Nodal function in 30 patients with atrioventricular nodal 1/1 conduction above 200/mn
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ABSTRACTS THE E~mmoP~YsIoLorx ASSESSMENT 0~ PATIENTS WITH TUESDAY, MARCH 17, 1981 PM INTRACARDIAC ELECTROPHYSIOLOGK STUDIES 2:00-3:30 RESULTS OF PROGRAMMED STIMULATION IN 80 PATIENTS HAVING A HISTORY BUT NO ELECTROCARDIOGRAPHIC DOCUMENTATION OF TACHYCARDIA. Hein J.J. Wellens, MD, FACC; Frits W.H.M. Bar, MD; Eddy J.D.M. Vanagt, MD; Pedro Brugada, MD; Willem R.M. Dassen, PhD, Dept. of Cardiology, University of Limburg, Annadal Hospital, Maastricht, The Netherlands. Identification of site of origin and mechanism of tachy- cardia(T) is important for proper selection of therapy. Therefore 80 consecutive patients(P) having a history of paroxysmal T but no electrocardiographic documentation were studied by programmed electrical stimulation(PES) of the heart. If no T could be initiated during PES, Atro- pine was given and PES repeated. Results: Sustained T could be initiated by PES in 53 P (66%). Site or origin of T was: Atria1 8, AV-nodal: 19 (in 7 P T could only be initiated after Atropine), Ven- tricular: 6. III 5 P a concealed accessory pathway was used during T. In all 15 P showing a WPW electrocardio- gram a circusmovement T with atrio-ventricular conduction over the AV-node and ventriculo-atria1 conduction over the accessory pathway could be initiated by PES. Conclusions: I) In all 15 P having a WPW electrocardio- gram and a history of T a circusmovement T could be initiated during PES. 2) In the remaining 65 P sustained T could be initiated in 38 P (= 58%). 3) T originated in different sites in the heart, AV-nodal T being the most common type. UNEXPLAINED SYNCOPE: RESULTS OF THERAPY BASED ON ELECTRO- PHYSIOLOGIC STUDIES. JOHN P. DIMARCO. MD, HASAN GARAN,HD, J. WARREN HARTHORNE, MD, FACC, JEREMY N. RUSKIN. MD,FACC. MASSACHUSETTS GENERAL HOSPITAL, BOSTON, MASS. Twenty-one patients with recurrent syncope that remained unexplained after thorough medical and neurologic evalua- tions underwent intracardiac electrophysiologic study (EPS) with atria1 and ventricular programmed stimulation (PS). Patients with bifascicular block and I’AV block on baseline ECG were excluded. Syncope had been present for from 3-96 months and each patient had had 3 or more prior episodes. Results of EPS were considered diagnostic in 6 patients with rapid ventricular tachycardia [271+11 (mean +S.D.) beats per minute] induced by PS, in 3 patients with intra-His conduction delays, in I patient with induced atria1 flutter and a rapid ventricular rate, and in 1 patient with sinus node dysfunction and induced atria1 flutter. In 3 other patients, EPS revealed a persistent prolongation of AV nodal refractoriness that was revers- ible with atropine suggesting increased vagal tone as a possible mediator for syncope. Based on these findings at EPS, therapy was instituted with either antiarrhythmic drugs (8 patients), ventricular pacing (5 patients), or both (1 patient) with complete relief from recurrent syn- cope in 12 patients, marked improvement in I patient, and no change in 1 patient over 17.8f5 months of follow-up. Syncope persists and remains unexplained in 3 of the 7 patients in whom EPS did not suggest an etiology. These observations indicate that EPS with PS should be utilized in the diagnostic evalaution of selected patients with recurrent unexplained syncope, since such testing may reveal arrhythmias or conduction system disease which are not demonstrable by noninvasive techniques. Specific pro- phylactic therapy directed against abnormalities detected by electrophysiologic testing is highly effective in preventing the recurrence of syncope. SYNCOPE Robert 0. Brandenburg, Jr., MD; David R. Holmes, Jr., MD, PGedffrev, FACC, Mayo Clinic, Mayo Foundation, A-cchester, MN.’ From 1977 to 1980, 92 patients (pts) with syncope of unknown etiology underwent invasive electrophysiologic (EP) studies to determine the mechanism of their syncope. Prestudy investigations including 12-lead electrccardio- graphy (92 pts), 24 hour Holter monitoring (75 pts), exercise testing (24 pts), and neurologic assessment in- cluding electroencephalograms (63 pts) had failed to identify an etiology in any patient. There were 55 males and 37 females (mean age 58 years) with a mean of 9.1 episodes of syncope per patient which had occurred over a mean of 20.8 months prior to the EP study. EP testing documented a probable cause for syncope in 59 of the 92 pts (64%). The most common abnormality was identifiable His-Purkinje conduction system disease which was found in 14 pts. The remaining pts were found to have carotid sinus hypersensitivity ill ptsl, hypervago- tonia (10 pts), ventricular dysrhythmias (10 ptsl, supraventricular tachycardia (9 pts), and intrinsic sinus node dysfunction (5 pts). Based on the EP testing, therapy directed at the specific mechanism of syncope was initiated. Follow-up data was available for 54 of the 59 pts (91%). During a mean follow-up of 14.2 months (range 4 to 38 months), 48 pts (89%) remained free of ,syncope on treatment. Two additional pts (4%) were improved on treatment but still had symptoms. The remaining 4 pts remained unchanged and in one of these an additional mechanism for syncope was documented. We conclude that EP testing plays a valuable role in the evaluation of pts with syncope of unknown etiology. It may identify the potential mechanism for syncope and facilitates selection of specific treatment modalities. NODAL FUNCTION IN 30 PATIENTS WITH ATRIOVENTRICLJLARNODAL 1/l CONDUCTION ABOVE ZOO/MN. Robert Frank, M.D., Guy Fontaine, M.D., Hoan Phan-Thuc. M.D.. Patrick Blanc. M.D. H8pital de la SalpOtriere. Paris, France. In normal adults, it has been considered that I:1 conduction of atria1 impulses to the ventricles above a rate of 20O/mn is indicative of an atrioventricular (AV) nodal bypass tract. In order to examine this contention, we reviewed the records of 600 consecutive adult patients who had electrophysiologic study and found 30 with l:I AV nodal conduction at atria1 rates above 2OO/mn. Under basal conditions, the AH time was abnormally short (5Oms or less) in 22 cases. The nodal effective refractory period was normal for the cycle length in 9, and could not be assessed in 21 because it was atria1 limited. The nodal functionnal refractory period was normal in all. HIH2 vs AlA curve by the extrastimulus techniques was normal in 15, 5 had a plateau, 4 had a dual curve and 6 were undetermined. AH vs RR curve with atria1 pacing by step of increasing rates had a constant slope in 15, 8 had 2 or 3 slopes and 7 had a plateau followed by a slope. In none of these 30 patients could AV nodal reentrant supraventricular tachycardia be indu- ced. Vagal stimulation was provoqued in each patient by injection of ATP (10 or 20mg IV bolus). In each patient first and second degree AV block occured within the AV node. Therefore I) since AV conduction prolonged or ceased in all patients with vagal stimulation, we concluded that an extranodal bypass tract was not responsible for an enhanced AV conduction, 2) enhanced AV conduction is not a prediction of AV reentrant supraventricular tachycardia, 3) an "enhanced" AV conduction may be due to a great variety of nodal responses. February 1981 The American Journal of CARDIOLOGY Volume 47 433
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Transcript of Nodal function in 30 patients with atrioventricular nodal 1/1 conduction above 200/mn
ABSTRACTS
THE E~mmoP~YsIoLorx ASSESSMENT 0~ PATIENTS WITH TUESDAY, MARCH 17, 1981 PM INTRACARDIAC ELECTROPHYSIOLOGK STUDIES 2:00-3:30
RESULTS OF PROGRAMMED STIMULATION IN 80 PATIENTS HAVING A HISTORY BUT NO ELECTROCARDIOGRAPHIC DOCUMENTATION OF TACHYCARDIA.
Hein J.J. Wellens, MD, FACC; Frits W.H.M. Bar, MD; Eddy J.D.M. Vanagt, MD; Pedro Brugada, MD; Willem R.M. Dassen, PhD, Dept. of Cardiology, University of Limburg, Annadal Hospital, Maastricht, The Netherlands.
Identification of site of origin and mechanism of tachy- cardia(T) is important for proper selection of therapy. Therefore 80 consecutive patients(P) having a history of paroxysmal T but no electrocardiographic documentation were studied by programmed electrical stimulation(PES) of the heart. If no T could be initiated during PES, Atro- pine was given and PES repeated. Results: Sustained T could be initiated by PES in 53 P (66%). Site or origin of T was: Atria1 8, AV-nodal: 19 (in 7 P T could only be initiated after Atropine), Ven- tricular: 6. III 5 P a concealed accessory pathway was used during T. In all 15 P showing a WPW electrocardio- gram a circusmovement T with atrio-ventricular conduction over the AV-node and ventriculo-atria1 conduction over the accessory pathway could be initiated by PES. Conclusions: I) In all 15 P having a WPW electrocardio- gram and a history of T a circusmovement T could be initiated during PES. 2) In the remaining 65 P sustained T could be initiated in 38 P (= 58%). 3) T originated in different sites in the heart, AV-nodal T being the most common type.
UNEXPLAINED SYNCOPE: RESULTS OF THERAPY BASED ON ELECTRO- PHYSIOLOGIC STUDIES. JOHN P. DIMARCO. MD, HASAN GARAN,HD, J. WARREN HARTHORNE, MD, FACC, JEREMY N. RUSKIN. MD,FACC. MASSACHUSETTS GENERAL HOSPITAL, BOSTON, MASS.
Twenty-one patients with recurrent syncope that remained unexplained after thorough medical and neurologic evalua- tions underwent intracardiac electrophysiologic study (EPS) with atria1 and ventricular programmed stimulation (PS). Patients with bifascicular block and I’AV block on baseline ECG were excluded. Syncope had been present for from 3-96 months and each patient had had 3 or more prior episodes. Results of EPS were considered diagnostic in 6 patients with rapid ventricular tachycardia [271+11 (mean +S.D.) beats per minute] induced by PS, in 3 patients with intra-His conduction delays, in I patient with induced atria1 flutter and a rapid ventricular rate, and in 1 patient with sinus node dysfunction and induced atria1 flutter. In 3 other patients, EPS revealed a persistent prolongation of AV nodal refractoriness that was revers- ible with atropine suggesting increased vagal tone as a possible mediator for syncope. Based on these findings at EPS, therapy was instituted with either antiarrhythmic drugs (8 patients), ventricular pacing (5 patients), or both (1 patient) with complete relief from recurrent syn- cope in 12 patients, marked improvement in I patient, and no change in 1 patient over 17.8f5 months of follow-up. Syncope persists and remains unexplained in 3 of the 7 patients in whom EPS did not suggest an etiology. These observations indicate that EPS with PS should be utilized in the diagnostic evalaution of selected patients with recurrent unexplained syncope, since such testing may reveal arrhythmias or conduction system disease which are not demonstrable by noninvasive techniques. Specific pro- phylactic therapy directed against abnormalities detected by electrophysiologic testing is highly effective in preventing the recurrence of syncope.
SYNCOPE Robert 0. Brandenburg, Jr., MD; David R. Holmes, Jr., MD, PGedffrev, FACC, Mayo Clinic, Mayo Foundation, A-cchester, MN.’
From 1977 to 1980, 92 patients (pts) with syncope of unknown etiology underwent invasive electrophysiologic (EP) studies to determine the mechanism of their syncope. Prestudy investigations including 12-lead electrccardio- graphy (92 pts), 24 hour Holter monitoring (75 pts), exercise testing (24 pts), and neurologic assessment in- cluding electroencephalograms (63 pts) had failed to identify an etiology in any patient. There were 55 males and 37 females (mean age 58 years) with a mean of 9.1 episodes of syncope per patient which had occurred over a mean of 20.8 months prior to the EP study.
EP testing documented a probable cause for syncope in 59 of the 92 pts (64%). The most common abnormality was identifiable His-Purkinje conduction system disease which was found in 14 pts. The remaining pts were found to have carotid sinus hypersensitivity ill ptsl, hypervago- tonia (10 pts), ventricular dysrhythmias (10 ptsl, supraventricular tachycardia (9 pts), and intrinsic sinus node dysfunction (5 pts). Based on the EP testing, therapy directed at the specific mechanism of syncope was initiated. Follow-up data was available for 54 of the 59 pts (91%). During a mean follow-up of 14.2 months (range 4 to 38 months), 48 pts (89%) remained free of ,syncope on treatment. Two additional pts (4%) were improved on treatment but still had symptoms. The remaining 4 pts remained unchanged and in one of these an additional mechanism for syncope was documented. We conclude that EP testing plays a valuable role in
the evaluation of pts with syncope of unknown etiology. It may identify the potential mechanism for syncope and facilitates selection of specific treatment modalities.
NODAL FUNCTION IN 30 PATIENTS WITH ATRIOVENTRICLJLAR NODAL 1/l CONDUCTION ABOVE ZOO/MN. Robert Frank, M.D., Guy Fontaine, M.D., Hoan Phan-Thuc. M.D.. Patrick Blanc. M.D. H8pital de la SalpOtriere. Paris, France.
In normal adults, it has been considered that I:1 conduction of atria1 impulses to the ventricles above a rate of 20O/mn is indicative of an atrioventricular (AV) nodal bypass tract. In order to examine this contention, we reviewed the records of 600 consecutive adult patients who had electrophysiologic study and found 30 with l:I AV nodal conduction at atria1 rates above 2OO/mn.
Under basal conditions, the AH time was abnormally short (5Oms or less) in 22 cases. The nodal effective refractory period was normal for the cycle length in 9, and could not be assessed in 21 because it was atria1 limited. The nodal functionnal refractory period was normal in all. HIH2 vs AlA curve by the extrastimulus techniques was normal in 15, 5 had a plateau, 4 had a dual curve and 6 were undetermined. AH vs RR curve with atria1 pacing by step of increasing rates had a constant slope in 15, 8 had 2 or 3 slopes and 7 had a plateau followed by a slope. In none of these 30 patients could AV nodal reentrant supraventricular tachycardia be indu- ced.
Vagal stimulation was provoqued in each patient by injection of ATP (10 or 20mg IV bolus). In each patient first and second degree AV block occured within the AV node.
Therefore I) since AV conduction prolonged or ceased in all patients with vagal stimulation, we concluded that an extranodal bypass tract was not responsible for an enhanced AV conduction, 2) enhanced AV conduction is not a prediction of AV reentrant supraventricular tachycardia, 3) an "enhanced" AV conduction may be due to a great variety of nodal responses.
February 1981 The American Journal of CARDIOLOGY Volume 47 433
