Postgraduate Medical Journal (January 1971) 47, 16-22.

Pacing after acute myocardial infarction

ALAN HARRISB.Sc., M.D., M.R.C.P.

Cardiac Department, St George's Hospital, London, S. W.1.

SummaryExperience of endocardial pacing in eighty-twopatients with atrioventricular block after myocardialinfarction is described. A unipolar pacing wire waspassed into an antecubital fossa vein and passed intothe right atrium and wedged into the apex of the rightventricle under radiological control using an imageintensifier. All patients were attached to an externaldemand unit set at 60/min which will pace if there isasystole longer than 1 sec. The disadvantages ofpacing are discussed.A fall in mortality occurred from 71% of unpaced

patients to 38% of thirty-seven patients where demandpacing was given. When suppressant drugs (lignocaine,procainamide and quinidine) were given in additionto pacing the mortality dropped to 11% of twenty-seven patients. The disadvantages of pacing are fewand it is considered that suppressant drugs are onlyused with safety when a pacing system has beeninstalled.

ACUTE myocardial infarction is complicated bycomplete heart block in 5-8% of all patients(Brown, Hunt & Sloman, 1969) and when untreatedcarries a mortality rate ranging between 48-71%Transvenous endocardial pacing for the manage-ment of Adams-Stokes disease is now established asa satisfactory method of treatment. More recentlytemporary transvenous pacing has been successfullyused for the treatment of the acute disturbances ofatrio-ventricular conduction which may follow acutemyocardial infarction (Epstein et al., 1966; Harris &Bluestone, 1966; Lassers & Julian, 1968). During thepast 9 years we have treated ninety-five patients withsecond degree or complete atrioventricular blockcomplicating acute myocardial infarction. Themajority of these patients have been referred to ourunit from other hospitals and hence there must besome element of selection which might have in-fluenced our results. Details of the first fifty-fivepatients and the technique used have been reported(Sutton, Chatterjee & Leatham, 1968).

MethodWe prefer to use a US Catheter Corporation uni-

polar C 5650 or bipolar C 5651 transvenous wirepassed via a medially placed antecubital fossa veinexposed under local anaesthesia. There are some whoadvocate the percutaneous subclavian vein approachbut this technique requires a high degree of skill toavoid local complications such as pneumothorax ordamage to the brachial plexus. We prefer not to usethe external jugular veins for temporary pacing butto preserve these in case long-term pacing is eventu-ally required. The transvenous wire is passed into theright atrium using a high-definition image intensifier.The bipolar electrode wire avoids the need for aseparate positive electrode but is slightly more rigidthan the unipolar wire. The electrode wire is passedthrough the tricuspid valve, usually by making a loopoff the right atrial wall, and then into the pulmonaryartery, thereby demonstrating that the electrode wirehas not been inadvertently placed in the coronarysinus. The electrode is then withdrawn from thepulmonary artery and its tip manoeuvred into aposition as low down and as far out in the apex ofthe right ventricle as possible (Fig. 1) and 'wedged'into position by gentle pressure. Sometimes manypositions at the apex of the right ventricle have to betried before a stable site is found. During themanipulation of the electrode tip within the rightventricle, ectopic rhythms may be induced but theyusually disappear once pacing is started. The wire isattached to an external demand pacing box (DevicesImplants Ltd.) and the threshold for pacing (voltagerequired) is measured and this should be less than1 volt at 2 sec duration. Pacing is then commenced atjust above the measured threshold and the stabilityof the electrode tip in the right ventricle is checkedby encouraging the patient to breathe deeply, and tocough; if these actions interrupt pacing even for onecycle, another position is found. If the electrode wireis 'wedged' with unnecessary force then perforationof the myocardium will occur (Fig. 2) leading toearly or late loss of pacing, but rarely causingtamponade.A further test of satisfactory electrode tip impac-

tion is obtained by recording the endocardial electro-cardium, by attaching all four limb leads of abattery-powered electrocardiograph to the patient

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Pacing after acute myocardial infarction 17

FIG. 1. Chest X-ray showing a satisfactory endocardialelectrode position. The electrode tip is 'wedged' at theapex of the right ventricle. The course of the wire throughthe right atrium is free from redundant loops.

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~..:...........|>FIG. 2. Chest X-ray showing myocardial perforation bythe electrode tip which is lying beneath the pericardium.

and the chest lead switched to V1 connected to thefree end of the endocardial electrode wire. When theendocardial electrode is well impacted into the rightventricular wall an injury pattern with elevation ofthe S-T segment of at least 2-3 mV is usually ob-tained (Fig. 3). The patient should then be screenedagain to observe that no redundant wire has beenleft in the right atrium (Fig. 4) since later a loop may

form in the electrode wire within the heart resultingin the withdrawal of the electrode tip from a stableposition and intermittent pacing may result.Once an ideal pacing position is obtained the

electrode wire is firmly tied to the antecubutal fossavein and neighbouring tissues with several silksutures. If a unipolar wire has been used then anindifferent electrode will have to be placed in the

TV ~~~~~~~~~~~~~~~~~~~~~~~~~~ .*.~~~~~~~~~~~~~~~.................

FIG. 3. Endocardial electrocardiogram showing in (A) a good injurypotential indicatingthe electrode tip is satisfactorily 'wedged' and in (B) a poor injury potential indicatingthe electrode tip is not in satisfEctory contact with the endocardium.

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Alan Harris

FIG. 4. Chest X-ray showing a redundant loop of elec-trode wire in the right atrium which later resulted in lossof pacing.

subcutaneous tissue and similarly fixed. The maindisadvantage with the use of an arm vein is the easeof displacement of the electrode tip from the'wedged' position if unrestricted arm movement ispermitted. We therefore always restrict arm move-ment with a special harness but satisfactory restric-tion can be obtained with a fracture board.

Occasionally the situation may demand thattransvenous pacing be carried out without X-rayscreening facilities. This may be quite rapidlyachieved by passing the electrode wire from anantecubital fossa vein, especially the left, and check-ing the position of the electrode tip by recording theintra-cardiac cavity electrocardiogram which clearlydifferentiates the right atrium, right ventricle andpulmonary artery position of the tip of the electrodewire (Chatterjee et a!., 1969). When the typical rightventricular cavity electrocardiogram is recorded theelectrode wire is advanced gently and impacted andoften a good injury current is recorded and a lowpacing threshold obtained. Pacing is then com-menced and the position of the electrode wire radio-logically checked with a portable chest X-ray.

All patients are attached to an external demandunit set at 60/min, which will pace if there is asystolelonger than 1 sec, at no more than twice the mini-mum voltage required to stimulate the right ventricle.Demand pacing with low power will theoretically

lower the risks of inducing ventricular fibrillation byinappropriate stimulation during ectopic rhythms orduring sinus competition (R on T). A unipolar elec-trode is recommended because a greater intracardiacpotential (which inhibits the demand pacemaker) isrecorded with a unipolar than with a bipolar elec-trode thereby reducing the risk of inappropriatestimulation due to low intracardial potential. Anumber of patients have been observed to suddenlydevelop competing fixed-rate pacing although at thetime their own heart rate was satisfactory; this wasfound to be due to a fall in the intracardiac potential(not usually reflected in the conventional externalelectrocardiogram) which often occurs followingacute myocardial infarction (Chatterjee et al., 1970).

All our patients now have suppressant therapyonce the pacing system is satisfactory, usually intra-venous infusion of lignocaine (1-3 mg/min) for3 days and then long acting quinidine as quinidinebisulphate (Kinidin Durules, Astra Chemicals) 0-25 gfour times daily, or procainamide 250-500 mg q.d.s.Oral quinidine seems to be more effective than oralprocainamide in suppressing ventricular ectopicbeats. Because of the risk of precipitating ventricularasystole, oral ventricular depressant drugs must notbe started until the pacing system is installed.Continuing ectopic beats despite increased dose ofsuppressant therapy are treated by increasing thepacing rate, but care must be taken when ventricularfunction is borderline since too fast a rate mayinduce heart failure.

Heart failure is treated by diuretics and digitalis,and lack of improvement with atrio-ventricularpacing (requiring a second transvenous wire to pacethe atrium) in order to obtain the benefit of atrialtransport.The threshold of stimulation is checked daily, and

pacing voltage should be set at not more than twicethe threshold value. A rise of threshold from anycause to above 2 volts at 2 msec is not treated byincreasing the power of the stimulus but by re-positioning the electrode wire to achieve a thresholdas low as possible.

Endocardial potentials should be checked daily toavoid inappropriate stimulation, particularly inpatients with shock and heart failure. Inappropriatestimulation from low cavity potential requires in-creased sensitivity of the demand pacemaker orcontinuous pacing at a higher rate to avoid competi-tion. Increasing the sensitivity of the inhibitingcircuit of the pacemaker will increase the risk ofinhibition of the pacemaker by external electricalinterference from, for example, electric razors,cleaning machines, physiotherapy appliances or evenby potentials from skeletal muscle activity (Fig. 5).The demand system is left in position for 1 weekafter return to sinus rhythm (average 2 days) and a

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Pacing afker acute myocardial infarction

S/2. ICP with arm movement

a L . .. .. -

Demand pacemaker inhibited by pectoral EMG

FIG. 5. The effect of the pectoral muscle electromyogram (EMG), during arm move-ment, on the endocardial electrocardiogram (ICP) in an unpaced subject (uni-polar system). Demand pacing with a sensitive box is interrupted by the pectoral EMG.

P. J. Reynolds pace beat counter is connected with anexternal demand pacemaker (set at 50) for the final24 hr to exclude intermittent block, which requiresprolongation of pacing care. If the pace-countershows no pacemaker action for 24 hr, the pacingsystem is removed but suppressant drugs are con-tinued.

ResultsThe first eighty-two patients were divided into

three groups according to the date of treatment andthe technique (Table 1). The thirty-two patients whowere unpaced (Table 1) were admitted to hospitalbefore our coronary care units were opened and werenot referred to the cardiac unit. Table 1 shows thatthe mortality in the paced groups has fallen from66 to 11%, although the population of patients withpoor prognosis, judged by anterior infarction, heart-failure and shock, was little different in the threegroups. Factors responsible for the improvement ingroup C were thought to be early pacing withavoidance of syncope, impairment in cardiac output,

demand-pacing with awareness of the possibility ofinappropriate stimulation, and the free use of sup-pressant drugs.

Early pacingIn this series of eighty-two patients syncope was

associated with a mortality of 52%, compared with20% in those without syncope (Table 2). Conclusionsof the effect of syncope must be provisional becausethese patients are also the worst risk group, but earlypacing to avoid syncope, and hence further deteriora-tion in the clinical cpndition, seems to be a primeobjective. Furthermore, the installation of a pacingsystem in a convulsing patient can be difficult.

Cardiac outputImprovement in the clinical state with pacing is

often remarkable, but, if shock and heart failurecontinue, indicating a bad prognosis (43% mortality),atrioventricular pacing may improve cardiac outputbecause of appropriate atrial systole (Martin &Cobb, 1966).

TABLE 1. Mortality of acute myocardial infarction complicated by heart block

Anterior Shock andNo. of Death infarct. heart failurecases (%) (%) (%)

Unpaced:1963-66 32 71 38

Paced:A. 1961-66

Fixed rate pacing 18 56 27 66B. 1966-68

Demand pacing 37 38 16 57C. 1968-69

Demand pacing andsuppressant therapy 27 11 22 66

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TABLE 2. Prognostic factors in eighty-two patients with post-infarctatrioventricular block (second or third degree)

MortalityNo. (%)

Anterior infarct 17 (20%) 76Inferior infarct 65 (800') 23Wide QRS 26 (31%) 73Narrow QRS 56 (69%) 16Onset known <24 hr after pain 25 (36%) 32Onset known > 24 hr after pain 45 (64%) 38Syncope 34 (42%) 52No syncope 48 (58%) 20Good clinical state 22 (26%) 13Shock and failure 60 (73°%) 43Return to sinus rhythm 60 (73%) 16No return to sinus rhythm 22 (27%) 82

Demand pacingThe fall in mortality with demand-pacing in 1966

coincided with a reduction of pacemaker power tojust above threshold level, tested daily. The theoreti-cal safety of demand pacing received a setback wheninappropriate stimulation due to transient falls inthe endocardial potential, used to inhibit the pace-maker, was found in some patients with shock (Fig.6). It is possible that the death of some of thepatients with shock who failed to improve withpacing could have been related to low cavitypotentials and inappropriate stimulation producingventricular dysrhythmias.

Suppressant drugsThe free use of suppressant drugs has been the

major factor in reducing the high mortality associ-ated with ectopic beats and ventricular dysrhythmiaswhich may continue despite satisfactory pacing(Table 3). Increasing the pacing rate alone was onlytransiently effective in suppressing ectopic rhythmsand intravenous lignocaine was far superior, thoughsometimes both were required.The disadvantages of pacing are summarized in

Table 4. Electrode displacement would have beenless frequent if subclavian or external jugular veinshad been used for electrode insertion, but the ante-cubital vein approach is much easier for nion-specialized staff, particularly in a sick patient, and isless worrying to the patient. There were four patientson demand pacemakers who were improving yetunexpectedly developed ventricular fibrillation and

FIG. 6. The upper trace shows the RV endocardial potential whichat times is too small to inhibit the demand pacemaker unit. The lowertrace shows sinus rhythm and two inappiopriate pacemaker stimuli. RV=right ventricle, III= lead IIl of the electrocardiogram, Thr Dem=minimumendocardial potential required to inhibit the demand pacemaker.

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Pacing after acule myocardial infacrtion

TABLE 3. Deaths among thirty-nine patients (47%of the eighty-two patients) with ventricular dys-

rhythmia not abolished by pacing

No. of Deathspatients (No.) ( O)

Suppressant drugs 23 3 13No suppressant drugs 16 11 68

TABLE 4 Disadvantages of pacing in eighty-two patients

No. Deaths

VT or VF during electrode insertion 6 0Electrode displacement 19 0Suspected perforation (rise of threshold) 3 0Phlebitis 6 0Ectopic beats induced by pacing 2 0Unexpected VF (demand) 4 3Unexpected VF (fixed rate) 1 1

VT=ventricular tachycaidia, VF=ventricular fibrillation.

three died. Inappropriate stimulation without ade-quate ventricular suppressant therapy was probablya major factor.

Following a period of ventricular pacing theunpaced electrocardiogram shows massive T waveinversion and ST depression which persists for avarying length of time depending on the duration of

Pra - nanf-inav Flecftrorde sitad

FIG. 7. The pre-paced electrocardiogram shows sinusrhythm with normal S-T segments and T waves. After7 days of continuous ventricular pacing, an unpacedelectrocardiogram shows conspicuous T inversion inII, III, aVF, and V3-V7.

pacing (Figs 7 and 8). If the period of pacing is onlya few minutes' duration (Fig. 9), then the ST and Twave changes rapidly regress, but if pacing hascontinued for several days, then the changes maypersist for weeks. There is, however, nothing tosuggest that the changes which occur in the STsegments and T wave after depolarization from an

I5 Min nr1inn

FIG. 8. Series of electrocardiograms obtained from the same patient during15 days of endocardial pacing. The T wave inversion progressively increasedin It, III and aVF, reaching a maximum on day 15.

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22 Alan Harris

Pre- pacing 10 min pacing

Recovery5 Mln 10 Min

10 Min pacing

FIG. 9. A series of electrocardiograms obtained fromthe same patient pre-pacing and after short intervals ofendocardial pacing. Immediately after 10 min of endo-cardial pacingT inversion occurred in V3-V4 which fullyregressed within 10 min. A further 10 min of pacingproduced T inversion again.

abnormal site are of any clinical importance, exceptthat they may be misinterpreted as evidence of pro-gressive coronary disease.

In conclusion, immediate low-power demand

pacing for second and third degree block followinginfarction, together with the liberal use of myo-cardial depressant drugs, appears to be lowering themortality of this serious complication of myocardialinfarction. With the safeguards described, the dis-advantages of pacing are few and it is only when apacing system has been installed that it is safe to usesuppressant drugs.

ReferencesBROWN, R.W., HUNT, D. & SLOMAN, J.G. (1969) The natural

history of atrioventricular conduction defects in acutemyocardial infarction. American Heart Journal, 78, 460.

EPSTEIN, E.J., COULSHED, N., MCKENDRICK, C.S., CLARKE,J. & KEARNS, W.E. (1966) Artificial pacing by electrodecatheter for heart block or asystole complicating acutemyocardial infarction. British Heari Journal, 28, 546.

CHATTERJEE, K., HARRIS, A., LEATHAM, A. & DAVIES, G.(1970) Fall on endocardial potentials after acute myo-cardial infarction. Lancet, i, 1308.

CHATTERJEE, K., SUTTON, R., LAYTON, C.A. & EDWARDS, A.(1969) The cavity electrocardiogram in emergency arti-ficial pacing. Postgraduate Medical Journal, 45, 713.

HARRIS, A. & BLUESTONE. R. (1966) Treatment of slow heartrates following acute myocardial infarction. British HeartJournal, 28, 631.

LASSERS, B.W. & JULIAN, D.G. (1968) Artificial pacing inmanagement of complete heart block complicating acutemyocardial infarction. British Medical Journal, 2, 142.

MARTIN, R.H. & COBB, L.A. (1966) Observations on theeffect of atrial systole in man. Journal of Laboratory andClinical Medicine, 68, 224.

SUTTON, R., CHATTERJEE, K. & LEATHAM, A. (1968) Heartblock following acute myocardial infarction. Lancet, ii,645.

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