LONG GANONG LEVINE SYNDROME PDF

Last Update: December 14, Introduction Pre-excitation is a term that refers to the premature activation of the ventricles. Previously used when referring to Wolff-Parkinson-White WPW , pre-excitation has been expanded to include any rhythm with antegrade ventricular or retrograde atrial activation via an accessory pathway. These pathways may be partially or completely separate from the normal conduction system.

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Last Update: December 14, Introduction Pre-excitation is a term that refers to the premature activation of the ventricles. Previously used when referring to Wolff-Parkinson-White WPW , pre-excitation has been expanded to include any rhythm with antegrade ventricular or retrograde atrial activation via an accessory pathway. These pathways may be partially or completely separate from the normal conduction system.

Multiple studies have evaluated the underlying pathway for WPW, which researchers call the bundle of Kent. The bundle of Kent takes the form of myocytes that bypass the AV node junction resulting in the direct activation of the ventricular myocardium by the accessory pathway. The current theory is that Lown-Ganong-Levine syndrome may result from multiple underlying causes involving pathways that partially or completely bypass the AV node with subsequent normal conduction down the bundle of His.

Epidemiology The Lown-Ganong-Levine pattern has been reported in a wide age range of patients and has not been shown to display increased incidence in one particular sex or ethnic background.

This number compares to an incidence of less than 0. Previously, Lown-Ganong-Levine was thought to utilize the bundle of James, which is an accessory pathway connecting the atria to the distal segments of the AV nodes or the proximal bundle of His. However, studies have been unable to isolate a unique pathway in multiple individuals. Other potential anatomic tracts by which the Lown-Ganong-Levine pattern may occur include Brechenmacher fibers or intranodal bypass tracts.

Brechenmacher fibers are quite rare, reported in less than 0. Regardless, these fibers are theorized to serve as bypass tracts that run from the atrium to the bundle of His and as a result, are considered to represent a potential cause of LGL. Intranodal bypass tracts are anatomically located with the AV node but allow for rapid conduction through the AV node. As a result, there are also proposals for intranodal bypass tracts as a cause of the LGL pattern.

History and Physical Findings that may be associated with the history and physical in patients with Lown-Ganong-Levine are rather scarce. Occasionally, while taking a history, some patients will note occasional palpitations or endorse a prior history of paroxysmal atrial fibrillation or other atrial arrhythmias.

On physical exam, again, findings are limited in LGL. During cardiac auscultation or palpating pulses, the examiner could potentially sense the irregular rhythm with a change of underlying rhythm. The finding of a short PR interval and the normal QRS complex is thought to be the result of a perinodal accessory pathway utilizing the bundle of James. Routine laboratory evaluation, including hormone levels thyroid-stimulating hormone and electrolytes potassium or magnesium , may require monitoring; however, replacement in deficiency has not at this time been shown to affect Lown-Ganong-Levine pattern.

Vagal maneuvers have previously demonstrated accentuation of a variety of arrhythmias and may be an option; their use in the identification of LGL pattern has not been studied at this time. While use has not previously been a target of research in the evaluation of LGL, outpatient ambulatory monitoring with Holter monitors of loop recorders should be a decision left to the discretion of the treating physician.

Emergency treatment is not typically necessary as LGL pattern itself has no established correlations with hemodynamic compromise. Instead, treatment focuses on the prevention of tachyarrhythmias via the accessory pathway. Medications utilized previously include digitalis, beta-blockers, calcium channel blockers CCB and either class I or III antiarrhythmics. At this time, minimal randomized control trials have taken place, and the data regarding the management of LGL in reported cases has been controversial.

In cases refractory to medical therapy, as with other supraventricular tachycardias or accessory pathways, radiofrequency catheter ablation has become a preferred treatment. Patients who display reentrant tachycardia with short PR intervals may benefit from an accessory pathway or partial AV nodal ablation. In a patient with atrial flutter or fibrillation and rapid ventricular response suspected to be secondary to LGL, complete heart block is inducable via RFA followed by implantation of a pacemaker.

Prognosis Prognosis appears to be good in patients with Lown-Ganong-Levine syndrome. While patients with LGL patterns are typically asymptomatic, due to a propensity to develop atrial fibrillation, atrial flutter, AVRT or another tachyarrhythmia, these patients have been known to report palpitations or other associated symptoms.

As a result, they are often considered to be at similar risk for stroke or other associated complications as patients with these tachyarrhythmias.

In rare cases, there have been suggestions regarding the development of more concerning rhythms such as ventricular tachycardia. Certain medications that enhance conduction through the AV node make AVRT, and some atrial tachycardias occur; this is thought to occur due to alteration in the conduction and refractoriness of the AV node or atrial myocardium.

As a result, some medications, such as sympathomimetics, should be utilized with caution in these patients. Consultations Patients with suspected Lown-Ganong-Levine may benefit from consultation by general cardiology and, if available, electrophysiology for the evaluation of potential bypass tracts within the conduction system.

The diagnosis of LGL requires the use of a resting EKG, where these patients typically display a pattern of short PR interval but normal QRS complex duration, however, electrophysiology should be consulted to evaluate for the presence of a bypass tract within the conduction system.

Pearls and Other Issues The description of the Lown-Ganong-Levine pattern is as an accessory pathway that partially or wholly bypasses the atrioventricular AV node resulting in the direct activation of the bundle of His by the sinoatrial SA node.

Findings associated with a routine history and physical are rather scarce. Cardiology specialty nursing staff trained in telemetry may aid in the diagnosis of Lown-Ganong-Levine pattern if patients with associated symptoms of palpitations or lightheadedness are found to display LGL pattern on telemetry, and can assist in monitoring and assessing treatment effectiveness once the treating physician has initiated therapy.

The healthcare team should also include a specialized cardiology pharmacist who can consult regarding anti-arrhythmic pharmaceutical therapy, verifying dosing, offering alternative agents as options if initial treatment is ineffective, and checking for drug-drug interactions.

Nurses, pharmacists, and other ancillary staff should have the freedom to voice concerns to the physicians and specialists on the case, ensuring they have a voice at the table in contributing to the overall success of the interprofessional team in directing patient outcomes positively.

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Lown-Ganong-Levine Syndrome ECG Review

The condition was first described in before the advent of electrophysiological testing, and some people dispute its existence as an entity[ 3 ]. Where there is a short PR interval but no history of supraventricular tachycardia SVT , it is probably just a variation of normal. Where arrhythmias have been investigated in people with the diagnostic criteria, another cause has often been found. Sometimes the duration of conduction through the AV node is fast and this is called enhanced atrioventricular nodal conduction EAVNC [ 1 ]. Although tachycardia, along with increased stroke volume, enables cardiac output to meet demands in exercise, a very fast tachycardia is inefficient and may cause compromise. The ventricles do not have adequate time to fill in diastole and this may reduce cardiac output. Tachycardia reduces the duration of both systole and diastole but it is diastole that is reduced more.

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