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Sinus node function after cardiac transplantation
ABSTRACTS
CHARACTERIZATION OF THE ONSET OF ECTOPIC ATRIAL TACHYCARDIA WITH A-V BLOCK. Joaquin G. Arciniegas, MD; Vance J. Plumb; Albert L. Waldo, MD, FACC, University of Alabama in Birmingham, Birmingham, Alabama
ATRIAL EXCITABILITY AND CONDUCTION IN PATIENTS PRONE TO ATRLAL FIBRILLATION Ross 3. Simpson. Jr., LID; James R. Foster, MD; Leonard S. Gettes, MD, University of North Carolina, Chapel Hill, N.C.
Ectopic atria1 tachycardia with A-V block (EAT) is a poorly understood rhythm. We analyzed the onset of 52 episodes of spontaneous EAT occurring in 9 patients free of digitalis toxicity. All patients were originally in sinus rhythm. During these episodes, bipolar atria1 electrograms (AEG) were recorded simultaneously with at least one surface ECG lead. To establish the presence of EAT, the rhythm had to have a cycle length less than 273 msec (220 beats/min), an isoelectric segment between P waves and evidence of A-V block at some time during the tachycardia. Three distinct patterns of onset of EAT were appreciated. In 6 instances, EAT was preceded by transient atria1 fibrillation of variable duration (12 to 120 seconds). In 4/6, gradual regularization of the AEG during atria1 fibrillation occurred. In 2/6, EAT abruptly replaced atria1 fibrillation. In 15 instances, EAT started de novo, the cycle length of the 1st beat being the same as the cycle length of the EAT. In 31 instances, EAT was started by a late premature atria1 beat (coupling interval 74-88% of the preceding sinus cycle). This was followed by progressive shortening of the cycle length of the 2nd and 3rd beats of EAT, followed by regularization of the EAT at a longer cycle length than that of the 3rd beat. In this latter group, the principles of traditionally accepted mechanisms (automaticity and reentry) of arrhythmias are not followed. These data show a close interrelationship between EAT and atria1 fibrillation and also suggest that more than one underlying mechanism of EAT may exist.
Atria1 fibrillation occurs frequently in patients (pts) tith prolonged P waves. To test the hypothesis that abnormalities of atria1 excitability or conductfon are found in these patients, we defined atria1 strength interval curves, late diastolic threshold, and the conduction tims of early and late premature beats in 7 pts with P waves of < 115 msec (Group I) and 13 pts with P waves ~115 msec (Group II). The increase in conduction time of early compared to late premature beats was measured from the high right atrium to low septal right atrium (AHRAAHIS) and coronary sinus (AH~-ALA). Only Group II patients had abnormal sinus node function (3/13) or history of atria1 fibrillation (6/13). The conduction time of premature beats in late diastole was similar in both groups. In Group I pts the conduction time of early premature beats increased slightly. In Group II pts conduction time of early premature beats increased dramatically and the difference between the maximum increase in conduction time of Group I and Group II ~~~~'~~~:'~~:,~~~~~~~~.5+10 vs 30220, ~<.'305;
SINUS NODE FUNCTION AFTER CARDIAC TRANSPLANTATION Alan F Mackintosh MRCP; David J Carmichael MRCP; Christopher Wren MRCP; Terence A English FRCS; Michael C Petch MD, Papworth Hospital, Cambridge, England Cardiac transplantation produces a permanently denervated donor sinus node and provides an opportunity for studying the human sinus node separated from the autonomic nervous system. Twelve patients have received transplants at Papworth Hospital and temporary atria1 epicardial wires were used in 6 to explore sinus node function during the first 3 weeks after operation. On most days recordings were made of the cycle length, the sinus node recovery time (SNRT), and the sinoatrial conduction time (SACT) calculated by pacing slightly faster than the spontaneous rate for 9 beats. For the first 4 days the rhythm was unstable and all 6 patients demonstrated abnormal nodal function. After this period 2 patients showed a stable atria1 rhythm with normal SNRT and SACT. Another patient temporarily developed a slow junctional rhythm soon after pacing associated with a prolonged SACT; both returned to normal after 9 days. These 3 patients are alive. The other 3 patients showed less stable rhythms. The SNRT was often markedly prolonged (maximum 12 seconds) and pronounced secondary slawing occurred after pacing. These 3 patients have died. One died while undergoing ambulatory monitoring; the tape showed progressive bradycardia leading to asystole after 16 minutes. One collapsed in circumstances suggestive of a fatal arrhythmia and the third died from uncontrolled rejection. In our experience sinus node dysfunction can occur after transplantation and when present may be particularly dangerous as the normal escape mechanisms seem unreliable.
496
February 1981
The American Journal of CARDIOLOGY
Late diastolic threshild was lower in Group I than in Group II pts (O.&t2 vs 1.322, p<.OO5). There was no difference between Group I and II in latency, refractory periods or presence of an early diastolic "supernormal" excitable period. Conclusion: The marked conduction slowing of early atria1 premature beats in patients with large P waves may explain their propensity to atria1 fibrillation.
ENHANCED VAGAL TONE SHORTENS ATRIAL RRFRACPORINESS AND FACILITATES INDUCTION OF REPETITIVE ATRIAL RESPONSES IN MAN. Eric N. Prystowsky. MD, FACC; Gerald V. Naccarelli, MD; Warren M. Jackman. MD: Robert L. Rinkenberner. MD: James J. Heger, MD; Douglas-P. Zipes, MD, FACC, l&&e& Institute of Cardiology, Indiana University School of Medicine and V.A. Medical Center, Indianapolis, Indiana. Although enhanced vagal tone @VT) decreases atria1 refractoriness in animals, published data on effects of ouabain and atropine suggest the opposite may occur in man. The purpose of this study was to determine the effect of EVT on right atria1 effective (ERP) and functional (FRP) refractory period in man. Twelve patients (pts) had electrophysiology study using standard intracardiac techniques. A specially made collar connected to a vacuum source was placed around the pt's neck. EVT was produced during neck suction using intracollar negative pressures (INP) of -50 to -60 m&g. INP, induced for 2 seconds during sinus rhythm, increased spontaneous sinus cycle length from 837 t 96 to 1136 f 273 msec (mean f lSD, pc.001). Atrial ERP and FRP were determined before and during application of INP. Atria1 ERP and FRP signiflcantly decreased during INP (241 t 24 to 230 + 20 maec, pc.01, and 272 f 32 to 262 + 29 maec, pq.01 respectively). During refractory period determinations, repetitive atria1 responses were induced in 3 pts and occurred only during EVT. Systemic arterial blood pressure remained constant during INP. After atropine (0.03 mglkg IV) no decrease in atria1 refractoriness occurred during INP (2/2 pte). In conclusion: 1) EVT mediated via muscarinic receptors shortens atria1 ERP and FRP in man, and-2) facilitates induction of repetitive atria1 responses; 3) the neck collar provides a method to evaluate the effects of EVT on electrophysiologic properties in man.
Volume 47
CHARACTERIZATION OF THE ONSET OF ECTOPIC ATRIAL TACHYCARDIA WITH A-V BLOCK. Joaquin G. Arciniegas, MD; Vance J. Plumb; Albert L. Waldo, MD, FACC, University of Alabama in Birmingham, Birmingham, Alabama
ATRIAL EXCITABILITY AND CONDUCTION IN PATIENTS PRONE TO ATRLAL FIBRILLATION Ross 3. Simpson. Jr., LID; James R. Foster, MD; Leonard S. Gettes, MD, University of North Carolina, Chapel Hill, N.C.
Ectopic atria1 tachycardia with A-V block (EAT) is a poorly understood rhythm. We analyzed the onset of 52 episodes of spontaneous EAT occurring in 9 patients free of digitalis toxicity. All patients were originally in sinus rhythm. During these episodes, bipolar atria1 electrograms (AEG) were recorded simultaneously with at least one surface ECG lead. To establish the presence of EAT, the rhythm had to have a cycle length less than 273 msec (220 beats/min), an isoelectric segment between P waves and evidence of A-V block at some time during the tachycardia. Three distinct patterns of onset of EAT were appreciated. In 6 instances, EAT was preceded by transient atria1 fibrillation of variable duration (12 to 120 seconds). In 4/6, gradual regularization of the AEG during atria1 fibrillation occurred. In 2/6, EAT abruptly replaced atria1 fibrillation. In 15 instances, EAT started de novo, the cycle length of the 1st beat being the same as the cycle length of the EAT. In 31 instances, EAT was started by a late premature atria1 beat (coupling interval 74-88% of the preceding sinus cycle). This was followed by progressive shortening of the cycle length of the 2nd and 3rd beats of EAT, followed by regularization of the EAT at a longer cycle length than that of the 3rd beat. In this latter group, the principles of traditionally accepted mechanisms (automaticity and reentry) of arrhythmias are not followed. These data show a close interrelationship between EAT and atria1 fibrillation and also suggest that more than one underlying mechanism of EAT may exist.
Atria1 fibrillation occurs frequently in patients (pts) tith prolonged P waves. To test the hypothesis that abnormalities of atria1 excitability or conductfon are found in these patients, we defined atria1 strength interval curves, late diastolic threshold, and the conduction tims of early and late premature beats in 7 pts with P waves of < 115 msec (Group I) and 13 pts with P waves ~115 msec (Group II). The increase in conduction time of early compared to late premature beats was measured from the high right atrium to low septal right atrium (AHRAAHIS) and coronary sinus (AH~-ALA). Only Group II patients had abnormal sinus node function (3/13) or history of atria1 fibrillation (6/13). The conduction time of premature beats in late diastole was similar in both groups. In Group I pts the conduction time of early premature beats increased slightly. In Group II pts conduction time of early premature beats increased dramatically and the difference between the maximum increase in conduction time of Group I and Group II ~~~~'~~~:'~~:,~~~~~~~~.5+10 vs 30220, ~<.'305;
SINUS NODE FUNCTION AFTER CARDIAC TRANSPLANTATION Alan F Mackintosh MRCP; David J Carmichael MRCP; Christopher Wren MRCP; Terence A English FRCS; Michael C Petch MD, Papworth Hospital, Cambridge, England Cardiac transplantation produces a permanently denervated donor sinus node and provides an opportunity for studying the human sinus node separated from the autonomic nervous system. Twelve patients have received transplants at Papworth Hospital and temporary atria1 epicardial wires were used in 6 to explore sinus node function during the first 3 weeks after operation. On most days recordings were made of the cycle length, the sinus node recovery time (SNRT), and the sinoatrial conduction time (SACT) calculated by pacing slightly faster than the spontaneous rate for 9 beats. For the first 4 days the rhythm was unstable and all 6 patients demonstrated abnormal nodal function. After this period 2 patients showed a stable atria1 rhythm with normal SNRT and SACT. Another patient temporarily developed a slow junctional rhythm soon after pacing associated with a prolonged SACT; both returned to normal after 9 days. These 3 patients are alive. The other 3 patients showed less stable rhythms. The SNRT was often markedly prolonged (maximum 12 seconds) and pronounced secondary slawing occurred after pacing. These 3 patients have died. One died while undergoing ambulatory monitoring; the tape showed progressive bradycardia leading to asystole after 16 minutes. One collapsed in circumstances suggestive of a fatal arrhythmia and the third died from uncontrolled rejection. In our experience sinus node dysfunction can occur after transplantation and when present may be particularly dangerous as the normal escape mechanisms seem unreliable.
496
February 1981
The American Journal of CARDIOLOGY
Late diastolic threshild was lower in Group I than in Group II pts (O.&t2 vs 1.322, p<.OO5). There was no difference between Group I and II in latency, refractory periods or presence of an early diastolic "supernormal" excitable period. Conclusion: The marked conduction slowing of early atria1 premature beats in patients with large P waves may explain their propensity to atria1 fibrillation.
ENHANCED VAGAL TONE SHORTENS ATRIAL RRFRACPORINESS AND FACILITATES INDUCTION OF REPETITIVE ATRIAL RESPONSES IN MAN. Eric N. Prystowsky. MD, FACC; Gerald V. Naccarelli, MD; Warren M. Jackman. MD: Robert L. Rinkenberner. MD: James J. Heger, MD; Douglas-P. Zipes, MD, FACC, l&&e& Institute of Cardiology, Indiana University School of Medicine and V.A. Medical Center, Indianapolis, Indiana. Although enhanced vagal tone @VT) decreases atria1 refractoriness in animals, published data on effects of ouabain and atropine suggest the opposite may occur in man. The purpose of this study was to determine the effect of EVT on right atria1 effective (ERP) and functional (FRP) refractory period in man. Twelve patients (pts) had electrophysiology study using standard intracardiac techniques. A specially made collar connected to a vacuum source was placed around the pt's neck. EVT was produced during neck suction using intracollar negative pressures (INP) of -50 to -60 m&g. INP, induced for 2 seconds during sinus rhythm, increased spontaneous sinus cycle length from 837 t 96 to 1136 f 273 msec (mean f lSD, pc.001). Atrial ERP and FRP were determined before and during application of INP. Atria1 ERP and FRP signiflcantly decreased during INP (241 t 24 to 230 + 20 maec, pc.01, and 272 f 32 to 262 + 29 maec, pq.01 respectively). During refractory period determinations, repetitive atria1 responses were induced in 3 pts and occurred only during EVT. Systemic arterial blood pressure remained constant during INP. After atropine (0.03 mglkg IV) no decrease in atria1 refractoriness occurred during INP (2/2 pte). In conclusion: 1) EVT mediated via muscarinic receptors shortens atria1 ERP and FRP in man, and-2) facilitates induction of repetitive atria1 responses; 3) the neck collar provides a method to evaluate the effects of EVT on electrophysiologic properties in man.
Volume 47