Paroxysmal tachycardia with widened QRS complexes was recorded in an eleven-year old boy who had suffered from brain damage, which had resulted from an episode of ventricular fibrillation. Atrial stimulation produced an increased AV conduction, sudden disappearance of the His bundle deflection and a complete left bundle branch block pattern. Tachycardias of this morphology were initiated by early atrial and ventricular premature beats. The findings suggested the presence of a macro re-entry circuit, utilizing a slow AV node- nodoventricular bypass tract as the anterograde limb and the His-Purkinje system--fast AV node as the retrograde limb. This supposition found further support by serial sectioning of the AV junctional area of the heart, which revealed a nodoventricular tract, which originated from the posterior extension of the compact part of the atrioventricular node and inserted into the crest of the ventricular septum.

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.

Congenital or acquired communication between the left ventricle and the right atrium is known as the Gerbode defect, which is rarely diagnosed since the defect is very unusual and for this reason often misinterpreted as an eccentric tricuspid regurgitation jet.The entity and reason of the defect is unknown to many physicians, so that profound knowledge and a careful and meticulous echocardiogram are necessary in order to prevent misinterpretation of this defect as a pulmonary hypertension.We report the case of a 76-year-old Austrian woman who developed such a Gerbode defect after a recent bioprosthetic aortic valve replacement.

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Summary:Electrophysiological studies were performed in a patient with paroxysmal supraventricular tachycardia and a normal surface ECG at the time of the study. Premature atrial stimulation revealed dual AV conduction and an echo zone during AV conduction over the fast and the slow pathway. The prolongation of the AV conduction time by a calcium antagonist, Ro 11-1781, permitted the induction of tachycardias via both pathways. Premature ventricular stimulation yielded constant VA conduction times with activation of the low right atrium before the high right atrium before the left atrium. During the tachycardia, premature right ventricular beats conducted to the atrium at a time when the AV node and the His bundle would be refractory. The study suggests the simultaneous occurrence of an occult accessory bundle connecting the right ventricle to the right atrium and dual AV conduction.Keywords: AV node, calcium antagonist, preexcitation, reentry, refractory period Supported by the ,,Fonds zur Forderung der wissenschaftlichen Forschung in Osterreich" (Project 1554).