Br Heart J 1991;66:185-91

WORKING PARTY REPORT

Recommendations for pacemaker prescription forsymptomatic bradycardia

Report of a working party of the British Pacing and Electrophysiology Group

Members of workingparty:

City General Hospital,Stoke-on-TrentMalcolm ClarkeWestminster Hospital,LondonRichard SuttonSt George's Hospital,LondonDavid WardSt George's Hospital,LondonA John CammRoyal National Heartand Chest Institute,LondonAnthony RickardsWestminster Hospital,LondonAnn IngramLeeds GeneralInfirmaryE John PerrinsBroadgreen Hospital,LiverpoolRichard CharlesRoyal National Heartand Chest Institute,LondonSue JonesGeneral Infirmary,GlasgowStuart CobbeCorrespondence toDr Malcolm Clarke,Honorary Secretary, BPEG,Cardiology Department,City General Hospital,London Road, Stoke-on-Trent ST4 6QG.Accepted for publication26 February 1991

After the first permanent pacemaker implanta-tion in 1958,' the initial developments inpacemaker technology were aimed towardsmore efficient pacemaker performance. Thestandard mode of pacing in these early yearswas single chamber ventricular stimulationand t-his became established as effective life-saving therapy.2 Over the past 10 years,however, there has been a wealth of different

Table 1 NBG pacemaker code

FIRST letter signifies the chamber(s) of the heart beingPACED

A (atrium)V (ventricle)D (atrium and ventricle)

SECOND letter indicates the chamber(s) being SENSEDA (atrium)V (ventricle)D (atrium and ventricle)

TTT"RT lpttpr intiirnti-c the MOTYR nf czpncinav~~~~~~~~~~~~~~~~~~ rIlnIJ ILLCr inuiaLebWtsnsivii VAOsensingfeatures incorporated into pacemaker design, I (inhibited)including programmability, telemetry, and T (triggered)different "modes" of pacing.6 D (inhibited and triggered)

The British Pacing and ElectrophysiologyGroup (BPEG) was formed as a specialistsubgroup of the British Cardiac Society in discussed in this document. Each of the pac-1976 and consists of cardiologists, technicians, ing modes under discussion is described in theand representatives from the pacemaker manu- Appendix.facturing industry. BPEG is organised for thepurposes of scientific communication,research, and education specifically related to AHA/ACC Guidelinescardiac pacing and electrophysiology. The Over the past 30 years the clinical indicationsgroup organises an -active scientific -and--- fbr pacing have increased to include a largeeducational programme and has more than number of different cardiac arrhythmias. To200 members. clarify the situation a combined workingA working party was formed by BPEG to group of the American Heart Association and

establish guidelines for the use of the different the American College of Cardiology has publ-modes of cardiac pacing. The nomenclature ished guidelines on the indications for pac-for pacemaker modes accepted for inter- ing.'4 There are three main classes of patients,national use is that produced by a combined which may be summarised as follows:working party of the North American Society Class I-Conditions in which there is gen-of Pacing and Electrophysiology (NASPE) eral agreement that permanent pacemakersand the British Pacing and Electrophysiology should be implanted. This includes syncopalGroup (BPEG) known as the NBG (NASPE/ patients with complete heart block or pro-BPEG generic) code.7 This is a code of five longed sinus arrest.letters of which the first three are most often Class II-Conditions in which permanentused (table 1). In addition, a fourth letter R is pacemakers are frequently used but there isused if adaptive rate pacing is programmed. some divergence of opinion about whetherIn adaptive rate (or rate responsive) pacing they are needed. Included within this groupthere is an additional sensor in the pacemaker are the sick sinus syndrome patients withoutsystem that detects a physiological or semi- syncope but with other symptoms and alsophysiological result of exercise or emotion and patients with symptomatic incompleteincreases the pacemaker rate on the basis of a atrioventricular block. Asymptomatic com-programmable algorithm. Sensors that are plete heart block is also in this category.presently successfully used in pacemakers Class III-Conditions in which there isinclude activity,8 respiratory rate9 and minute general agreement that pacemakers are not

ventilation,'0 right ventricular pressure (dP/ necessary. This includes asymptomaticdt),"1 central venous temperature,'2 evoked patients with sinus node disease or first or

QT interval,5 and oxygen saturation. 13 second degree atrioventricular block andWhatever the sensor effective adaptive rate patients with unexplained syncope withoutpacing can be used independently of atrial obvious cardiac arrhythmia.activity. Recently, activity sensing has beencombined with dual chamber pacing.6The NBG code also uses a fifth letter relat- BPEG Guidelines

ing to antitachycardia function which is not The AHA/ACC recommendations have

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provided a logical foundation to guidephysicians considering cardiac pacing as atreatment for their patients. There are,however, some areas where published dataindicate that pacing should be more widelyused as a first-line therapy.

Carotid sinus syndrome"5 and, morerecently, malignant vasovagal syncope"6 wouldnow qualify as firm indications for pacemakerimplantation when appropriate investigationshows a major cardioinhibitory effect.6 17 Fur-thermore, untreated persistent second degreeatrioventricular block, even in asymptomaticpatients, has been shown to be associated witha reduced expectation of life. In this group ofpatients prophylactic pacing restores lifeexpectation to normal.'8 The Wenckebachphenomenon can occur during sleep in normalindividuals with high vagal tone and thesepeople do not need to be considered for treat-ment. However, those asymptomatic patientswith either Wenckebach or Mobitz II seconddegree atrioventricular block occurring duringmuch of the day and night would qualify forpacemaker implantation,19 as would patientswith asymptomatic complete heart block.With these modifications, the AHA/ACCguidelines can be used both as a clinical aidand a basis for medical audit of the indicationsfor pacemaker implantation. However, recom-mendations about the choice of pacemakerprescription are limited.

Choice ofpacemaker modeWhen the choice of pacemaker mode for anindividual patient is considered, the ideal isproduction of a paced cardiac rhythm with asmany features of normal sinus rhythm aspossible (table 2). The guidelines proposed inthis paper are based on an attempt to allow thepacemaker response to behave asphysiologically as possible. This includes res-toration of atrioventricular synchrony and/orrate adaptive pacing wherever needed. Toachieve this ideal, detailed information of theunderlying cardiac rhythm should be obtainedbefore or during pacemaker implantation. Thefollowing features should be considered.

ATRIOVENTRICULAR SYNCHRONYPacemaker systems that maintain atrioven-tricular synchrony with a physiologicalatrioventricular interval have been shown toincrease cardiac output both at rest and onexercise in patients with normal and impairedleft ventricular function.20 Even in the absenceof an exercise induced rate response, atrioven-tricular synchrony reduces the number ofminor symptoms (dizziness, lethargy) that areassociated particularly with sinus node dis-ease.21

Table 2 General principles ofpacemaker choice

(1) The ventricle should be paced if there is actual orthreatened atrioventricular block.

(2) The atrium should be paced/sensed unlesscontraindicated.

(3) Rate response is not essential if the patient is inactive orhas a normal chronotropic response.

(4) Rate hysteresis may be valuable if the bradycardia isintermittent.

RATE MODULATIONAdaptive rate (or rate responsive) pacing sig-nificantly increases cardiac output on exercisein patients with atrioventricular block8 andsinus node disease.22 Patients treated with rateresponsive pacemakers achieve higher work-loads and greater exercise tolerances.822

ATRIAL PACINGEvidence is accumulating of a considerablereduction in the high spontaneous incidence ofthe development of atrial fibrillation23 and ofsystemic emboli" 2 in patients with sinus nodedisease treated by a pacing system that main-tains atrioventricular synchrony.

LEFT VENTRICULAR PERFORMANCESpontaneous (normal) ventricular contractionmay allow better ventricular function than apaced ventricular beat.26 Typically, the ven-tricular pacing lead is inserted into the rightventricle and delivery of the pacing stimulus atthis site results in the equivalent of left bundlebranch block. This causes measurable impair-ment of left ventricular contraction which maybe ofhaemodynamic relevance in both normal27and compromised left ventricles.28

RATE HYSTERESISHysteresis is a programmed feature wherebythe pacemaker paces at a faster rate than thesensing rate. For example, pacing at 80 pulses aminute with a hysteresis rate of 55 means thatthe pacemaker will be inhibited at all ratesdown to 55 beats per minute. Having beenactivated at a rate below 55, the pacemaker thenswitches on and paces at 80 pulses a minute.Unless careful record is made in the patient'snotes that hysteresis has been programmed,pacemaker malfunction could be incorrectlyinferred.

ATRIAL ARRHYTHMIASThe presence of atrial activity other thanchronic or frequently repetitive atrial flutter orfibrillation generally requires an atrialpacemaker electrode. Paroxysmal atrial arr-hythmias are not a contraindication to atrialpacing29 or sensing in most cases, because atrialpacing may stabilise the atrial rhythm30; inothers concomitant drug treatment may bebeneficial. In those patients with atrialbradycardia and intact atrioventricular con-duction, a single chamber atrial pacemaker canbe considered to be the treatment of choice.29However, the presence of minor abnormalitiesof atrioventricular conduction-for examplefirst degree atrioventricular block (PR intervalprolongation) or bundle branch disease withnormal atrioventricular conduction generallysuggests a need for placement of a ventricularlead in patients with symptomatic sinoatrialdisorders."3 32

TYPES OF ARRHYTHMIAS REQUIRING PACINGTable 3 shows the percentage occurrence ofarrhythmias in a typical population of patientswith bradycardia requiring pacing.3" For thepurposes of table 3, sinus node disease includes

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Recommendations for pacemaker prescription for symptomatic bradycardia

Table 3 Percentage incidence of variousbradyarrhythmias in a typical pacemaker population

Arrhythmia %

Sinus node disease 25AV block 42Sinus node disease + AV block 10Atrial fibrillation + AV block 13Carotid and vasovagal syndromes 10

AV, atrioventricular.

sinus bradycardia, sinus arrest, sinoatrialblock, and the tachycardia-bradycardia syn-dome, but does not include atrial bradyarr-hythmias associated with carotid sinus syn-drome or malignant vasovagal syndrome.

CAROTID SINUS AND MALIGNANT VASOVAGALSYNDROMESCarotid sinus syndrome can be diagnosed in apatient with syncope by the presence of apositive carotid sinus massage test. Thedevelopment of either a period of asystole inexcess of three seconds, or the appearance ofatrioventricular block, during five to sixseconds of firm carotid sinus massage (notcompression) is regarded as diagnostic."7 Thetest should not be performed in patients withcarotid artery bruits or documented stenosis,after recent myocardial infarction, or if thepatient is digitalised. Variations of carotidsinus syndrome include micturition syncope,34cough syncope,35 and deglutition syncope.'6Malignant vasovagal syncope can be demon-strated by performing a 600 head-up tilttest. Syncope associated with bradycardiaor hypotension or both occurs within 40minutes."

In patients with carotid sinus and malignantvasovagal syndromes there are two componentsto the syncope-bradycardia (cardio-inhibition) and peripheral and splanchnicvasodilation (vasodepression). In patients witha pronounced vasodepressor effect, pacing isless successful than in patients with a dominantcardioinhibitory effect.15 Ifpatients are suitableTable 4 Recommended pacemaker modes

Diagnosis Optimal Alternative Inappropriate

SND AAIR AAI VVIVDD

AVB DDD VDD AAIDDI

SND and AVB DDDR DDD AAIDDIR DDI VVI

Chronic AF VVIR VVI AAIwith AVB DDD

VDDCSS DDI DDD AAI

VVI* VDDMVVS DDI DDD AAI

VVItVDD

The optimal mode of pacing should be considered for mostpatients. The alternative mode should be regarded as beingless satisfactory, but acceptable in some groups of patients-for example those who are disabled by another disease, thosewith very intermittent symptoms, or those who have a shortlife expectancy because of another disease. When a patientwith, for example, a previous hemiplegia or with terminalneoplasia has atrioventricular block, VVI may suffice to reducesymptoms.*If VVI is ever chosen for the management of carotid sinussyndrome rate hysteresis is recommended.8 Patient selectionshould follow the guidelines suggested by Brignole et al.39tSee reference.'AVB, atrioventricular block; AF, atrial fibrillation or flutter;MV.VS, malignant vasovagal syndrome; SND, sinoatrial nodedisease; CSS, carotid sinus syndrome.

for pacing the mode of choice for carotid sinussyndrome and malignant vasovagal syndromeis DDI,37 frequently with hysteresis as anadded feature.38

ATRIAL TRACKING PACING SYSTEMSIt is recognised that the pacing system knownuniversally as DDD behaves for most of thetime as a VDD system. The only difference isthe behaviour at the lower programmed rate,where the DDD paces into the atrium and theVDD has a back-up VVI mode. For the patientwith bradycardia that is slower than the lowerprogrammed rate, this may have significantdisadvantages including pacemaker syndrome.In sinus node disease the potential benefit ofpacing the atria is not available in VDD mode.Table 4 shows the recommended modes,

based on these principles, for patients withall varieties of bradyarrhythmias requiringpacing.

Complications of inappropriate modeselectionInappropriate pacemaker modes (table 4)should be avoided to prevent the followingcomplications:

(a) Pacemaker syndrome,4' which is causedeither by retrograde conduction from the ven-tricle to the atrium or by lack of synchronousatrioventricular activity that results in loss ofatrial transport function. Pacemaker syndromemay cause symptoms of syncope or pre-syn-cope as a result of retrograde conduction.4'Dyspnoea may occur where there is high pul-monary venous pressure and low cardiac out-put and associated mitral regurgitation(demonstrable by Doppler echocardiography)caused by a lack of atrioventricular syn-chrony.42 Neck pulsation may be seen whenretrograde atrioventricular conduction causestricuspid regurgitation or right atrial contrac-tion against a closed tricuspid valve. The trueincidence of pacemaker syndrome is not welldefined but it is thought that 10% of patientspaced VVI have quite severe symptoms andanother 15% have a reduced quality of life as aresult.4' All these symptoms can be relieved bya more appropriate pacing mode.

(b) Inappropriate atrial tracking of atrialtachyarrhythmias by aDDD or VDD system.43Atrial tachycardia, flutter, or fibrillationproduce an electrogram which can be easilydetected by the atrial sensing amplifier of thepacemaker, which will then track this rhythmat its upper pacing rate. Newer dual chamberrate adaptive systems incorporate algorithmsthat prevent or minimise inappropriate ven-tricular pacing in response to atrial fibrillation.

(c) Additional atrioventricular block in apatient with sinus node dysfunction may not beeasily detected initially." Normal 1:1 atrioven-tricular conduction at atrial pacing at rates of140 usually indicates adequate atrioventricularnodal function. The appearance of the atrio-ventricular Wenckebach block at slower rates

may be considered indicative of importantimpairment of atrioventricular node conduc-tion which warrants placement of a ventricular

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lead. There may be other evidence ofinadequate atrioventricular conduction fromHolter monitoring, exercise stress testing, orHis bundle electrography.

(d) Lack ofphysiological heart rate responseon exercise. Unrecognised sinus node dysfunc-tion in a patient with atrioventricular blockwould result in inadequate performance of anatrial tracking (DDD) pacemaker. In addition,there are some patients with sinus node diseasetreated by atrial rate modulated pacing systemswho may develop abnormal atrioventricularconduction on exercise45 resulting in anunusual variety of pacemaker syndrome.

Additional guidelinesThe following additional guidelines are recom-mended to enable accurate assessment of apatient requiring pacemaker implantation:

(a) In selected patients atrioventricular con-duction should be assessed by Holter, carotidsinus massage, and atrial pacing to assess theatrioventricular Wenckebach point at the timeof implant if atrial pacing (AAI) is beingConsidered.

(b) Retrograde atrioventricular conductionshould be assessed by ventricular pacing ifVVIor VVIR pacing is considered. Head-up tiltingduring ventricular pacing may reveal latentsymptoms.

(c) If VDD or DDD pacing is being con-sidered in active patients the chronotropicresponse of the sinus node should be assessedby Holter or exercise testing. If the response isinadequate an appropriate sensor driven sys-tem may be needed.

Consequences of increased use of dualchamber and rate responsive pacingCOSTA VVIR unit costs about 40-50% more and adual chamber unit costs 40-100% more than amultiprogrammable single chamber pace-maker. In addition, a dual chamber systemrequires two pacing leads which furtherincrease the cost. Rate-responsive pacing sys-tems have a shorter battery lifetime than non-rate responsive modes because of their overallfaster pacing rate and the inherent currentdrain of the sensor.However, pacing is cost effective in terms of

relief of symptoms, prolongation of life, andimprovement of the quality of life.20' 50Patients with pacemakers rarely need to bereadmitted to hospital because of problems. Soa tailored pacemaker prescription that followsthe guidelines in this report will offer good valuefor money.

FOLLOW UPPatient follow up with VVIR and dual chambersystems is initially more complex and timeconsuming. Additional programming is neces-sary together with Holter taping and exercisetesting where required. Support staff need to

be trained. When the pacing system has been"fine tuned" to the individual patient'srequirements, however, subsequent follow upis less time consuming.

COMPLICATIONSComplex pacing systems are more susceptibleto problems. Dual chamber systems requiretwo endocardial leads and lead related com-plications are therefore slightly increased.5"Inappropriate programming may also give riseto difficulties. A badly programmed sensor maygive excessive or inadequate rate responses. Itis possible to select an inappropriate sensorsystem for an individual patient-for example,an activity sensor in a bedbound patient or aminute-ventilation sensor in a patient withchronic lung disease are as inappropriate as aDDD system would be in a patient with atrialflutter.

Which hospitals should implant andfollow up pacemakers?Over recent years, it has been the policy ofsome regional health authorities to encouragepacemaker implantation in district general hos-pitals. This is acceptable but it demands at leastone cardiologist fully trained in the complexdisciplines of dual chamber pacing and followup, together with at least one similarly trainedphysiological measurement technician. Hosp-itals with only one cardiologist would need tomake arrangements with similarly trained staffin a neighbouring district to cover periods ofabsence.

Choice of pacing systemWhen choosing a pacemaker system for apatient, a physician usually adopts one of threepolicies:

(a) A basic VVI system for everyone,irrespective of need, symptoms, or electro-cardiographic findings. This policy is clearlyinappropriate.

(b) The routine use of the most sophisticateddual chamber rate adaptive pacemaker(DDDR) for every patient, programmed tomatch the patients' needs. This is medicallyacceptable, but inappropriate on grounds ofcost.

(c) A device that is carefully prescribedaccording to the guidelines in this report. Thisagain is medically sound, but this policyrequires thorough assessment of the patientbefore pacemaker implantation and meticulousfollow up.This working party of BPEG recommends

that selection of the appropriate pacemakermode should follow the basic principles andguidelines discussed above. This will require afairly radical change of practice in somepacemaker centres in the United Kingdom andadditional funding for the more complexpacemaker systems and their subsequentfollow up.

1 Elmqvist R, Senning A. An implantable pacemaker for theheart. Smyth CN, ed. In: Medical electronics. Proceedingsof the second international conference on medical electronics.London: Illife, 1959:253.

2 Ginks W, Leatham A, Siddons H. Prognosis of patientspaced for chronic atrioventricular block. Br Heart J1979;41:633-6.

3 Sutton R, Citron P, Perrins J. Physiological cardiac pacing.PACE 1980;3:207-17.

188

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Recommendations for pacemaker prescription for symptomatic bradycardia

4 Clarke M, Allen A. Use of telemetered electrograms in theassessment ofnormal pacemaker function. JElectrophysiol1987;1:388-95.

5 Rickards AF, Norman J. Relation between QT interval andheart rate. New design of a physiologically adaptivecardiac pacemaker. Br Heart J 1981;45:56-61.

6 Kappenberger L, Hepers L. Rate responsive dual chamberpacing. PACE 1986;9:987-91.

7 Bernstein A, Camn J, Fletcher R, et al. The NASPE/BPEGgeneric pacing code for antibradyarrhythmia and adaptiverate pacing and antitachycardia devices. PACE 1987;10:794-9.

8 Humen D, Anderson K, Brumwell D, Huntley S, Klein G. Apacemaker which automatically increases its rate withphysical activity. In: Steinbach K, Glogard A, Laszk-ovicsa D, Schneibelhofer W, Weber H, eds. Cardiacpacing. Darmstadt: Steinkopff Verlag, 1983:252-64.

9 Rossi P, Plicchi G, Canducci G, Rognoni G, Aina F.Respiration as a reliable physiological sensor for controll-ing cardiac pacing rate. Br Heart J 1984;51:7-14.

10 Lau C, Antoniou A, Ward D, Camm AJ. Reliability ofminute ventilation as a parameter for rate responsivepacing. PACE 1989;12:321-30.

11 Sutton R, Sharma A, Ingram A, Camm J, Lindemans F,Bennett T. First derivative of right ventricular pressure asa sensor for an implantable rate responsive VVI pacemaker[abstract]. PACE 1988;11:487.

12 Alt E, Volker R, Hogl B, MacCarter D. First clinical resultswith a new temperature-controlled rate responsivepacemaker. Circulation 1988;78 (suppl III): 116-24.

13 Stangl K, Wirtzfeld A, Heinze R, Laule M. First clinicalexperience with an oxygen saturation controlledpacemaker in man. PACE 1988;11:1882-7.

14 Frye RL, Collins JJ, DeSanctis RW, et al. Guidelines forpermanant pacemaker implantation-May 1984. A reportof the joint American College of Cardiology/AmericanHeart Association Task Force on assessment of Car-diovascular Procedures (Subcommittee on PacemakerImplantation). J Am Coll Cardiol 1984;4:434-42.

15 Morley CA, Perrins EJ, Grant P, Chan SL, McBrien DJ,Sutton R. Carotid sinus syncope treated by pacing.Analysis of persistent symptoms and role of atrioven-tricular sequential pacing. Br Heart J 1982;47:411-8.

16 Fitzpatrick A, Sutton R. Tilting towards a diagnosis inrecurrent unexplained syncope. Lancet 1988;i:658-60.

17 Morley C, Sutton R. Carotid sinus syndrome--editorialreview. Int J Cardiol 1984;6:287-93.

18 Shaw D, Kekwick C, Veale D, Gowers J, Whistance T.Survival in second degree atrioventricular block. Br HeartJ 1985;53:587-93.

19 Campbell RWF. Chronic Mobitz type I second degreeatrioventicular block. Has its importance been underes-timated? Br Heart J 1985;53:585-6.

20 Kruse I, Armman K, Conradson T, Ryden L. A comparisonof the acute and long-term haemodynamic effects ofventricular inhibited and atrial synchronous ventricularinhibited pacing. Circulation 1981;65:846-55.

21 Mitsuoka T, Kenny RA, Yeung TA, Chan SL, Perrins JE,Sutton R. Benefits of dual chamber pacing in sick sinussyndrome. Br Heart J 1988;60:338-47.

22 Rognoni G, Bolognese L, Aina F, Occhetta E, Magnani A,Rossi P. Respiratory dependant atrial pacing, man-agement of sinus node disease. PACE 1988;11:1853-9.

23 Rosenqvist M, Brandt J, Schuller H. Long-term pacingin sinus node disease; effects of stimulation mode oncardiovascular morbidity and mortality. Am Heart J1988;116:16-22.

24 Santini M, Alexidou G, Porto M, Santini A, Ammirati F,Ansalone G. The sick sinus syndrome: prognosis asfunction of age, conduction defects and pacing mode[abstract]. PACE 1989;12:1237.

25 Bianconi L, Boccadamo R, Di Florio A, et al. Atrial versusventricular stimulation in sick sinus syndrome; effects onmorbidity and mortality [abstract]. PACE 1989;12:1236.

26 Theodorakis G, Fitzpatrick A, Ahmed R, Travill C, SuttonR. Doppler estimation of cardiac output during AAI andDDD pacing (with varying AV delay) at different pacingrates [abstract]. PACE 1989;12:1185.

27 DeNardo D, Antolini M, Pitucco 0, et al. Effects of leftbundle branch block on left ventricular function inapparently normal subjects. Cardiology 1988;75:365-71.

28 Gibson DG, Chamberlain DA, Coltart DJ, Mercer J. Effectof changes in ventricular activation on cardiac haemo-

dynamics in man. Comparison of right ventricular, leftventricular, and simultaneous pacing of both ventricles.Br Heart J 1971;33:397-400.

29 Ryden L. Atrial inhibited pacing-an underused mode ofcardiac stimulation. PACE 1988;1 1:1375-9.

30 Egobasti A, Gueunoun M, Sasdjian A, et al. Long-termfollow-up ofpatients treated with VVI pacing and sequen-tial pacing with special reference to VA retrograde con-duction. PACE 1988;11:1929-34.

31 Sutton R, Kenny R. Natural history of sick sinus syndrome.PACE 1986;9:1110-4.

32 Rosenqvist M, Obel I. Atrial pacing and the risk for AVblock: Is there a time for change of attitude? PACE1989;12:97-101.

33 British Pacing and Electrophysiology Group Database-statistics for the City General Hospital, Stoke-on-Trent,1986-1989.

34 Haldane JH. Micturition syncope. Can Med Assoc J 1969;101:712-4.

35 Hart G, Oldershaw P, Cull R, Humphrey P, Ward D.Syncope caused by cough-induced complete atrioven-tricular block. PACE 1982;5:564-66.

36 Igaluer S, Swartz B. Heart block periodically induced by theswallowing of food in a patient with cardiospasm(vasovagal syncope). Ann Otol Rhinol Laryngol 1936;45:875-81.

37 Sutton R, Ingram A, Clarke M. DDI pacing in the treatmentof sick sinus, carotid sinus and vasovagal syndromes[abstract]. PACE 1988;11:827.

38 Morley C, Perrins EJ, Chan SL, Sutton R. The role of ratehysteresis pacing in the hypersensitive carotid sinussyndrome. PACE 1983;6:1224-8.

39 Brignole M, Menozzi C, Lolli G, Oddone D, Roti S. When isDDD pacing necessary and when is VVI pacing sufficientin carotid sinus syndrome? [abstract]. PACE 1989;12:1169.

40 Fitzpatrick AP, Travill CM, Vardas PE, et al. Recurrentsymptoms after ventricular pacing in unexplained syn-cope. PACE 1990;13:619-24.

41 Ausubel K, Furman S. The pacemaker syndrome. AnnIntern Med 1985;103:420-9.

42 Naito M, Dreyfus L, David D, Nicholson E, Mardela T,Kmetzo J. Re-evaluation of the role of atrial systole incardiac hemodynamics: evidence for pulmonary venous

regurgitation during abnormal atrioventricular sequenc-ing. Am Heart J 1983;105:295-302.

43 Castellanos A, Lemberg L, Rodriquez-Tocker L, et al.Atrial synchronised pacemaker arrhythmias, revisited.Am Heart J 1968;76:199-205.

44 Steinbach K, Forohner K, Meisl F, et al. Atrial stimulation.In: Perez G6mez F, ed. Cardiac pacing. Madrid: Grouz,1985:629.

45 Clarke M, Allen A. Rate responsive atrial pacing resulting inpacemaker syndrome [abstract]. PACE 1987;10:1209.

46 Perrins JE, Morley CA, Chan SL, Sutton R. Randomisedcontrolled trial of physiological and ventricular pacing. BrHeart J 1983;50:112-7.

47 Lau CP, Rushby J, Leigh-Jones M, et al. A double blindcross-over study on the symptomatology and quality of lifein patients with rate responsive pacemakers [abstract].JAm Coll Cardiol 1989;13:113.

48 Fitzgerald WR, Graham IM, Cole T, Evans DW. Age, sex,and ischaemic heart disease as prognostic indicators inlong-term cardiac pacing. Br Heart J 1979;42:57-60.

49 Edhag 0, Swann A. Prognosis of patients with completeheart block or arrhythmic syncope who were not treated bycardiac pacemakers. Acta Med Scand 1976;200:457-63.

50 Williams A. Economics of coronary artery bypass grafting.BMJ 1985;291:326-9.

51 Sutton R, Ingram A, Briers L, et al. Ten years ofphysiological cardiac pacing. In: Belhassen B, Feldman S5Copperman Y, eds. Cardiac pacing and electrophysiology.Jerusalem: R & L Creative Communications, 1987:141-2.

52 Cunningham T. Pacemaker syndrome due to retrogradeconduction in DDI pacemaker. Am Heart J 1988;115:478-9.

53 Ricci D, Rider A, Mason J. Recurrent tachyarrhythmiaassociated with a bifocal demand pacemaker. Chest 1977;72:120-3.

54 Den Dulk K, Lindemans FW, Banf W, et al. Pacemakerrelated tachycardia. PACE 1982;5:476-85.

55 Torresani J, Egobasti A, Allard-Latour G. Pacemakersyndrome with DDD pacing. PACE 1984;7:1148-51.

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