Intraoperative endocardial mapping during sinus rhythm

DIAGNOSTIC METHODSVENTRICULAR TACHYCARDIA

Intraoperative endocardial mapping during sinus

rhythm: relationship to site of origin of ventriculartachycardiaMICHAEL G. KIENZLE, M.D., JOHN MILLER, M.D., RITA A. FALCONE, M.S.,ALDEN HARKEN, M.D., AND MARK E. JOSEPHSON, M.D.

ABSTRACT Mapping-guided endocardial resection has proved to be an effective therapy for recur-

rent sustained ventricular tachycardia. However, some patients cannot be mapped during ventriculartachycardia, so that guidance from findings during normal sinus rhythm would be highly desirable. Weexamined the frequency, timing, and duration of several abnormal types of electrograms recordedendocardially during sinus rhythm and related these findings to activation mapping during sustainedventricular tachycardia. Thirteen patients with extensive myocardial infarction complicated by recur-

rent sustained ventricular tachycardia were studied intraoperatively during sinus rhythm and inducedventricular tachycardia with a standardized mapping scheme involving the entire endocardial surface.Fractionated electrograms (multicomponent with amplitude <1 mV and duration >50 msec) were

recorded in all patients. This type of electrogram could be recorded at up to 36% of mapped sites. Splitelectrograms (two components separated by isoelectric period) were also frequently seen but involvedonly a mean of 5.8% of mapped sites. Late electrograms (inscribed entirely after the QRS complex)were only recorded in four of 13 patients at a mean of 5% of mapped sites. The location of theseelectrograms was related to an arbitrary 8 cm2 zone around the earliest site of endocardial activationrecorded during ventricular tachycardia. The longest fractionated electrogram was closely related tonine of 22 morphologies of induced ventricular tachycardia, split electrograms were related to seven of16 morphologies, and late clectrograms to two of four morphologies. We have concluded that extreme-ly abnormal electrograms recorded endocardially during sinus rhythm are widespread in patients withextensive myocardial infarction complicated by ventricular tachycardia. These electrograms may beassociated with, but are not specific for, sites of origin of ventricular tachycardia. Surgical proceduresbased on sinus rhythm mapping of these electrogram types would likely result in more extensivesurgical excision than those guided by endocardial activation during ventricular tachycardia.Circulation 70, No. 6, 957-965, 1984.

PREOPERATIVE and intraoperative mapping of en-docardial activation of ventricular tachycardia hasbeen used to guide subendocardial resection in patientswith refractory ventricular tachycardia.' - In some pa-tients, however, tachycardias cannot be mapped as aresult of such factors as cycle length of tachycardia,hemodynamic embarrassment, changing morphology

From the Clinical Electrophysiology Laboratory, CardiovascularSection, Department of Medicine, and the Cardiothoracic Surgery Sec-tion, Department of Surgery, Hospital of the University of Pennsylva-nia, Philadelphia.

Supported in part by grants from the American Heart Association,Southeastern Pennsylvania Chapter, Philadelphia, grant Nos. HL00361and HL24278 from the National Heart, Lung, and Blood Institute,Bethesda, and a grant from the Fannie E. Ripple Foundation, Morris-town, NJ.

Address for correspondence: Mark E. Josephson, M.D., Cardiovas-cular Section, 658 Ravdin Bldg., Hospital of the University of Pennsyl-vania, 3400 Spruce St., Philadelphia, PA 19104.

Received June 4, 1984; revision accepted Aug. 13, 1984.

of tachycardia, or failure to induce tachycardia. Frac-tionated and other abnormal electrograms recordedfrom the endocardium have been noted in patients withventricular tachycardia>7 and have been suggested asmarkers for the substrate of reentry. If these abnormalelectrograms were reliably associated with the site ofearliest endocardial activation during ventriculartachycardia, mapping during sinus rhythm could beused to guide surgical therapy. In the present study weevaluated the characteristics of abnormal endocardialelectrograms measured in sinus rhythm during surgeryfor refractory ventricular tachycardia, and related thefindings to the earliest site of endocardial activationduring induced ventricular tachycardia.

MethodsThe clinical characteristics of the study population are listed

in table 1. There were eight men and five women with a mean

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TABLE 1Clinical characteristics of patients (n = 13; eight men and fivewomen)

Mean age 52 years (range 37-61)Ischemic heart disease 13

Vessels >70% occluded 1.8 + 0.8Aneurysm 13Mean ejection fraction 0.29 ±0.06

SurgeryEndocardial resection 13Aneurysmectomy 13CABG 10

CABG -coronary artery bypass graft.

age of 52 years. All patients had ischemic heart disease with ahistory of distant myocardial infarction. A mean of 1 .8 coronaryvessels had at least a 70% obstructive lesion. Each patient hadangiographic evidence of anterior left ventricular aneurysm.The mean ejection fraction was 29%. Seven patients hadintraventricular conduction delay on their electrocardiograms.No patient had a bundle branch block pattern. The indicationfor surgery was medically refractory, sustained ventriculartachycardia in all patients. Each underwent subendocardial re-section and aneurysmectomy and 10 underwent coronary by-pass grafting.

Endocardial mapping was performed, under normothermicconditions and while the patient was on cardiopulmonary by-pass, through a ventriculotomy using a fingertip bipolar elec-trode with an interelectrode distance of 1.5 mm. Signals werefiltered at 40 to 500 Hz. Electrograms from each site wererecorded simultaneously with surface leads I, F, and VSR or V6,as well as with right and left ventricular reference electrograms.A 1 mV calibration signal was recorded at each site during sinusrhythm and all recordings were obtained at a paper speed of 200mm/sec on an ink-jet recorder (Elema Mingograph). The mo-ment of activation at each site was taken as the point at whichthe largest rapid deflection crossed the baseline, or at sites atwhich no rapid deflection was present as the earliest deviationfrom the baseline at that site. After the endocardial sinus mapwas obtained, induction of tachycardia was carried out with useof programmed ventricular extrastimuli delivered through aright ventricular endocardial electrode catheter positioned be-fore surgery at the right ventricular apex. Mapping of the mor-phology of each induced venricular tachycardia was done at thesame endocardial site as was used for the sinus rhythm record-ing. The earliest sites of endocardial activation during ventricu-lar tachycardia was defined as the earliest electrical activationoccurring before the surface QRS in the last half of electricaldiastole.

Electrograms were recorded during sinus rhythm and duringventricular tachycardia by the scheme shown in figure 1A andfigure 1, B and C. Electrograms were recorded sequentially ateach of 12 "clock" sites, starting at the palpable border of theaneurysm. This pattem of recording was repeated at each of upto five rows spaced approximately 1 cm apart, which are repre-sented in figure LA as a series of planes cutting through the leftventricle from apex to base.The electrograms recorded in patients in sinus rhythm were

classified into three types and are illustrated in figure 2. Frac-tionated electrograms were arbitrarily defined as high-frequen-cy, multicomponent signals with an amplitude of less than 1 mVand a duration greater than or equal to 50 msec. Fractionatedelectrograms outlasting the end of the QRS complex were desig-nated as delayed. Split potentials were defined as two-compo-nent electrograms with isoelectric periods between the compo-

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nents of at least 30 msec. Late potentials were defined aselectrograms inscribed entirely after the end of the QRS com-plex recorded on the body surface, either alone or as part of asplit electrogram.

Results

Electrogram distribution. Thirty-five to 60 sites weremeasured during sinus rhythm in the 13 patients, witha mean of 48 sites each. All 13 patients had fractionat-ed electrograms recorded on the endocardial surface ata mean of 10 sites per patient (or 21% of all measuredsites). Split potentials were detected in 10 patients. Inthe 10 patients in whom split potentials were present, amean of 2.7 sites (range 1 to 5) with split potentialswere recorded. This represented 5.8% of the totalnumber of mapped sites in the patients in whom splitelectrograms were present. Late potentials were re-corded in only four patients at a mean of 2.3 sites, or5%, of the total number of mapped sites (table 2).

Characteristics of fractionated electrograms. The char-acteristics of recorded fractionated electrograms arelisted in table 3. The mean width for all fractionatedelectrograms was 86 msec. The mean width of thelongest fractionated electrogram for patients in sinusrhythm was 129 msec. This was significantly longerthan the mean width for all other fractionated electro-grams measured. In 12 of 13 patients, fractionatedelectrograms starting within the QRS complex outlast-ed the end of the QRS. In these patients, a mean of 3.3sites (1 to 6) had such delayed electrograms. In ninepatients the latest fractionated electrogram was also thelongest, and in four the latest and longest electrogramswere recorded at disparate sites. The total endocardialactivation time measured from the earliest onset to theend of electrical activity recorded on the endocardiumwas a mean of 171 msec and exceeded the surface QRSby a mean of 59 msec.

Spatial distribution of fractionated electrograms. Frac-tionated electrograms were widely distributed in mostpatients. They were found to coincide with areas ofhealed myocardial infarction, and in this group of pa-tients were found predominantly on the ventricularseptum (figure 3). Expressed as the number of clocksites in which the fractionated electrogram could berecorded, these electrograms could be found to covertwo to nine segments, and in the majority of patientsseven to nine clock segments were involved (figure 4).The greatest density of fractionated electrograms wasfound in the first two sequential rows recorded fromthe aneurysm edge (figures 1 and 4); however, up tofive sequential rows contained fractionated electro-grams in individual patients.

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DIAGNOSTIC METHODS-VENTRICULAR TACHYCARDIA

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FIGURE IA. Intraoperative endocardial mapping during sinus rhythm and ventricular tachycardia of two morphologies. Themapping scheme is shown at the bottom. This represents the opened left ventricle with the observer facing the interventricularseptum. The numbers around the ventriculotomy represent the clock sites mapped at each offour rows spaced 1 cm apart. Locallyrecorded electrograms are displayed from noon to 11:00, along with surface leads I, II, V5R, right and left ventricular referenceelectrograms, and 1 mV calibration signals. Time lines are displayed at the bottom of each row. The extensive number and widespatial distribution of low-amplitude wide electrograms recorded during sinus rhythm is well illustrated. In this patient,fractionated and other bizarre electrograms can be recorded at many sites in each row and from apex to base. The longestfractionated electrograms are designated by small black arrows.

Spatial distribution of split and late potentials. Split andlate potentials were fewer in number and less widelydistributed than fractionated electrograms. They were

almost uniformly observed in close proximity to frac-tionated electrograms in general, and specifically wereoften closely associated with the longest fractionatedelectrogram recorded during sinus rhythm. Six of ninelate potentials were part of a split electrogram.

Relationship of abnormal sinus rhythm electrograms to

site of tachycardia origin. The sites of origin of inducedventricular tachycardia, defined as the sites of earliest

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endocardial activation during ventricular tachycardiarelative to the onset of the surface QRS, were com-pared with the locations of the longest fractionatedelectrograms, as well as the locations of any observedsplit or late potentials. Any of these type of electro-grams falling within an area defined by one radialsegment or clock site on either side of the site of originof ventricular tachycardia and 2 cm toward the apex orthe base (approximate area 8 cm2) were considered tobe close to the site of origin of ventricular tachycardia.Those outside this arbitrary boundary were called dis-

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FIGURE 1, B and C. B, Activation mapping during one of two morphologically distinct ventricular tachycardias. Surface

electrocardiographic leads and electrograms are arranged as in figure IA. Presystolic electrical activity is designated by the dark

arrows. The asterisk denotes the earliest site of activation during ventricular tachycardia of this morphology. The open arrow

represents an electrogram that exactly straddles electrical diastole. The longest fractionated electrogram illustrated in figure IAwas considered close to the site of origin of ventricular tachycardia in B. C., Endocardial activation mapping during the second of

two morphologically distinct morphologies of ventricular tachycardia. The data is arranged in the same manner as before. Theearliest sites of endocardial activation during ventricular tachycardia are designated by the black arrows. The asterisk denotes the

earliest site. As before, the open arrow designates electrograms that straddle electrical diastole. The earliest site of endocardial

activation during ventricular tachycardia of this morphology was considered distant from the most abnormal findings duringsinus rhythm (see text).

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tant from the site of origin. Analyzed in this way, thelongest fractionated electrogram was close to the siteof origin in nine of 22 morphologically distinct tachy-cardias and distant from the earliest site of endocardialactivation during 13 types of tachycardia (table 4).Sixteen distinct types of ventricular tachycardia were

mapped in the 10 patients in whom split potentialswere recorded during sinus rhythm. One or more splitpotentials were close to the site of origin of ventriculartachycardia for seven tachycardias and distant for nine.In the four patients in whom late potentials were re-

corded, one or more late potentials were close to the

FIGURE 2. Electrogram types and definitions. In each example isshown surface leads I, II, and V5R, a right ventricular reference electro-gram, and recordings from the left ventricular endocardial probe. Tenmillisecond time lines and 1 mV calibration signals are also displayed.

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TABLE 2Electrogram frequency

Fractionated Split Late

Patients (n) 13 10 4Mean sites per patient

(range) 10 (2-17) 2.7 (1-5) 2.3 (1-4)% Total mapped sites

(range) 21 (4-36) 5.8 (2-10) 5.0 (2-8)

sites of origin of two types of ventricular tachycardiaand distant from those of two others. The longest frac-tionated electrogram recorded during sinus rhythmwas close to at least one type of ventricular tachycardiain seven patients, and far from all sites of origin ofventricular tachycardia in six patients. Of the four pa-tients in whom the longest and latest fractionated elec-trograms were at disparate sites, the site of latest activ-ity in sinus rhythm was close to the site of a ventriculartachycardia of another morphology in two. Examplesof maps obtained during sinus rhythm and during ven-tricular tachycardia are shown in figures 1 and 5.The mean width of fractionated electrograms within

an area defined as one radial segment on either side of

TABLE 3Mean characteristics of fractionated electrograms

Electrogram width (msec) 86 ± 29Longest electrogram (msec) 129 ± 31Exceed surface QRS 12/13 patients

Total endocardial activation (msec) 171 + 30Surface QRS width (msec) 112± 13

the earliest site of endocardial activation during eachventricular tachycardia did not differ from the meanwidth of those recorded from the remainder of the leftventricle (figure 6).

DiscussionFractionated and other type of abnormal electro-

grams have been recorded from epicardial, intramyo-cardial, and endocardial sites of previous myocardialinfarction in a variety of animal preparations as well asin human beings. These electrograms share the charac-teristics of high-frequency components with diminish-ed amplitude, prolonged duration, or both.-10 Frac-tionated electrograms have been of special interestbecause of reports of the association of these electro-grams with the initiation, maintenance, and termina-

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FIGURE 3. Detailed endocardial septal map during sinus rhythm. Local electrograms were recorded from multiple septal sites ina grid pattern as illustrated in the drawing and arbitrarily numbered 1 to 9. Electrograms recorded in this way are positioned asrecorded on a grid represented by the dotted lines. Also shown are 1 mV calibration signals for each row, or for individualelectrograms when change of gain occurred. Multiple bizarre low-amplitude multicomponent electrograms were recorded fromnearly the entire left ventricular septum. Such findings are characteristic of patients with extensive anteroseptal infarctioncomplicated by ventricular tachycardia. The dark arrows indicate His-Purkinje spikes and underline the survival of His-Purkinjetissue despite extensive infarction.

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FIGURE 4. Distribution of fractionated electrograms. A, The absolute

number of clock segments in which fractionated electrograms could be

found are shown on the horizontal axis and the number of patients is

displayed on the vertical axis. The majority of patients had seven to nine

clock segments in which fractionated electrograms could be found. B,

The absolute number of rows (as measured from apex to base) in which

fractionated electrograms could be found is displayed in the horizontal

axis and the number of patients is on the vertical axis. Most patients hadthree to five rows in which fractionated electrograms could be detected.

tion of ventricular tachycardias arising after myocardi-al infarction.4 " These electrograms have been felt to

represent slow and disorganized conduction throughischemically damaged tissue, which may form the sub-strate for reentrant ventricular arrhythmias. This inter-pretation has not been uniformly accepted, however,and some have maintained that fractionated electricalactivity may represent characteristics unrelated toreentrant activity, such as artifact resulting from cath-eter movement or other phenomena.5 12

Ischemically damaged myocardium has been shownin a variety of preparations to be composed of fibroustissue intermingled with partially damaged and com-

pletely normal surviving myocardial cells.' 13 Thisanatomic heterogeneity is also reflected in electro-physiologic heterogeneity.8-11 1416 Gardner et al.'6

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TABLE 4Relationship of electrogram to ventricular tachycardia

Longestfractionated Split Late

Close 9 7 2Far 13 9 2Total VTs 22 16 4

VTs = ventricular tachycardias.

have demonstrated that the origin of fractionated elec-trograms is surviving myocardial cells that have beenuncoupled and electrically isolated by intervening fi-brous tissue. This results in a slow and desynchronizeddepolarization of normal cells (nonuniform aniso-tropy) that inscribes a high-frequency multicomponentelectrogram of low amplitude and long duration whenrecorded extracellularly.

Fractionated electrograms recorded during sinusrhythm have been reported in patients with coronaryartery disease after myocardial infarction.4 6, 1 Further-more, patients with ventricular tachycardia have morefrequent and longer fractionated electrograms.7' 17 Inour patients, fractionated electrograms were widelydistributed and frequently found on the endocardialsurface. Up to 36% of sites in these uniformly andcompletely mapped ventricles showed fractionatedelectrical activity. The distribution and degree of in-volvement cannot be directly compared with that inother studies because of differences in mapping detailand technique. The frequency of finding fractionatedand other abnormal electrograms is consistent with theextensive myocardial damage that is associated withchronic recurrent ventricular tachycardia. Split elec-trograms have been recorded during sinus rhythm inpatients with ventricular arrhythmias with or withoutmyocardial infarction.6' '1 These electrograms are be-lieved to possibly represent desynchronized activationof tissue by one or more wave fronts. Like others, wehave recorded these electrograms in fewer patients andat fewer sites than fractionated electrograms.67

These fractionated and other abnormal electrogramsare associated with a prolonged endocardial activationtime, as has been noted in both animal and humanpreparations.6-.0 11, 18 In these studies total endocardialactivation was markedly prolonged, with one or morelong fractionated electrograms extending beyond theend of the surface QRS in all but one patient.

If these prolonged and delayed electrograms repre-sent slow conduction manifest during sinus rhythm, intheory the longest or latest electrogram during sinusrhythm might be a likely site for reentry to occur. Theappearance of locally recorded electrograms has been

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suggested as being useful in determining the bound-aries of viable and nonviable myocardial tissue duringperformance of aneurysmectomy and coronary by-pass.'9 In addition, it has been suggested that findingsduring sinus rhythm could be helpful in directing surgi-cal therapy for ventricular tachycardia arising in thesetting of coronary disease or right ventricular dyspla-

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sia. 18 This would be highly desirable, since activationmapping during ventricular tachycardia cannot alwaysbe performed due to characteristics such as tachycardiacycle length and failure of induction of tachycardia.The results of detailed mapping in our patients

would suggest that neither the type, duration, nor tim-ing of electrograms recorded during sinus rhythm is

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FIGURE 5. The relationship of abnormal electrograms recorded during sinus rhythm to site of origin of ventricular tachycardia.A, The fractionated electrograms recorded during sinus rhythm in one patient in whom 42 sites were mapped is shown, along witha 1 mV calibration signal and time lines at the bottom. This patient had an extensive anteroseptal infarction. The asterisk denotesthe longest fractionated electrogram recorded during sinus rhythm. B and C, Endocardial activation mapping during two

morphologically distinct ventricular tachycardias. Surface leads I, Il, and VSR, right ventricular and left ventricular references,and the earliest site of endocardial activation and its adjoining site are shown for both panels. The longest fractionatedelectrogram recorded during sinus rhythm, shown in A (asterisk), was associated with the ventricular tachycardia shown in B.

The local electrogram associated with the ventricular tachycardia in C, while abnormal, was far from being the most abnormal.

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FIGURE 6. The mean width of the fractionated electrogram recorded insinus rhythm surrounding the site of origin of ventricular tachycardiacompared with the remainder of mapped sites. The mean width of

fractionated electrograms around each site of origin was not significant-ly longer than that of the fractionated activity recorded in the remainderof the ventricle (see text).

completely reliable in localizing all sites of earliestendocardial activation during ventricular tachycardia.Too many extremely abnormal electrograms can befound during sinus rhythm on the endocardial surfaceto permit a localized endocardial resection. Resectionof all sites of fractionated, split, and delayed electro-grams would require resections of up to one-third ofthe endocardial surface of the left ventricle. Reportshave appeared of removal of all visually abnormalendocardium in patients with ventricular tachycardia,resulting in ablation of the arrhythmia.20 In some cases

this has required removal of papillary muscle and mi-tral valve replacement. It is still unclear whether resec-

tion of all tissue that appears abnormal results in an

undue hemodynamic burden in these patients with al-ready-compromised left ventricular function.The poor correlation between abnormalities noted in

sinus rhythm and the earliest site of endocardial activa-tion during ventricular tachycardia is not totally sur-

prising. To assume that the most abnormal electro-grams represent slow and abnormal conduction isjustifiable. However, one cannot assume linearity ofconduction through areas under the bipolar electrode.Furthermore, slow conduction is not the only determi-nant of reentry. In theory, the area in which there is thelongest conduction and shortest refractoriness wouldbe the most likely site for reentry. However, refractori-ness also appears to have a heterogeneous distributionin infarcted tissue"5 and ischemically damaged myo-

cardium may, in fact, be more refractory than normaltissue.21 The appropriate combination of conductionand refractoriness may not occur at a site at whichconduction is longest.

Influences of the autonomic nervous system are only

964

beginning to be understood with respect to ventriculartachycardia and may also be a determinant not reflect-ed by the duration of the local electrogram. It is alsopossible that failure to show a relationship betweenabnormalities in sinus rhythm and ventricular tachy-cardia is related to the mapping procedure itself. Map-ping done during sinus rhythm and ventricular tachy-cardia are not simultaneous and are open to errors ofreproducibility of site selection. In this study, howev-er, we used a detailed and uniform grid of the leftventricular endocardial surface and thereby minimizedany discrepancy between sites of origin of ventriculartachycardia and sinus rhythm abnormalities arising asa result of failure to return to the same mapping site.Errors in localizing the earliest site of endocardial acti-vation could also add to observed inaccuracy, butagain they have been minimized by the standarddetailed mapping scheme. Techniques such as high-density simultaneous recording of endocardial andtransmural electrograms during sinus rhythm and ven-tricular tachycardia may be required to further clarifythe relationship between conduction in sinus rhythmand the occurrence of local reentry. The response oflocal electrograms to perturbations such as atrial andventricular pacing and extrastimuli may provide moreinformation about potential sites of reentry than dosinus rhythm recordings. This possibility requires fu-ture study.

Abnormal electrograms recorded during normal si-nus rhythm are widespread in patients with coronaryartery disease, distant myocardial infarction, and ven-tricular tachycardia. The most common of these abnor-mal electrograms are fractionated. Split potentials canbe recorded in most patients but are fewer in numberthan fractionated electrograms. Many of the fraction-ated electrograms recorded during sinus rhythm extendbeyond the inscription of the surface QRS and result ina markedly prolonged endocardial activation time.Discrete electrograms inscribed after the surface QRSare infrequently seen, however. These electrogramsmay be associated with, but are not specific for, sitesof origin of ventricular tachycardia. Therefore, sur-gery procedures based on sinus rhythm mapping ofthese electrograms would likely result in more exten-sive surgical excision than those guided by endocardialactivation during ventricular tachycardia.

We are indebted to Ms. Nancy Walker for her skillful prep-aration of this manuscript.

References1. Josephson ME, Harken AH, Horowitz LN: Endocardial excision: a

new surgical technique for the treatment of recurrent ventriculartachycardia. Circulation 60: 1430, 1979

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4. Josephson ME, Horowitz LN, Farshidi A: Continuous local electri-cal activity: A mechanism of recurrent ventricular tachycardia.Circulation 57: 659, 1978

5. Waxman HL, Sung RJ: Significance of fragmented ventricularelectrograms observed using intracardiac recording techniques inman. Circulation 62: 1349, 1980

6. Klein H, Karp RB, Kouchoukos NT, Zorn GL, James TN, WaldoAL: Intraoperative electrophysiologic mapping of the ventriclesduring sinus rhythm in patients with a previous myocardial infarc-tion. Identification of the electrophysiologic substrate of ventricu-lar arrhythmias. Circulation 66: 847, 1982

7. Weiner I, Mindich B, Pitchon R: Determinants of ventriculartachycardia in patients with ventricular aneurysm: results of intra-operative epicardial and endocardial mapping. Circulation 65:856, 1982

8. Boineau JP, Cox JL: Slow ventricular activation in acute myocardi-al infarction, a source of re-entrant premature ventricular contrac-tions. Circulation 43: 702, 1973

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M G Kienzle, J Miller, R A Falcone, A Harken and M E Josephsonventricular tachycardia.

Intraoperative endocardial mapping during sinus rhythm: relationship to site of origin of

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