ABSTRACTS

EPICARDIAL MAPPING OF VENTRICULAR REENTRANT PATHWAYS IN

THE LATE MYOCARDIAL INFARCTION PERIOD

Ruth Ann Smith, MD; Nabi1 El-Sherif, MD, FACC; A. Kerry

Evans, ME: University of Utah, Salt Lake City, Utah: and

the VA Hospital and University of Miami, Miami, Florida

Epicardial activation sequence was mapped during ventric-

ular arrhythmias (VAIA) induced by premature stimulation in

4 dogs 3-5 days after anterior descending coronary artery ligation. A 17 cm2 rectangular grid of 48 equally spaced bipolar electrodes with 2 mm interpolar distance was ap- plied to the infarct zone (12) and surrounding normal zone. Electrograms were recorded simultaneously with a multiplexing system and were computer processed. Activa- tion times permitted detailed description of activation sequence in the IZ during the VA. Following the premature stimulation, activation fronts circumvented a central area of functional unidirectional block which was about 1 cm*

in size. The reentrant paths were completed when delayed activation entered the central area and progressed through

the previous site of block to reexcite the ventricle. The epicardial sequence and length of the reentrant pathway, as well as the QRS configuration of the reentrant beat, varied in the same animal. The conduction velocity, as suggested by the activation times, varied in different segments of the reentrant pathway. In some reentrant beats, activation times bridged the entire diastolic in- terval reflecting a predominant epicardial location of the reentrant path. During other beats, gaps in the epicar- dial activation times suggested intramyocardial segments of the reentrant pathway. The study has demonstrated a reentrant mechanism of VA at 3-5 days after coronary liga-

tion and has clearly shown the feasibility of tracing re-

entrant paths by activation sequence mapping.

ENDOCARDIAL MAPPING OF VENTRICULAR TACHYCARDIA IN MAN Mark E. Josephson, MD, FACC; Leonard N. Horowitz, MD; Ardeshir Farshidi, MD; Joseph F. Spear, PhD, FACC, John A. Kastor, MD, FACC; E. Neil Moore, DVM, FACC, University of Pennsylvania, Philadelphia, Pa.

Endocardial ventricular mapping (EVM) of 25 ventricular tachycardias (VT) was performed using electrode catheters (1 cm interelectrode distance). Mapping sites included the atrioventricular junction, coronary sinus, apex, mid- septum, anterior wall, lateral inflow tract and outflow tract of the right ventricle (RV); and high, mid, and low septum, apex, lateral wall and posterior basal area of the left ventricle (LV); and at least one site within a LV aneurysm when present. Twelve VT had a left bundle branch block pattern (VT-LBBB) and 13 VT had a right bun- dle branch block pattern (VT-RBBB). In all VT-RBBB the earliest site of activation was in the LV or septum. In VT-LBBB the earliest site was either in the RV (4/12), the LV (6/12), or the septum (2/12). In all VT with QRS 5140 msec (4/25) the site of origin was in the septum. In patients (pts) with LV aneurysms the site of origin of VT was always in the area of the aneurysm. All VT-LBBB arising from the LV originated in an aneurysm involving the septum. Spontaneous or pacing-induced QRS changes during VT were associated with alterations in the pattern of ventricular activation and in 3 pts continuing activi- ty in an aneuyrsm was unaffected during the change in morphology. In 2 pts VT-RBBB changed to VT-LBBB upon the development of exit block. In 3 pts the site of origin predicted by EVM was confirmed intra-operatively by epi- and/or endocardial mapping. We conclude that EVM demon- strates the limitations of the surface ECG in localizing the site of origin of VT and may provide important data upon which the surgical treatment of VT is based.

CRITICAL ROLE OF SUBENDOCARDIAL ACTIVATION IN THE GENESIS OF MALIGNANT VENTRICULAR TACHYCARDIA AND FIBRILLATION. Eleiser Kaplinsky, MD, Satoshi Ogawa, MD, Leonard S. Dreifus, MD, FACC, Lankenau Hospital, Philadelphia, Pa.

Continuous electrical activity during diastole prior to ventricular premature complexes (VPC) or ventricular tachycardia (VT) is a critical determinant of ventricular reentry in acute myocardial infarction. However, the pre- cise re-excitation pathway from the infarcted zone (12) to the normal tissue (NT) has not been shown. VPC, VT and ventricular fibrillation (VF) were produced in 11 open chest dogs by a ligation and perfusion techniques of the left anterior descending coronary artery. Lead II and 7 close bipolar and composite electrograms were simultan- eously recorded from endocardial and epicardial surfaces in the IZ (Endo IZ and Epi IZ) and NT. Low frequency spikes as well as various Epi IZ conduction ratios (2:1, 3:l and Wenckebach periods) inducine VPC and VT were ob- served. The hiehest degree of fraementation was observed well within the Eoi LZ with uerioheral decrement. Ven- tricular oacine at sinele or multiole (simultaneous) uoints and raoid atria1 oacine increased fraementation. Endo IZ soikes, followine the diastol.ic EDi 17. activitv, were alwavs observed prior to each ectopic activation of the adjacent NT. VF could be predicted by prior frag- mentation of the Endo IZ electrograms. Continuous fib- rillatory activity in the Epi IZ was transmitted to the NT only through prior activation of Endo IZ. It is con- cluded that (1) delayed activation in Epi IZ did not necessarily result in VPC or VT, (2) Endo IZ activity predictably preceded VPC, VT and VF, (3) VF occurred with prior fragmentation of Endo IZ electrograms, (4) Endo 17. appears to be the necessary link of reentry between the tissue of origin of reentrant activity (the Epi IZ) and the NT.

DIVERSE ELECTROPHYSIOLOGICAL MECHANISMS UNDER-

LYING MALIGNANT VENTRICULAR DYSRHYTHMIA

Patricia A. Penkoske, MD; Burton E. Sobel, MD, FACC;

Peter B. Corr, PhD, Washington University, St. Louis, Missouri

Both coronary occlusion and reperfusion result in malignant ventri-

cular dysrhythmia in experimental animals and either may precipi-

tote sudden death in man. In the present study, electrophysiologi-

cal properties of the two dysrhythmios were delineated in 57 chlor-

alose-anesthetized cots with proximol LAD occlusion and subse-

quent reperfusion 35 minutes later. Both coronary occlusion and

reperfusion gave rise to reproducible bouts of malignant ventricu-

lar dysrhythmia. Simultaneous bipolar electrogmms (epi-, myo-,

and endocardial) from ischemic and normal zones were continuous-

ly analyzed by computer. Dysrhythmia after occlusion was preced-

ed by slowed conduction in the ischemic electrode-zone (dV/dt

decreased by 66+6% (meanfSE)), delayed endo- to epicardial

conduction (2901!-91% of control), asynchronous depolarization

(pulse width increased by 59X-76%) a slow idioventricular escape

rate elicited with maximal vagal stimulation (62f6 beats/min),

exacerbation with rapid atrial stimulotion, and shortening of the

refmctory period in ischemic zones (by 15.k2%). In contrast, dys-

rhythmia after reperfusion was chamcterized by normalized con-

duction in the ischemic electrode-zone, normal endo- to epicar-

dial conduction time (129+15% of control), a return to synchro-

nous depolarization (pulse width = 126$13% of control), a rapid

idioventricular escape rate (188*12 beats/min), suppression by

atrial pacing, and no change in ischemic zone refractory period.

Thus, dysrhythmia due to coronary occlusion alone appeared to

depend on reentry in contrast to dysrhythmia following reperfusion

in which enhanced ventricular automaticity was the apparent

progenitor.

February 1978 The American Journal ol CARDIOLOGY Volume 41 427