Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q96S42 (nodal)
 22,877 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of tiapamil was studied in 9 patients with the Wolff-Parkinson-White syndrome using programmed stimulation of the heart. Before the drug, sustained orthodromic tachycardias could be initiated in 7 patients and antidromic tachycardia in 2 by premature atrial and/or ventricular stimulation. An intravenous bolus of tiapamil, 2 mg/kg, terminated the tachycardia in 7 out of 8 cases by a block in the atrioventricular (AV) node. Tiapamil lengthened the effective refractory period of the AV node in the only patient in whom it could be measured and the atrial effective refractory period in 1 out of 9 cases, but the drug had no influence on antegrade or retrograde refractory periods of the accessory pathway or on that of the ventricle. The AV nodal conduction time (A-H interval) was prolonged. Following tiapamil, it was not possible to initiate the tachycardia in 4 cases, in 2 patients the tachycardia zone widened, and in 3 it was unaltered. In the latter cases, the cycle length of the tachycardia was increased. Tiapamil appears to be useful for the termination of tachycardia and also for its prevention in some cases. In others, it may facilitate the inhibition of tachycardia. The delayed AV nodal conduction during sinus rhythm augments the area of ventricular preexcitation, which may facilitate the electrocardiographic localization of the accessory pathway.
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PMID:Effect of tiapamil in the Wolff-Parkinson-White syndrome. 616 96

The effect of 2 mg/kg intravenous tiapamil was studied by programmed stimulation of the heart in 6 patients. Before tiapamil, sustained tachycardias were initiated in 5, and only atrial echoes in 1. In all patients, the reentrant circuit involved an accessory pathway conducting only in the ventriculoatrial direction. When administered during tachycardia, tiapamil promptly terminated the arrhythmia in 5 cases. Tiapamil lengthened the atrio-His (A-H) interval and the effective refractory period of the A-V node. As a result of these changes, it was not possible to initiate the tachycardia in 1 patient. In 1 case, tiapamil permitted the induction of sustained tachycardia, while only echoes had been initiated before the drug. In 2 cases, the tachycardia zone narrowed, in 2 others it widened following tiapamil. The ability to sustain the arrhythmia was lost in 1 patient. Tiapamil may be useful for the termination of reentrant supraventricular tachycardia involving concealed accessory pathways. Whether tiapamil prevents or favors the initiation of tachycardia in these patients depends on the interplay between the prolongation of the effective A-V nodal refractory period and the prolongation of the transnodal conduction time in individual patients.
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PMID:Electrophysiology of tiapamil in concealed accessory pathways. 715 Oct 74

The effects of tiapamil were studied in 10 patients with antegrade preexcitation using programmed stimulation of the heart. Before administration of the drug, it was possible to initiate sustained orthodromic tachycardia in 7 patients, antidromic tachycardia in 2 and atrial echoes in 1 case by premature atrial and/or ventricular stimulation. An intravenous bolus of 2 mg/kg tiapamil terminated the tachycardia in 7 out of 8 cases by blocking the A-V node. The tachycardia continued at a reduced heart rate in 1 case with a nodoventricular bypass. Tiapamil lengthened the effective A-V nodal refractory period in 1 patient in whom it could be measured and the atrial effective refractory period in 1 case but did not prolong the antegrade or retrograde refractory periods of the accessory pathway. Only in 1 case was the antegrade effective refractory period of the accessory pathway shortened by tiapamil. The A-V nodal conduction time (A-H interval) was prolonged. Following tiapamil it was not possible to initiate the tachycardia in 4 cases and atrial echoes in 1 case; in 2 patients the tachycardia zone widened and in 3 it was not altered. In the latter, the cycle length of the tachycardia increased. Tiapamil appears to be of therapeutic value for the termination of tachycardia and also for its prevention in some cases. In others, it may facilitate the initiation of tachycardia. The delayed A-V nodal conduction during sinus rhythm augments the area of ventricular preexcitation which may facilitate the electrocardiographic localization of the accessory pathway.
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PMID:Effect of tiapamil in the preexcitation syndrome. 715 Oct 77