Journal, Sinus bradycardiaSinus bradycardia 745 was not present at rest at sometime. Brady-cardia...

British Heart Journal, I97I, 33, 742-749.

Sinus bradycardia

Dennis Eraut and David B. ShawFrom the Cardiac Department, Royal Devon and Exeter Hospital, Exeter, Devon

This paper presents the features of 46 patients with unexplained bradycardia. Patients were ad-mitted to the study if their resting atrial rate was below 56 a minute on two consecutive occasions.Previous electrocardiograms and the response to exercise, atropine, and isoprenaline were studied.

The ages of the patients variedfrom I3 to 88years. Only 8 had a past history of cardiovasculardisease other than bradycardia, but 36 hJd syncopal or dizzy attacks. Of the 46 patients, 35 hadanother arrhythmia in addition to bradycardia; at some stage, i6 had sinus arrest, i.5 hadjunc-tional rhythm, 12 had fast atrial arrhythmia, I6 had frequent extrasystoles, and 6 had atrio-ventricular block. None had the classical features of sinoatrial block. Arrhythmias were oftenproduced by exercise, atropine, or isoprenaline. Drug treatment was rarely satisfactory, but onlyi patient needed a permanent pacemaker.

It is suggested that the majority of the patients were suffering from a pathological form ofsinus bradycardia. The aetiology remains unproven, but the most likely explanation is a loss ofthe inherent rhythmicity of the sinoatrial node due to a primary degenerative disease. Thedescriptive title of 'the lazy sinus syndrome' is suggested.

Bradycardia with a slow atrial rate is usuallyregarded as an innocent condition common incertain types of well-trained athlete, but occa-sionally it may occur in patients with symp-toms of heart disease. Laslett in I909 de-scribed a 40-year-old woman who had a slowpulse and complained of fainting attacks.Using a MacKenzie Polygraph, he showedthat the attacks were associated with arrestof the whole heart. Subsequently, there havebeen a number of reports of patients whotended to have a slow atrial rate and weresubject to other disorders of cardiac rhythm.In some instances the bradycardia was con-sidered to be sinus (Campbell, I943; Pearson,1945; Short, I954; Birchfield, Menefee, andBryant, I957), while in others sinoatrial blockwas suggested as the mechanism (Levine,I9I6; Cowan, I939; Stock, I969; Rokseth etal., 1970). The clinical details have variedfrom case to case, but commonly reportedfeatures both in those described as havingsinus bradycardia and those with sinoatrialblock are syncope and episodes of tachycardia.The cardiograms have on occasions shownsinus arrhythmia, wandering pacemaker, sinusarrest, with and without junctional (nodal)escape, paroxysmal atrial tachycardia, atrialflutter, and atrial fibrillation. The study pre-sented in this paper was undertaken in an

Received 7 October 1970.

attempt to define the clinical syndrome ofbradycardia with a pathologically slow atrialrate and to clarify the nature of the arrhyth-mia.

Plan of studyPatients were admitted to the study if their restingatrial rate was below 56 a minute on two consecu-tive visits, providing they were not taking drugsof the digitalis group, or propranolol, quinidine,procainamide, methyldopa, or bethanidine.Patients with untreated myxoedema, jaundice, orknown raised intracranial tension were excludedas were those with temporary slowing of the heartin association with recent myocardial infarction(within 28 days), or acute carditis.

Forty-six patients fulfilled the criteria of thestudy. Most of these were found after a directapproach was made to the family doctors in theclinical area. Two hundred and ninety doctorswere asked to give details of patients with heartblock or pulse rates below 56 a minute, and replieswere obtained from all but 8. A full report of thissurvey has been given by Shaw and Eraut (1970).Nineteen patients were seen in routine hospitalpractice over a period of 6 years and 2 were re-ported to us by colleagues who knew of ourinterest in the condition. The patients have beenfollowed up at intervals for periods up to 6 years.Previous electrocardiograms were obtained in 23of the 46 patients, the average time between thefirst and last cardiogram being approximately 5years.Most of the patients were seen in the Cardiac

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Sinus bradycardia 743

Department at the Royal Devon and ExeterHospital. Six were unable to attend and werevisited at their homes only. One patient (Case 20)was not seen by us; Dr. Cosh of Bath has kindly

, sent serial reports. The patients were asked if theysuffered from syncopal attacks, dizziness, dys-pnoea, or chest pain on effort, and inquiry wasmade for a past history of diphtheria, rheumaticfever, or myocardial infarction. After a generalphysical examination, a standard 12-lead cardio-gram was recorded and the resting heart rate wastaken from a 3-foot strip of lead II. In 32 patientsa continuous recording was made for 3 minutesat a slow speed with a 3-channel mingographrecorder. Records were repeated after exercise in42 patients, and in 27 patients records were takenthroughout the standard exercise test used in thedepartment. This consists of walking up and downsteps at a fixed rate for 3 minutes, followed by a3-minute rest with continuous cardiogram record-ing. The effect of o06-i mg atropine was studiedby serial cardiograms in 22 patients, the drugbeing given by intravenous injection in 3 andorally in the others. All experienced dryness ofthe mouth. Isoprenaline was given by intravenousinjection in 3 patients and sublingual tablets (20mg) in 24 patients.The cardiogram was examined to check the

rhythm and atrial rate at rest and during exercise.A search was made for junctional (nodal) rhythm,periods of sinus arrest with or without escapebeats, fast atrial arrhythmia, atrial tachycardia,flutter or fibrillation, coupled and frequent extra-systoles (more than i for io sinus beats), and forany evidence of abnormal atrioventricular con-duction. The PR interval and the duration andheight of the P waves were measured in lead II.Where atrial arrest occurred, the duration of thearrest and the preceding and following PP inter-vals were measured to assess the presence or ab-sence of single blocked complexes of sinoatrialblock or of Wenckebach conduction in sinoatrialblock. First and third degree sinoatrial block can-not be recognized from the cardiogram (McGarry,I966). The criteria for the diagnosis of seconddegree sinoatrial block used in this study are

-based on the work of Winton (1948), McGarry'(i966), and Stock (I969), and are as follows.

i Isolated single dropped beats with a prolongedPP cycle, length twice the length of the predomin-ant PP interval.2 Several consecutive dropped beats with a pro-longed PP length 3, 4, or 5 times the predominantPP interval.3 Sudden doubling or trebling of the atrial rate,often in response to exercise or atropine and im-plying a relatively fixed 2: 1 or 3: I sinoatrialblock.4 Wenckebach conduction in sinoatrial blockwith beats dropped more or less regularly. In thisinstance there should be progressive shortening,of the PP interval up to the pause, the PP intervalincluding a blocked sinoatrial impulse is shorterthan twice the length of the PP interval precedingit (provided that only one impulse is blocked), and

the PP interval following the dropped sinoatrialimpulse is longer than the PP interval precedingit. In cases of doubt the duration of the sinuscycle can be calculated and the presence or absenceof sinoatrial block tested by formulae suggestedby Schamroth and Dove (I966).

ResultsBasic clinical data are given in Table i. Theage range of the patients with bradycardia waswide (I3 to 88), but over half were elderly,being within the range 55 to 75. Only 8 pa-tients had a history of heart disease other thanthe bradycardia. Four patients had had amyocardial infarction. Two patients had con-genital heart disease: one of these had anatrial septal defect, and one had dextrocardiaand situs inversus. One patient was consideredto have an idiopathic cardiomyopathy. Onepatient had rheumatic heart disease and afurther 4 gave a history of childhood rheu-matic fever, but had no clinical history ofheart disease. Neurological disease was alsorare. Three had had cerebrovascular acci-dents, and 3 had been considered to haveepilepsy, though on review this diagnosis wassubsequently abandoned in one who had mildpresenile cerebral degeneration, and was un-substantiated in another. Two patients hadsuffered from myxoedema and were onthyroxine, and one had had a partial thyroid-ectomy but was euthyroid at the time of thestudy.

Thirty-six of the 46 patients had symptomsof circulatory impairment. Twenty-three ex-perienced disturbance of consciousness, in I4there were episodes of complete loss of con-sciousness, and iS had attacks of dizziness; 6patients had both. Central chest pain on exer-tion was complained of by 17 patients; only3 of these had a past history or cardiographicevidence of myocardial infarction. Twenty-nine patients complained of breathlessnesson exercise, and I0 patients complained ofswollen ankles.The mean blood pressure for the group was

I50/77 mmHg, the range being Ioo/6o to240/I00 mmHg. Only i had a diastolic bloodpressure above ioo mmHg.The resting atrial rate at the time of the last

assessment when sinus rhythm was dominantranged from 28 to 54 a minute, the mean forthe group being 44 (see Table i). The rateincreased with exercise but not to the sameextent as observed in normal subjects. Themean maximal exercise atrial rate in the pa-tients fully studied was some 20 a minutebelow the mean normal value for this depart-ment. Eleven of the patients developed anarrhythmia during or just after exercise, which



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TABLE I Clinical data on 46 patients studied

Case Age Sex Minimum Symptoms Atrial ArrhythmiaNo. (yr) length of rate/min

history (yr) Sinus Junctional Fast atrialarrest rhythm arrhythmia

36 I3 M43 I5 M6 I7 M34 i8 M46 26 M

27 38 M13 39 M20 40 F40 42 M

38 43 M32 43 F42 44 M41 47 M35 47 M

4 49 M3 54 M

31 54 FI9 59 F

25 6o M

10 62 M

26 62 M

33 62 M5 62 F

7 63 M

I5 64 F

I 65 M2 69 M17 69 M8 70 F

22 70 F

III

'9

29I

I33

2

35I

433

5I

I3

5

'5

32

'53

2

I

III

5

Breathlessness 54Disturbance of consciousness 38

43Disturbance of consciousness 35Breathlessness, disturbance of 40

consciousness36

Angina, breathlessness 52Disturbance of consciousness 35Angina, breathlessness, 36

disturbance of consciousness50

Disturbance of consciousness 52Angina 48Breathlessness 48Angina, breathlessness, 38

disturbance of consciousnessAngina, breathlessness 44Breathlessness, disturbance of 50

consciousness50

Breathlessness, disturbance of 47consciousness, oedema

Breathlessness, disturbance of 50consciousness



Breathlessness 40Disturbance of consciousness, 30oedema


Angina, disturbance of 50consciousness

5250

Angina, breathlessness 45Angina, breathlessness, oedema 50Angina, breathlessness, dis- 40

turbance of consciousness,oedema

i6 7I M 8 42ii8 7I M I Angina 4844 7I M 50 Angina, breathlessness, dis- 40

turbance of consciousness,oedema

45 7I M 6i Breathlessness, disturbance of 30consciousness

9 73 F 14 Breathlessness, oedema 54II 74 M 38 Breathlessness, disturbance of 40

consciousness12 75 M 14 Angina, breathlessness 52I4 75 F 9 Angina, breathlessness, oedema 362I 75 F 3 Angina, breathlessness, dis- 45

turbance of consciousness23 76 M 3 Angina, breathlessness 4028 77 M 6 Angina 5424 79 M i8 Angina, breathlessness, dis- 28

turbance of consciousness39 8o M 8 Breathlessness, oedema 4237 8i M I Breathlessness 5029 84 M I8 Breathlessness, disturbance of 36

consciousness, oedema30 88 M 5 Disturbance of consciousness, 54

oedema

* **

*

* * *

*

*

*

*

* *

* ** *

*

*

**

* *

* *

*

*

* *

* *

* *

*

*

***

*



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was not present at rest at some time. Brady-cardia tended to persist despite atropine. Inthe 22 patients given this drug the mean atrialrate only increased from 44 to 60 a minute,

a while 6 patients developed an arrhythmia.The mean atrial rate in the 26 patients givenisoprenaline rose to 54 a minute, an increaseof I0 a minute, and arrhythmias developed in3 patients.The cardiograms showed that the P waves

tended to be of low voltage, being difficult to

c distinguish in lead I and in 4 patients werehardly discernible in lead II. In those in whomserial cardiograms were available, the ampli-tude of the P waves decreased over the years.The P waves were broad (o-io sec or more inlead II) in 26 of the 46 patients, and io hadP waves of o i i sec or more. The PR intervalwas prolonged in excess of 0-2 sec in 4 pa-tients, the time intervals being 0o28, 0-3, 0-34,and 0-52 sec. One patient was in partial atrio-ventricular block on some occasions and com-

plete block on others, and one (Case 40) hadepisodes of complete block.

In i6 patients there were periods when theatrium failed to depolarize at the expected

; time and there would be a pause in atrialelectrical activity for from I14 tO 3-5 sec

(Fig. i and 2). Their occurrence was quiteunrelated to respiration. The duration ofatrial standstill bore no relation to the pre-ceding PP interval, nor was there a tendencyfor the PP intervals to shorten before atrialstandstill. The pauses in atrial activity in thesepatients, therefore, were considered to beassociated with sinus arrest. These wereusually followed by a junctional escape beat(Fig. i), though in several the sinoatrial noderestarted spontaneously on occasions (Fig. 2).Sinus arrhythmia was present in 7 of the 46patients but coincided with sinus arrest inonly i. In 4 the PP interval varied by over0 75 sec over the respiratory cycle; even inthese cases analysis of the cycle lengths usingthe formula of Schamroth and Dove (I966)failed to conform to sinoatrial block.

Junctional rhythm was observed at one timeor another in I5 patients. In I2 the sinus ratewas so slow at rest that on occasion the atrio-ventricular junctional tissue took over as pace-

maker, and in 3 additional patients junctionalrhythm was precipitated by drugs or exercise.In 2 patients a ventricular centre at times com-peted with the sinoatrial node (Fig. 3). Fivepatients showed atrioventricular dissociation.In 4 of these the rates of the atrium and thelower pacemaking centre were so similar thatatrioventricular synchrony (accrochage) was

suspected.Fast atrial arrhythmia was recorded in I28

LedtCase oo., ^ .,._ S. . ..... ......t. a .wC.se t4o. 5

170 170

170 170 19Z V

FIG. I Cardiogram from Case 5 showing 3sinus beats followed by sinus arrest and ajunctional escape. The figures for the timeintervals are in hundredths of a second.

patients, in 4 atrial tachycardia occurred, andin 3 there was atrial flutter. One patient withatrial tachycardia and one with flutter laterdeveloped atrial fibrillation. Seven patientshad episodes of atrial fibrillation. Atrial flutteror fibrillation became established in 9 patients.One patient (Case 27) was defibrillated byDC shock and settled down to an asymptom-atic sinus bradycardia at a rate of 36. Sub-sequent questions revealed that he had abradycardia dating back to his student dayswhen he was found to have a pulse in the40's and that this had been present up to theonset of fibrillation.

Thirty-five of the patients had one or morearrhythmia in addition to the bradycardia,and 24 had a major disturbance of rhythmsuch as sinus arrest, junctional rhythm, orfast atrial arrhythmia (see Table 2).

FIG. 2 This recording from Case 22 shows 2sinus beats followed by sinus arrest. The sinusnode restarts spontaneously after a 2i-secondpause. The figures for the time intervals arein hundredths of a second.-------- ----t-,---,,,,,,,,,,,,,_,~~~~~; 1~ Zb...........................\ .i.

,.,,,,V



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eJm

c... N..U... .U

FIG. 3 Slow speed recording of the 3 standard leads in Case II. The trace shows runs of sinusbeats at a rate of 42 a minute alternating with beats from a ventricular pacemaker at 40 a

minute and 2 fusion beats.

Cardiograms have been obtained antedatingthe study in i8 patients, and these show thatbradycardia had been present for up to 14years, the average being 7 years. The averagelength of the history of bradycardia in the 35patients with one or more arrhythmia was 14years, and in ii patients the history suggestedthat bradycardia was noted in childhood or

early adult life. The length of the history ofbradycardia in the i i patients who showed no

arrhythmia was i year or less, apart from one

patient with a 2-year history.Long-term treatment was undertaken in ii

patients in the attempt to increase the heartrate. Nine patients were given 'saventrine'(isoprenaline hydrochloride), but the doserequired to increase the sinoatrial rate alsotended to provoke fast atrial arrhythmia or

multiple atrial or ventricular extrasystoles,and only 4 patients are still taking the drug.Tincture of belladonna was used in 3 patients.Again, it tended to produce abnormal rhythmsand unpleasant side effects, and no long-termbenefit was achieved when this drug was usedalone. However, the heart rate in anotherpatient who required propranolol to controlattacks of paroxysmal atrial tachycardia wasincreased when belladonna was added to theregimen. In one patient (Case 5) with frequentsyncopal attacks, the heart rate decreased to30 a minute despite treatment with bella-donna and isoprenaline hydrochloride, andan on-demand pacemaker was fitted. Thepacemaker has now been in place for over 2

years and there have been no further syncopalattacks.

DiscussionChronic bradycardia is usually regarded as

physiological, so that it might be expectedthat the majority of patients in the presentstudy would have a slow atrial rate for physio-logical reasons. However, most had symptomsof cardiovascular disease, and some abnor-mality of rhythm, in addition to bradycardia,was found in all but ii of the 46 patients. Itseems, therefore, that in these 35 patients theslow atrial rate was a manifestation of heartdisease and was in fact a pathological atrialbradycardia. The mechanism could be sino-atrial block or sinus bradycardia. Since de-polarization of the sinoatrial node cannot be

TABLE 2 Cross reference of types ofdisturbance in rhythm or conduction in 35

patients who had arrhythmia in addition tobradycardia

Sinus Junctional Fast atrial Frequent A Varrest rhythm arrhythmia extrasystoles block

Sinus arrest I6 I2 6 5 IJunctional rhythm I2 I5 5 5 2Fast atrial arrhythmia 6 5 12 4 2Frequent extrasystoles 4 5 4 i6 IAV block I 2 2 I 6



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recorded (McGarry, I966), it is impossible todisprove the existence of sinoatrial block.However, none of the patients in the presentstudy had the classical features of this condi-tion, nor could a change in block be producedby measures that release the parasympatheticdrive on the sinoatrial node, such as exerciseor the administration of atropine. Indeed, inthe majority of the patients the increase in therate of depolarization of the sinus node inresponse to exercise and other agents was ab-normally small, while in 7 cases the responsewas so poor that the atrioventricular junc-tional tissue took over as pacemaker. A fur-ther point of distinction between the patientsof the present study and those of cases of sino-atrial block is the amplitude of the P wave inthe cardiogram. The very low wave, oftenindiscernible in lead I, seen in the patientswith bradycardia, is in marked contrast to thesharply demarcated P waves illustrated byLevine (I9I6) in his classic description ofsinoatrial block. It seems reasonable, there-fore, to attribute the slow atrial rate to sinusbradycardia rather than to sinoatrial block.Most of the arrhythmias seen in this study

have been reported to occur in patients withsinus bradycardia by previous authors,though the frequency of junctional rhythmdoes not appear to have been emphasized.Periods of sinus standstill were described byPearson (I945), Short (I954), and Birchfieldet al. (I957), and alternating episodes ofbradycardia with atrial tachycardia, atrialflutter, or atrial fibrillation were observed byShort (I954) and Birchfield et al. (1957).These workers also recorded junctionalrhythm after the administration of atropine.The spontaneous onset of junctional rhythmwhich alternated with atrial tachycardia andatrial flutter was found in a patient with sinusbradycardia by Cohen, Kahn, and Donoso(I967), and a similar case with permanentjunctional rhythm and 'periods of standstill ofthe whole heart' and obvious bradycardia wasdescribed by Wedd and Wilson (1930).There have been reports of patients with

bradycardia ascribed to sinoatrial block whohave developed other arrhythmias or respon-ded abnormally to exercise or atropine(Cowan, 1939; Stock, I969; Rokseth et al.,I970). Cowan (I939) reported a group ofpatients showing periods of atrial standstillwhich he attributed to sinoatrial block. In atleast 2 of these cases the periods of standstillwere followed by escape beats and at timesjunctional rhythm alternated with sinusrhythm in a way similar to that seen in sinusbradycardia. Stock (I969) describes 3 patientswith bradycardia and syncopal attacks, 2 of

whom subsequently developed atrial fibrilla-tion. In i of these cases intravenous atropinewas followed by junctional rhythm. As theauthor implies, this is not the response to beexpected had the patient been suffering fromsinoatrial block, and it seems probable thatone or more of these were cases of sinus brady-cardia. Rokseth et al. (I970) described I4patients, I2 with symptoms of dizziness andsyncopal attacks that they attributed to sino-atrial block. Six of their patients had paroxys-mal supraventricular tachycardia and 7 pa-tients were described as having sinus arrest,the pause being terminated by a junctionalescape beat. From the data available it seemsthat I0 of the I4 patients present features verysimilar to those seen in sinus bradycardia, andit is tempting to consider that some had thiscondition. It is possible that sinoatrial blockand sinus bradycardia may coexist in the samepatient; Laake (I946) described a patientwith sinus bradycardia who developed sino-atrial block after digitalis and quinidine.Again, Lown (I966) described a group ofpatients who after electrical defibrillationfailed to develop a sustained sinus rhythm,but had erratically recurring atrial complexesof varying morphology associated with bothsinoatrial standstill and sinoatrial block.The cause of the sinus bradycardia remains

unexplained in the majority of cases. The casereported by Pearson (1945) later was foundto have carcinomatous infiltration of the car-diac plexus (Pearson, I950). Theoretically,this might have increased the parasympatheticdrive on the sinus node, though the authorconsidered it unlikely. Laslett (I909) sug-gested that excessive vagal tone was a possiblecause for the bradycardia and episodes ofcardiac standstill in the patient he described,and Wedd and Wilson (I930) also attributedthe cardiac standstill in their case to vagalactivity. Short (I954), however, did not con-sider that this mechanism was likely to havebeen responsible for the bradycardia in his 4patients. As already stated, in the presentstudy atropine tended to precipitate ratherthan correct the rhythm disturbances. Itseems likely, therefore, that at least in themajority of patients with sinus bradycardiathere is a primary loss of the automatic de-polarizing activity in the sinoatrial node,rather than suppression of the node by abnor-mal parasympathetic drive.

Kirk and Kvorning (1952) found brady-cardia in 3 patients with diseases of the centralnervous system, and the patient with brady-cardia described by Wedd and Wilson (I930)also had a hemiplegia from a lesion of the in-ternal capsule. Limitation of the normal re-



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sponse of the pulse rate to exercise has beendescribed in 2 patients with brainstem lesionsby Frick, Hartel, and Punsar (i964) and Frick,Heinonen, and Heikkild (i966), but, unlikepatients with sinus bradycardia, their restingpulse rates were normal. Clinical evidence ofnervous system lesions was rare in the patientsof the present study. Only 3 had had cerebro-vascular accidents, i was thought to have someunspecified brain atrophy, and none wasknown to have had encephalitis. In 3 a diag-nosis of epilepsy had been made on account ofthe recurrent blackouts, though this was onlysubstantiated by electroencephalogram in i.

It is possible that in sinus bradycardia sino-atrial function is disturbed by a faulty nodalblood supply. Sinus node arrest and brady-cardia are well recognized after myocardialinfarction (James, i96i; Lippestad and Mar-ton, i967), but usually these arrhythmias per-sist for a few days only (Fluck et al., i967). Itseems unlikely that such a mechanism playeda part in many of the patients of the presentstudy, since only 4 had any evidence of pastcardiac infarction. Rokseth et al. (1970) com-mented that 5 of their I4 patients with brady-cardia had had rheumatic fever or diphtheriaimplying a causal relation. However, in thepresent study this seems unlikely since theseillnesses had occurred in only a minority ofthe patients. Fowler et al. (i969) suggestedthat the bradycardia might be due to primarydegenerative disease affecting the sinoatrialnode, and likened the aetiology to that of idio-pathic heart block. Certainly, the frequency ofpossible aetiological features such as a pasthistory of coronary artery disease or rheumaticfever or diphtheria is remarkably similar tothat of patients with atrioventricular block.This is illustrated in Table 3 which comparesthe past illnesses of the patients with sinusbradycardia with those recorded in ioo con-secutive patients with 2nd and 3rd degreeheart block seen in this department (Shawand Eraut, I970). Another similarity is thefrequency of fast atrial arrhythmias in the twoconditions. Thus paroxysmal atrial tachy-cardia or atrial flutter or fibrillation occurredin i2 of the 46 patients with bradycardia andiS of the ioo with heart block. Further, 6 ofthe 46 patients with sinus bradycardia hadevidence of disturbed atrioventricular conduc-tion, and in view of the rarity of the two con-ditions this association is likely to be signifi-cant.The common finding of broad low voltage

P waves in the patients with sinus bradycardiaimplies that the pathological process, whateverit may be, often involves the atria in additionto the sinoatrial node. The frequency of atrial

TABLE 3 Comparison of possible aetiologicalfactors in past history of patients with heartblock and those with sinus bradycardia

Past history Heart block Sinus(ioo patients) bradycardia(%) (46 patients)

(%)

Cardiac infarction 13 9Rheumatic fever I I I IDiphtheria I2 I ICongenital heart disease 2 4Miscellaneous I 2None of these 65 67

fibrillation in patients with sinus bradycardiais further evidence of this, since though patho-logical changes in the sinoatrial node are usualin patients 'dying' in atrial fibrillation (Hud-son, i960), ischaemia or injury to the nodealone is inadequate to produce the arrhythmia(James, i96i).

From the data presented it is suggestedthat sinus bradycardia exists as a pathologicalentity distinct from sinoatrial block and thatpatients with the condition tend to presentthe following features: (i) a long history of aslow pulse rate; (2) a tendency to syncopal ordizzy attacks; (3) evidence of failure of sino-atrial node rhythmicity (sinus arrest withjunctional or ventricular escape); (4) abnor-mally broad and low amplitude P waves in thecardiogram; (5) excessive irritability of theatria leading to fast atrial arrhythmias or fre-quent atrial ectopic beats; and (6) an abnor-mal response to the stimulus of exercise,atropine, or isoprenaline.The aetiology remains unproven but the

most probable seems to be the loss of the in-herent rhythmicity of the sinoatrial nodeassociated with a primary degenerative disease.While awaiting further evidence to establishthe mechanism of the condition, the descrip-tive title of 'the lazy sinus syndrome' issuggested.

We would like to thank the family doctors in theExeter clinical area for their help and co-operationon which this study depended. We are gratefulto Dr. J. A. Cosh of Bath and Dr. M. G. Thorneof Torbay for supplying the details of two of thepatients and for the support of other physiciansin the Devon clinical area who kindly allowed usto borrow case notes. Part of this work wasfinanced by a grant from the Department ofHealth and Social Security.



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