Dispersion of atrial refractoriness in patients with sinus node dysfunction

Dispersion of atrial refractoriness in patients with sinus node dysfunction

ABSTRACTS TUESDA Y, MARCH 13, 1979 PM CLINICAL ELECTROPHYSIOLOG Y-I 2:00-5:30 FUNCTION OF THE DENERVATED HUMAN SINUS NODE. Jay W. Mason, M D, Stanfor...

234KB Sizes 2 Downloads 127 Views

ABSTRACTS

TUESDA Y, MARCH 13, 1979 PM CLINICAL ELECTROPHYSIOLOG Y-I 2:00-5:30 FUNCTION OF THE DENERVATED HUMAN SINUS NODE. Jay W. Mason, M D, Stanford University, Stanford,

THE ONSET OF CLASSICAL ATRIAL FLUTTER - STUDIES IN MAN FOLLOWING OPEN HEART SURGERY. Terry B. Cooper, M.D.; Michael G r i f f i t h , B.S.; Vance J. Plumb, M.D.; William A. H. MacLean, M.D., FACC; Albert L. Waldo, M.D., FACC. University of Alabama, Birmingham, Alabama. CA.

Autonomic influences obscure intrinsic properties of the sinus node (SN). To assess the effect of autonomic innervation upon SN recovery time (SNRT) 2170 atrial cycles after 434 atrial pacing episodes in 14 human cardiac transplant recipients (pts) were analyzed. These pts retain their own SN's and atrial remants, which can be recorded and stimulated and remain innervated, while their donor (D) atria are denervated. Each pts innervated, remant (R) and denervated D atria were separately paced at up to i0 rates between 85 and 200 beats/min once for 60 and once for 15 sec and the first 5 recovery cycles were measured. Data obtained from 60 sec overdrive periods are reported, but findings obtained with 15 sec overdrive were not significantly different. SNRT increased with decreasing pacing cycle lengths (CL) for D "but no predictable relationship between overdrive CL and length of the post pacing pause existed for R atria. Corrected SNRTmax occurred at a pacing CL of 400 msec or less in 14/14 D but only 5/14 R atria (p primary pauses; 2) lengthens SNRT/spontaneous CL; and 3) protects against progressive, excessive lengthening of the post pacing pause at more rapid stimulation rates, perhaps by promoting SN entrance block. Also, overdrive pacing for 15 sec produces responses indistinguishable from longer pacing periods.

DISPERSION OF ATRIAL REFRACTORINESS IN PATIENTS WITH SINUS NODEDYSFUNCTION Jerry C. Luck, MD, Toby R. Engel, HD,FACC, The Medical College of Pennsylvania, Philadelphia, Pennsylvania Abnormal atrial refractoriness was examined as a cause of atrial f i b r i l l a t i o n / f l u t t e r (AFF) in patients.(pts) with bradycardia. We compared refractory periods among 3 disparate right atrial sites in 16 pts with sinus node dysfunction (SND, heart rate 61.6 bts/min_+3.4 SE) and 13cont r o l s {heart rate 73.5+2.2). Effective and functional refractory periods (ERP,FRP) were measured by twice threshold atrial extrastimulation after every 8th sinus beat and after 8 beats of a t r i a l pacing at 120/min. Atrial pacing shortened refractory periods (eg, in SND pts average ERP shortened from 324+19 to 258-+9 msec, p
388

February 1979

The American Journal of CARDIOLOGY

The onset of classical (Type I) atrial f l u t t e r (AFI) was studied during 27 episodes of the spontaneous conversion of sinus rhythm to AFI in 16 patients following open heart surgery. Bipolar atrial electrograms were recorded from epicardial wire electrodes along with a surface ECG during all episodes. In all instances, sinus rhythm wes interrupted by a premature atrial beat with a mean coupling interval of 352 ±12 msec (range 275-587 msec) which ranged from 45-83% (mean 58 ±I.9%) of the preceding sinus cycle length. This premature beat was always followed by a transitional rhythm which had a mean duration of 9.3 ±2.4 seconds (range 1-60 sec) before Type I AFI was established. The transitional rhythm, which was distinct from both sinus rhythm and AFI was consistent with atrial f i b r i l l a t i o n in 24 episodes and with Type I I (veryrapid) AFI in three episodes. The mean atrial cycle length of 178 ~3 msec (range 153-204 msec) and the mean beat-to-beat change in cycle length of 16 ±2.7 msec (range 7-33 msec) during the transitional rhythm differed significantly from the mean cycle length of 198 ±2.4 (176-214 msec) and the mean beat-to-beat change ~n cycle length of 4 ±0.4 msec (range2-11 msec) during the subsequent Type I AFI (P <.OOl for each comparison). Data from this selected population demonstrate that l) the coupling interval of the premature atrial beat which i,terrupted sinus rhythm was very long and beyond the expected atrial vulnerable period; 2) Type I AFI developed after a transitional rhythm, rather than de novo; and 3) a close relationship exists between atrial f i b r i l l a t i o n , Type I AFI, and Type II AFI.

O F BYPASS TRACT IN HUMAN A-V JUNCTIONAL TACHYCARDIA: SLOW CONDUCTING ACCESSORY PAT~gAYS Jerdnimo Farr4,MD;Isaac wiener,MD;David L.Ross,FRACP;Frits W.B~r,MD;Hein J.J.Wellens,MD,FACC;Annadal Hospital,University of Limburg,Maastricht,The Netherlands. A NEW TYPE

Accessory Pathways(AP) characteristically have conduction times shorter than those of the A-V node-His-Purkinje(AVNHP)axis. A new type of AP,with very long conduction times (280-320 ms),was demonstrated to be part of a reentrant circuit in three patients(pts) with circusmovement tachycardia(CMT).Two pts had spontaneously recurring CMT with antegrade conduction over the AVN-HP and retrograde via the AP.Evidence for AP conduction was:1)advance of atrial activity by a VPB given during CMT at a time when the His Bundle(HB)was refractory,2)different sequence of retrograde a t r i a l a c t i v a t i o n via the AVN and the AP during ventricular stimulation,the latter sequence being identical to that during CMT.Criteria number 2 plus the fact that APBs during CMT advanced the HB spike without advancing the coronary sinus atrial electrogram,make a Mahaim tract unlikely and point towards an anomalous atrioventricular connection. In both pts exercise shortened V'A conduction via the AP.Atropine was tested in one patient and V-A time over the AP was shortened by 60 m s . T h e t h i r d patient had a wide QRS during CMT,the slow conducting AP being used antegradely and the AVN retrogradely.Evidence for antegrade AP conduction was:l)absence of HB spike before QRS complex,2)initiation of CMT by APBs blocked in the AVN, 3)advance of QRS during CMT by APBs which did not capture the HB~CMT was terminated by:l)APBs which did not capture the HB or ventricle,2)V~Ps only when they were retrogradely blocked in the AVN.CONCLUSiONS:Two forms of CMT incorporating a new type of AP a r e d e s c r i b e d . T h e s e APs are characterized by:1)long conduction times,2)acceleration of conduction velocity by atropine and exercise.

Volume 43