Disease relevance of Wolff-Parkinson-White Syndrome

• Mutations in PRKAG2, the gene for the gamma 2 regulatory subunit of AMP-activated protein kinase, cause cardiac hypertrophy and electrophysiologic abnormalities, particularly preexcitation (Wolff-Parkinson-White syndrome) and atrioventricular conduction block [1].
• Lidocaine in Wolff-Parkinson-White syndrome with atrial fibrillation [2].
• This study shows that long-term treatment with sotalol is highly effective in patients with the Wolff-Parkinson-White syndrome and regular supraventricular tachycardia [3].
• Encainide is well tolerated and prevents recurrence of reentrant tachycardia in patients with Wolff-Parkinson-White syndrome very effectively [4].
• In 12 patients (nine with Wolff-Parkinson-White syndrome and three with ventricular tachycardia) the electrophysiologic effects of intravenous (5 mg/kg body weight in 1 min) and oral (total dose 9800 to 11,200 mg) amiodarone were studied with programmed stimulation of the heart [5].

Psychiatry related information on Wolff-Parkinson-White Syndrome

• CASE SUMMARY: A 77-year-old woman with a history of hypertension, insulin-dependent diabetes mellitus, temporal arteritis, and Wolff-Parkinson-White syndrome who had taken procainamide for six weeks presented to the hospital with disorientation and acute renal and hepatic dysfunction [6].

High impact information on Wolff-Parkinson-White Syndrome

• RESULTS: A total of 31 members (23 from Family 1 and 8 from Family 2) had the Wolff-Parkinson-White syndrome [7].
• Overall, 5 of 51 LHON patients and 9 of 112 symptom-free maternal relatives had Wolff-Parkinson-White syndrome (9%) [8].
• Proarrhythmia in patients with the Wolff-Parkinson-White syndrome after standard doses of intravenous adenosine [9].
• Procainamide infusion test: inability to identify patients with Wolff-Parkinson-White syndrome who are potentially at risk of sudden death [10].
• Sotalol in patients with Wolff-Parkinson-White syndrome [3].

Chemical compound and disease context of Wolff-Parkinson-White Syndrome

• Intravenous amiodarone slowed (p less than .05) the rate of circus-movement tachycardia in patients with Wolff-Parkinson-White syndrome, and further slowing was observed after oral amiodarone [5].
• We examined the electrophysiologic effects of verapamil in eight patients with the Wolff-Parkinson-White syndrome [11].
• Electrophysiologic effects of disopyramide phosphate in patients with Wolff-Parkinson-White syndrome [12].
• Clinical efficacy and electrophysiologic effects of encainide in patients with Wolff-Parkinson-White syndrome [4].
• Effects of procainamide and quinidine sulfate in the Wolff-Parkinson-White syndrome [13].

Biological context of Wolff-Parkinson-White Syndrome

• CONCLUSION: In the setting of electrophysiology testing, adenosine triphosphate is a safe agent, even when administered inappropriately during arrhythmias for which it is relatively ineffective, such as ventricular tachycardia, and Wolff-Parkinson-White syndrome with atrial fibrillation [14].
• Molecular genetic analysis of PRKAG2 in sporadic Wolff-Parkinson-White syndrome [15].

Anatomical context of Wolff-Parkinson-White Syndrome

• Propofol has no direct effect on sinoatrial node function or on normal atrioventricular and accessory pathway conduction in Wolff-Parkinson-White syndrome during alfentanil/midazolam anesthesia [16].
• Concomitant operative procedures were performed upon four patients, including division of the accessory atrioventricular pathway for the Wolff-Parkinson-White syndrome in two patients, plication of the right atrium for idiopathic right atrial dilatation in one patient, and a closure of the atrial septal defect in one patient [17].
• This study was designed to assess the effects of isoflurane (ISO) on the electrophysiological properties of the accessory pathway, atrium, ventricle, and AV node in children with the Wolff-Parkinson-White (WPW) syndrome [18].
• A surgically treated case of both Wolff-Parkinson-White syndrome and atrial septal defect complicating single coronary artery and partial pericardial defect [19].
• The effects of atropine on atrio-ventricular conduction in patients with Wolff-Parkinson-White syndrome. Studies with His bundle electrogram [20].

Gene context of Wolff-Parkinson-White Syndrome

• We now describe mutations in PRKAG2, encoding the gamma(2) subunit of AMP-activated protein kinase (AMPK), in two families with severe HCM and aberrant conduction from atria to ventricles in some affected individuals (pre-excitation or Wolff-Parkinson-White syndrome) [21].
• Transgenic mouse model of ventricular preexcitation and atrioventricular reentrant tachycardia induced by an AMP-activated protein kinase loss-of-function mutation responsible for Wolff-Parkinson-White syndrome [22].
• This is a report of a 10-year-old child who underwent surgery for complex congenital heart disease consisting of corrected transposition of the great vessels, ventricular septal defect, patent ductus arterisus, severe left-sided atrioventricular (AV) valve insuffieicney (Ebstein's deformity) and Wolff-Parkinson-White syndrome [23].
• Tuberous sclerosis and Wolff-Parkinson-White syndrome [24].
• The child has hypertrophic cardiomyopathy with Wolff-Parkinson-White syndrome [25].

Analytical, diagnostic and therapeutic context of Wolff-Parkinson-White Syndrome

• Many patients with the WPW syndrome require long-term maintenance drug therapy (propranolol, digitalis or quinidine in most cases) [26].
• The electrophysiologic effects of encainide were studied in 10 patients with Wolff-Parkinson-White syndrome after intravenous (1 mg kg-1 in 60 minutes) and oral administration of two dose regimens (75 and 150 mg daily) [27].
• The effect of amiodarone in the Wolff-Parkinson-White syndrome was studied with programmed electrical stimulation of the heart in 15 patients [28].
• Propranolol, by rapid intravenous infusion administration, is unlikely to be effective primary therapy for PSVT in the WPW syndrome [29].
• Effects of intravenous injection of 0.6 mg/kg sotalol, a beta-blocking agent with additional class III properties, were studied by means of electrophysiologic techniques in 14 patients, seven with the Wolff-Parkinson-White syndrome and seven with concealed atrioventricular (AV) accessory pathways [30].

References