'ah FRIDAY
- Surah 63 - Al Munafiqun THE HYPOCRITES
- Surah 64 - Al Taghabun THE MUTUAL LOSS AND GAIN
- Surah 65 - Al Talaq DIVORCE
- Surah 66 - Al Tahrim PROHIBITION
- Surah 67 - Al Mulk THE DOMINION
- Surah 68 - Al Qalam THE PEN
- Surah 69 - Al Haqqah THE SURE REALITY
- Surah 70 - Al Ma'arij THE WAYS OF ASCENT
- Surah 71 - Nuh NOAH
- Surah 72 - Al Jinn THE SPIRITS
- Surah 73 - Al Muzzammil THE ENFOLDED ONE
- Surah 74 - Al Muddaththir THE ONE WRAPPED UP
- Surah 75 - Al Qiyamah THE RESURRECTION
- Surah 76 - Al Insan MAN
- Surah 77 - Al Mursalat THOSE SENT FORTH
- Surah 78 - Al Naba' THE GREAT NEWS
- Surah 79 - Al Nazi'at THOSE WHO TEAR OUT
- Surah 80 - 'Abasa HE FROWNED
- Surah 81 - Al Takwir THE FOLDING UP
- Surah 82 - Al Infitar THE CLEAVING ASUNDER
- Surah 83 - Al Mutaffifin THE DEALERS IN FRAUD
- Surah 84 - Al Inshiqaq THE RENDING ASUNDER
- Surah 85 - Al Buruj THE CONSTELLATIONS
- Surah 86 - Al Tariq THE NIGHT STAR
- Surah 87 - Al A'la THE MOST HIGH
- Surah 88 - Al Ghashiyah THE OVERWHELMING EVENT
- Surah 89 - Al Fajr THE DAWN
- Surah 90 - Al Balad THE CITY
- Surah 91 - Al Shams THE SUN
- Surah 92 - Al Layl THE NIGHT
- Surah 93 - Al Duha THE GLORIOUS MORNING LIGHT
- Surah 94 - Al Sharh THE EXPANSION OF THE BREAST
- Surah 95 - Al Tin THE FIG
- Surah 96 - Al Alaq THE CLINGING CLOT
- Surah 97 - Al Qadr THE NIGHT OF POWER
- Surah 98 - Al Bayyinah THE CLEAR EVIDENCE
- Surah 99 - Al Zalzalah THE EARTHQUAKE
- Surah 100 - Al 'Adiyat THOSE THAT RUN
- Surah 101 - Al Qari'ah THE GREAT CALAMITY
- Surah 102 - Al Takathur THE PILING UP
- Surah 103 - Al 'Asr TIME THROUGH THE AGES
- Surah 104 - Al Humazah THE SCANDALMONGER
- Surah 105 - Al Fil THE ELEPHANT
- Surah 106 - Quraysh THE TRIBE OF QURAYSH
- Surah 107 - Al Ma'un THE NEIGHBOURLY ASSISTANCE
- Surah 108 - Al Kawthar THE ABUNDANCE
- Surah 109 - Al Kafirun THOSE WHO REJECT FAITH
- Surah 110 - Al Nasr THE HELP
- Surah 111 - Al Masad THE PLAITED ROPE
- Surah 112 - Al Ikhlas THE PURITY OF FAITH
- Surah 113 - Al Falaq THE DAYBREAK
- Surah 114 - Al Nas MANKIND
- Acute Coronary Syndromes
- Angina Pectoris
- Anomalous Left Coronary Artery From the Pulmonary Artery
- Aortic Coarctation
- Aortic Dissection
- Aortic Regurgitation
- Aortic Stenosis
- Aortic Stenosis, Subaortic
- Aortic Stenosis, Supravalvar
- Ashman Phenomenon
- Atrial Fibrillation
- Atrial Flutter
- Atrial Myxoma
- Atrial Septal Defect
- Atrial Tachycardia
- Atrioventricular Block
- Atrioventricular Dissociation
- Atrioventricular Nodal Reentry Tachycardia (AVNRT)
- Benign Cardiac Tumors
- Brugada Syndrome
- Complications of Myocardial Infarction
- Coronary Artery Atherosclerosis
- Coronary Artery Vasospasm
- Digitalis Toxicity
- Dissection, Aortic
- Ebstein Anomaly
- Eisenmenger Syndrome
- First-Degree Atrioventricular Block
- HACEK Group Infections (Infective Endocarditis)
- Heart Failure - Decompensatio Cordis
- Holiday Heart Syndrome
- Hypertensive Heart Disease
- Junctional Rhythm
- Loeffler Endocarditis
- Long QT Syndrome
- Lutembacher Syndrome
- Mitral Regurgitation
- Mitral Stenosis
- Mitral Valve Prolapse
- Myocardial Infarction
- Myocardial Rupture
- Paroxysmal Supraventricular Tachycardia
- Patent Ductus Arteriosus
- Patent Foramen Ovale
- Pericardial Effusion
- Pericarditis Acute
- Pericarditis, Constrictive
- Pericarditis, Constrictive-Effusive
- Pulmonic Regurgitation
- Pulmonic Stenosis
- Right Ventricular Infarction
- Saphenous Vein Graft Aneurysms
- Second-Degree Atrioventricular Block
- Sinus of Valsalva Aneurysm
- Sudden Cardiac Death
- Tetralogy of Fallot
- Third-Degree Atrioventricular Block
- Torsade de Pointes
- Tricuspid Regurgitation
- Tricuspid Stenosis
- Unstable Angina
- Ventricular Fibrillation
- Ventricular Septal Defect
- Ventricular Tachycardia
- Wolff-Parkinson-White Syndrome