Electrophysiologic findings in patients suffering cardiac arrest

ABSTRACTS

ROLE OF VENTRICULAR FRAGMENTATION IN DEFINING THE MECHANISM OF VENTRICULAR TACHYCARDIA IN MAN Harvey L. Waxman, MD; Ruey J. Sung, MD, FACC, University of Miami School of Medicine, Miami, Florida Ventricular fragmentation(VF be observed during experimental myocardial infarction in the canine heart.It is postulated that VF is a marker for conduction delay in the ischemic myocardium which is a requisite condition for development of reentrant ventricular tachycardia(VT). Recent studies using intracardiac recordings(ICR)suggest that VF can be detected in patients(pts)with chronic VT associated with cardiomyopathy(CM) or ischemic heart disease(HD) ventricular aneurysm.Nevertheless,no systematic evaluation of VF has been performed in man.To define the role of VF in the genesis of VT,we studied 17 pts(l2 without and 5 with VT)during ICR.Of these 17 pts,Z had CM,5 ischemic HD(3/5 had ventricular aneurysm),5 rheumatic HD,Z congenital HD,and the remaining 3 no apparent HD. The left ventricular electrogram(LVE) and right ventricular electrogram(RVE) were recorded at multiple sites with variable interelectrode distances(IED) and filter frequency settings(FFS).Following adjustment of ICRlocation, VF "a& observed in the RVE in 3 pts without VT and 1 pt with VT,but in the LVE in all 17 pts using IED of 1 cm or greater and FFS of 40-500 Hz or less.Incremental atria1 pacing resulted in progressive prolongation of VF without leading to VT,and the initiation of VT required no antecedent prolongation of VF.Moreover, during VT,interruption of VF with ventricular extrastimulation could neither reset nor terminate VT.We conclude that:l)recordings of VF depend on ICR location,IED,and FFS;Z)VF is most likely related to intracardiac catheter electrode movement associated with mechanical systole and diastole,and can thus be recorded in pts with or bithout VT;and 3)VF recorded using ICR probably has no significance in defining the mechanism of VT in man.

NON CLINICAL POLYMORPHIC VENTRICULAR TACHYCARDIA INDUCED BY PROGRAMMED CARDIAC STlMULATION: INCIDENCE AND CLINICAL IMF'LICATIONS. C. Pratap Reddy, MD, FACC; John Sartini, MD, VA and University of Kentucky Medical Centers, Lexington, Kentucky. Acute drug testing during programmed cardiac stimulation (PCS) is increasingly relied upon in designing the treatment of recurrent (R) ventricdlar (V) tachycardia (T). This approach to the treatment of RVT is based on the premise that PCS reliably reproduces the morphology and In order to test this assumprate of spontaneous VT. tion, we analyzed the morphology and rate of VT induced by PCS in 20 patients (pts) with RVT who exhibited only The induced one type of VT during spontaneous episodes. VT was clinical, i.e. similar to spontaneous VT in 10 pts (Group A) and non clinical, i.e. different from spontaneous VT in 10 pts (Group B). During PCS 8/10 pts in Group B exhibited multiple morphologies (polymorphism). T morphology and rate could be changed by changing the basic cycle length (2 pts), the method of initiation of T (1 pt) and by introducing paced V beats during T (5 The table shows clinical data for both groups. pts). Group B p value Group A N.S. 8 pts Coronarv arterv disease 7 Pts N.S. 1 ;t 2 pts v aneurysm co.01 8 pts Intraventricular conduction 4 pts defects (IVCD) 64+19
406

February 1960

The American Journal of CARDIOLOGY

REPETITIVE

VENTRICULAR

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N.

Ruskin,

Massachusetts

MD,

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ELECTROPHYSIOLOGIC FINDINGS IN PATIENTS SUFFERING CARDIAC ARREST Mark E. Josephson, MD,FACC; Leonard N. Horowitz, MD,FACC; Allan M. Greenspan, MD; Scott R. Spielman, MD; John A. Kastor, MD,FACC, Hospital of the University of Pennsylvania, Philadelphia, Pa. Fifty-two patients (pts) resuscitated from cardiac arrest (CA) underwent electrophysioloqical studies (EPS). There were 40 men and 12 "omen ranging in age from 21-75 Years. The earliest documented arrhythmia at the time of initial or recurrent (15 pts) CA "as ventricular fibrillation (VF, 30 pts), ventricular tachycardia (VT) degenerating to VF In two pts no (vT/VF, 15 pts), and sustained VT (5 pts). arrhythmia had been documented prior to defibrillation. EPS revealed normal sinus node function in 51/52 pts. A-H intervals ranging from 45-140 msec with a mean of 85.9 msec, and H-V intervals ranging from 35-100 msec with a EPS revealed inducible arrhythmias mean of 57.6 msec. (IA) in 33 pts (63%) and no inducible arrhythmia (NIA) in 17 pts (37%). Of 30 pts with documented VF, 13 had IA Of 20pts (VF in 4 pts. VT/VF in 5 pts. and VT in 4 pts). with VT or VT/VF, 18 had IA (VT in 16 pts and VT/VF in 2 VT and VT/VF were induced in the two pts with unpts). Pts with IA had longer A-H indocumented CA mechanism. tervals than those with NIA - 91.1 vs 76.6 (p <.002) and Prolonged H-V 61.4 vs 50.8 msec (p c.007) respectively. intervals (>55 msec) and intraventricular conduction defects were each observed in 18/33 (55%) pts with IA and were observed in 5/19 (26%) and 7/19 (37%) pts with NIA We conclude that: a) pts resuscitated from respectively. CA have a high incidence of IA; b) IA are more frequent if the mechanism of CA is VT or VT/VF; c) pts with IA have a high incidence of infra-nodal and intraventricular conduction defects which may predispose to VT, VT/VF and VT; and d) EPS may provide data upon which to base therapy in pts resuscitated from CA.

Volume 45