Wolff-Parkinson-White syndrome conduction

Conduction abnormalities Use caution in patients with sick sinus syndrome, Wolff-Parkinson-White syndrome or bundle branch block. 

Zolmitriptan- Patients with symptomatic Wolff-Parkinson-White syndrome or arrhythmias associated with other cardiac accessory conduction pathway disorders should not receive zolmitriptan. 

Cardiomyopathy Conduction blocks Wolff-Parkinson-White syndrome Inner ear... 

Digitalis should be avoided in the therapy of arrhythmias associated with Wolff-Parkinson-White syndrome because it increases the probability of conduction of arrhythmic atrial impulses through the alternative rapidly conducting atrioventricular pathway. It is explicitly contraindicated in patients with Wolff-Parkinson-White syndrome and atrial fibrillation (see Chapter 14 Agents Used in Cardiac Arrhythmias). 

It was recognized at the start of the 20th century that reentry in simple in vitro models (eg, rings of conducting tissues) was permanently interrupted by transecting the reentry circuit. This concept has now been applied to treat clinical arrhythmias that occur as a result of reentry in anatomically delineated pathways. For example, interruption of accessory atrio-ventricular connections can permanently cure arrhythmias in patients with the Wolff-Parkinson-White syndrome. Such... 

Some patients may experience hearing loss, which may accompany diabetes. Usually, type 2 diabetes is described in individuals with MELAS, although type 1 or insulin-dependent diabetes also may be observed. Palpitations and shortness of breath may be present in some patients with MELAS secondary to cardiac conduction abnormalities such as Wolff-Parkinson-White syndrome. Acute onset of gastrointestinal manifestations (e.g., acute onset of abdominal pain) may reflect pancreatitis, ischemic colitis, and intestinal obstruction. Numbness, tingling sensation, and pain in the extremities can be manifestations of peripheral neuropathy. Some patients may have the presentation of Leigh syndrome (i.e., subacute necrotizing encephalopathy). 

Adenosine is contraindicated in patients with aberrant conduction pathways, because it can cause cardiac dysrhythmias. Supraventricular dysrhythmias occurred in three children with Wolff-Parkinson-White syndrome who were given intravenous adenosine (22). 

Problems can also occur in patients with aberrant conduction pathways for example, verapamil caused an increased ventricular response in patients with Wolff-Parkinson-White syndrome associated with atrial fibrillation (9-11). The danger lies in provocation of ventricular fibrillation from advanced anterograde conduction in accessory pathways (12). 

The only calcium channel blocking drug to have been licensed for the treatment of cardiac arrhythmias is verapamil. Its main uses are in the treatment of supraventricular tachycardia (SVT) and paroxysmal SVT. Because verapamil lengthens the ERP and FRP of the AV node and prolongs AV nodal conduction time [16], it can be used to control the ventricular rate in atrial fibrillation or atrial flutter and it usually terminates re-entry arrhythmias involving the AV node [208, 209], However, intravenous verapamil should not be given to patients who have the Wolff-Parkinson-White syndrome and atrial... 

Supraventricular arrhythmias arising from accessory conduction pathways include Wolff-Parkinson-White syndrome (re-entrant arrhythmias). In this case, a depolarization and conduction occur in an accessory pathway, which circumvents the upper portion of the AV node and weakly depolarizes AV nodal tissue. Then, because the tissue is quickly repolarized, it is able to rapidly depolarize the upper portion of the AV node after depolarization of myocardial tissue, causing a re-entrant loop or circus rhythm. (The nodal tissue is normally refractory to stimulus, and thus serves as the termination stimulus for ventricular conduction.) The therapy of supraventricular arrhythmias involves partial blockade of the AV node. 

Flecainide slows conduction in all cardiac cells including the anomalous pathways responsible for the Wolff-Parkinson-White (WPW) syndrome. Together with encainide and moricizine, it underwent clinical trials to establish if suppression of asymptomatic premature beats with antiarrhythmic drugs would reduce the risk of death from arrhythmia after myocardial infarction. The study was terminated after preliminary analysis of 1727 patients revealed that mortality in the groups treated with flecainide or encainide was 7.7% compared with 3.0% in controls. The most likely explanation for the result was the induction of lethal ventricular arrhythmias possibly due to ischaemia by flecainide and encainide, i.e. a proarrhythmic effect. In the light of these findings the indications for flecainide are restricted to patients with no evidence of structural heart disease. The most common indication, indeed where it is the drug of choice, is atrioventricular re-entrant tachycardia, such as AV nodal tachycardia or in the tachycardias associated with the WPW syndrome or similar conditions with anomalous pathways. This should be as a prelude to definitive treatment with radiofrequency ablation. Flecainide may also be useful in patients with paroxysmal atrial fibrillation. 

Electrical impulses don t always follow normal conduction pathways in the heart. In preexcitation syndromes, electrical impulses enter the ventricles from the atria through an accessory pathway that bypasses the atrioventricular junction. Wolff-Parkinson-White (WPW) syndrome is a common type of preexcitation syndrome. 

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