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PRECORDIAL PAINBy BRUCE MACLEAN, M.D., F.R.C.P.

Physician and Cardiologist, North Staffordshire Royal lnfirmary

During the 1939-4S war, the incidence of pre-cordial pain increased, organic disease accounting,in my experience, for rather less than half thecases. Often the diagnosis is difficult because ofmisleading symptoms and a paucity of clinicalsigns. Sometimes the symptoms alone make thediagnosis easy; and in between these extremesare cases of such a curious mixture that it is fair toconclude that in the past the combination of bothfunctional and organic factors has not beensufficiently emphasized.

Common Causes of Chest PainThe commonest cause of pain in the chest is

the functional disorder usually termed benigncardiac pain or angina innocens, but betterdescribed as left-sided infra-mammary pain. It isdue to an anxiety state and is discussed below.

Pectoral fibrositis is very common and isdiagnosed not only by the presence of tender areaselicited by deep palpation but also by the patient'sstatement that the pain arises on movement of thethorax and on muscular contraction in the affectedarea. When the upper part of the chest is in-volved, it is possible to produce referred pain inthe arm by pressing on the painful site. In manyinstances there has been strain of the pectoraltissues and a toxic state provokes persistence ofthe symptoms and signs. Introspection followingstrain of the pectoral muscles and-giving rise tochronic tenderness and aching of the left breast isregarded by Mendlowitz' as the second mostcommon cause of pectoral pain in Americansoldiers and recruits to military service.

Arthritis of the shoulder-joint is not infrequentlyassociated with fibrositis and should always besought in suspicious cases with pains in the upperpart of the chest.

True angina and pain from coronary thrombosisare dealt with below.

Paroxysmal tachycardia (with its coronary in-sufficiency), pericarditis, and pleurisy are notdifficult to exclude by their special characteristics.Here one may refer to those cases of coronaryinfarction where deep breathing also causes painin the precordial area as the result of pericardialinvolvement.

Mitral stenosis is sometimes accompanied by

left-sided infra-mammary pain. The statementthat pain in this area is never due to heart disease isincorrect. Though it is usually a symptom ofneurosis, when it accompanies mitral disease painis probably the result of both mental and physicalfatigue.

Apart from invasion of the spine, pleura andadnexa by neoplasm, other causes of pectoral painare not common. A pneumothorax causing painand dyspnoea, especially on exertion, is easilyconfused with true angina particularly when thereis a partially collapsed left lung difficult to diagnoseon clinical examination. A sudden onset in par-ticular simulates a thrombotic attack.

Left-sided Infra-Mammary PainNomenclature. This syndrome was first

described by Da Costa (I87I) during the AmericanCivil War and was often associated with dysentery.During the I914-I8 war, it came into prominenceonce more under the heading of D.A.H. (dis-orderly action of the heart), irritable heart, effortsyndrome, soldier's heart, and neuro-circulatoryasthenia; but these descriptions do not alwaysfit the bill. There may be no disorderly action,such as tachycardia or irregularity of the heart-beat, and occasionally no complaint of dyspnoea.The syndrome occurred in civilians in the I939-45war more than in soldiers,2 for the obvious reasonsthat past experience had taught us to weed outrecruits undergoing medical examinations whoshowed any likelihood of this disorder, and be-cause the civilian population were subjected notonly to real warfare but also to general anxiety.

Aetiology. Left-sided infra-mammary pain iscommonly encountered in overworked and highlystrung people. In peace-time, females with hyper-tension form the majority of such patients, butduring I939-45 a large proportion has consisted ofmales aged seventeen or more. Cardiologists con-sider that the condition is due to mental fatigueand not to coronary insufficiency. A strainedpectoral muscle can initiate fear, with psycho-somatic disturbance, and infection lowers theresistance and morale. Certain it is that re-assurance can effect a cure, provided the mentalstress at the same time is removed.

Infection (focal sepsis) appears to play a part.

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In contradistinction to the association withdysentery noted by Da Costa, I have foundpharyngeal infection to be the most constant toxicfactor.

Experiments point to the hypothalamus, withits sympathetic centres, as the probable site ofdisorder. The auriculo-ventricular conductiontime can be lengthened by stimulation of the hypo-thalamus in dogs; and sweating and even ulcera-tion of the duodenum can be produced by trau-matic lesions of the hypothalamus in man.

SymptomsThe patient usually complains that pain arises

in or under the left breast, coming on at any time,day or night, and sometimes waking him in thenight, though he is more likely to wake first. Thepain is described as stabbing, throbbing, burning,and lasting hours, sometimes all day. It mayarise with, but usually after, effort; but in sodoing it tenos to persist and is not relieved bycessation of activity. It often spreads to the leftarm, usually the inner border, and this limb mayfeel numb and useless ; sometimes the pain ex-tends to the left side of the neck. I have onlytwice known the pain to spread to the right arm;it has been stated that such a spread excludes thepsychosomatic illness and indicates true coronaryocclusion, but this is incorrect.

Occasionally the symptoms overlie true angina,and then the patient's story is of real service;his attitude and reaction will probably give theclue to the assessment. It is in such cases thatwe tend to make a wrong diagnosis of pureneurosis, the symptoms of true angina beingovershadowed.

SignsThere is not infrequently tenderness to pressure

over the area of pain. Thomas Lewis3 pointed outduring the I914-I8 war that pinching the sterno-mastoids, trapezii, and pectorals provoked morediscomfort on the left side:

Hyperaesthesia has often been described. I havefound the left mammnary tissue, in both male andfemale, tender to the grasp, and believe that thehyperaesthesia of the left chest described byvarious authorities probably refers to tendernesson deeper palpation. True hypersensitiveness ofthe skin is rare.

Electrocardiography and radioscopy reveal nosigns of disease. The exercise-tolerance test may befaulty, the systolic blood-pressure infrequentlyraised, tachycardia present, and a soft systolicmurmur detected at the apex of the heart, none ofthese features being contingent upon organicdefect.

TreatmentIt is a pity that the word ' angina' is used so

often in connection with what is described asbenign cardiac pain; it is better to discard a namewhich to the layman is associated with the dreadof sudden death. In fact the terms ' angina,'' tired heart,' and ' flabby heart-muscle ' shouldnever be mentioned to the patient, for they mayhaunt him for the rest of his life. Herein lies thefirst principle in the treatment-reassurance. Tothe intelligent inquiring patient it must be ex-plained that there is no organic disease, and thatthe symptoms, though real to him, are the resultof fatigue and anxiety. This is often a difficult pillfor the patient to swallow. Likening him to asensitive wireless set, tuned in to distant stationsand reacting accordingly, compared with the in-ferior models, does much to satisfy his doubts. Itis explained that if the mind is tuned in to dis-comforts they become so much more apparent andmust be faded out and in this way eventuallyobliterated. I have known an understanding talkwith a patient abolish the precordial pain at oneconsultation. Moreover, once the diagnosis hasbeen established, further cardiac examinations areredundant and harmful, provoking introspectionby raising doubts as to the state of the myocardium.Some patients need physical rest, but rest in bed

is bad for those with nothing but an anxiety state.It is a different story where the neurosis is super-imposed on organic pathological conditions such ashypertension, valvulitis, and coronary dysfunction.

In any case sedation is necessary. Bromides area good standby though used far too in-discriminately; if they are given for too long theymay cause depression, lack of concentration, andeven incoordination with nystagmus. Restlessnessand insomnia may require barbiturates, par-ticularly in a hypertensive patient. It is wise tosubstitute a non-barbiturate from time to time,such as carbromal, or bromo-iso-valeryl urea(B.V.U.); isobrom is a happy combination ofthese latter drugs with enhanced action, and canbe used during the day with little narcotic effect.For those who cannot sleep on retiring a quick-acting sedative is best, such as Seconal or Car-brital. Hexobarbitone is rapid in action but doseslarger than 4 gr. may upset the digestion and causevomiting. Evidorm, a combination of quick andslow acting barbiturates, has a rapid and morelasting effect. Digitalis is often useless in cardiacneurosis except for its vagotonic effect in dampingdown the pacemaker at the sino-auricular node inpatients with tachycardia and overaction of thesympathetic supply. Small doses of belladonnaalso stimulate the vagal nerve endings and slowthe heart-rate; large doses paralyse and provoketachycardia.

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True AnginaAetiology. True angina, coronary pain, effort

angina, or angina pectoris occurs usually in middleage, mainly in men, but has been observed in thefourth decade, and I have described it in a childaged fourteen with progeria (premature senility).4

Angina pectoris should be regarded more as asyndrome than a disease, for it may accompanyspasmodic conditions of the arteries further afield,as in intermittent claudication; it may occur inpeople without evidence of arterial disease; andit is a symptom found not only in atheroma of thecoronary vessels but also in thrombosis and in-farction of those vessels, in syphilitic endarteritis,and in rheumatic aortic lesions. It also occurs inadvanced anaemia and in untreated myxoedema,from myocardial anoxaemia, when the pain iscaused by the toxic effects of accumulatingmetabolites.The precordial discomfort is nearly always

caused by effort; but emotion, cold, or dyspepsiamay also bring it on. The pain is quantitativelyrelated to effort and s increased by fatigue oranxiety and lessened by a carefree holiday. Acardiovascular lesion is surely not responsible forthese changes; it is the overlabile autonomicsystem and the exaggerated response to stimuliwith increased vasoconstriction or failure of avasodilator response of the coronary arteries whichcauses the ischaemia. There is therefore anadditional qualitative factor. This overactiveautonomic system explains why the effect of over-work and fatigue, with inadequate leisure, invokesangina; and why the business man during the,week develops pain on walking to the railway'station, yet can play a game of golf without dis-comfort and be free from attacks while on holiday.

Only 15 per cent. of patients with calcificationof the coronary arteries have been known to re-port an anginal syndrome. Few persons with thiscomplaint experience pain on going upstairs orwalking about their business premises; some caneven run upstairs without discomfort, but it isthe slow incline that catches them out. The factthat belching seems to relieve the pain suggestsassociated gall-bladder disease, but belchingprobably denotes the cessation of the attack.Oesophageal spasm may also be present; it canbe regarded as a counterpart of anginal pain, forit can be prevented or relieved by nitroglycerine.The statement that this eructation is due in mostcases to air swallowing is erroneous. Somepatients, thinking their symptoms are due todyspepsia, swallow air while attempting to dis-lodge the wind, but they are in the minority. It isalso a fact that many patients with angina of effortdo not complain of associated flatulence. On theother hand, true angina is often associated with

gall-bladder disease, which then excites the anginaand can be likened to the trigger of a loaded gun.Cases are on record where cholecystectomy hasabolished angina for a long time. Similarly, insome cases the provoking factors are a distendedcolon or stomach, the result of overfeeding or ofindigestion. ;

Anginal pain can be incited by exposure to cold,as in coming out of a warm theatre or walkingfrom a warm room to a cold one, and then it is notthe effort but the alteration in temperature whichinduces the attack, the result, no doubt, of a risein the blood pressure which increases the work ofthe heart. Getting into bed with cold sheets has alike effect. This pain must be regarded as ofspasmodic reflex character and associated withcoronary spasm. a

Tobacco is a rare primary cause of angina, yetthe symptoms at times are relieved by abstention,especially from cigarette inhaling. It seems feasiblethat some people may become more sensitive totobacco with advancing age. Coronary restrictioncan be produced experimentally in animals withnicotine. Repeated arterial spasm is likely to leadeventually to arteritis and thrombosis.A special type of angina develops during anaemia

and is then due to the smaller supply of oxygen tothe muscle when an extra call is made on the heart.This can be cured by restoration of the haemo-globin level. Any anaemia may cause thissymptom, whether from haemorrhage, perniciousor hypochromic anaemia, or leukaemia; but youngpeople and children with severe anaemia do notget angina.

Campbell6 holds the view that people with thistype of angina will eventually develop true anginaof effort, believing that the anaemia alone cannotcause the angina unless associated with coronarysclerosis. Other cardiologists incline to the beliefthat the lack of oxygen suffices to explain the pain,in the absence of coronary disease.Angina has also been described in association

with thyrotoxicosis and with myxoedema; it hasbeen alleviated by thyroidectomy in thyrotoxicosisand by thyroid administration in myxoedema. Itmust be remembered that, when thyroid extract isadministered in overdosage, a state of overaction ofthe sympathetic is induced, with the consequenttendency in some people to coronary spasm.

SymptomsTrue angina used to be regarded as a sudden

severe pain associated with a sensation of im-pending dissolution. We know now that the painmay be mild, even a dull ache, and rarely associatedwith the fear of death. It is in the so-calledvasovagal syncopal attacks and in sensory epilepsythat this dread is more commonly experienced.

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There is always a positive history of the symp-toms produced by effort and relieved in a shortspace of time by rest or by nitroglycerine; fre-quently aggravated by exposure to cold or effortafter a meal. Cold raises the blood pressure andthrows greater strain on the heart; while a fullstomach with increased blood supply reduces thecoronary flow.Some patients get pain first thing on making an

effort after breakfast, and then are relieved for therest of the day. There is a story of a doctor whopreferred to wind up his car and get the troubleover rather than have the symptoms tending topersist over a longer period. Other patients com-plain mainly at the end of the day when they aretired ; in this instance the sympathetic nervoussystem comes strongly into play.Some patients lose their angina for a time. This

fact does not indicate an error in diagnosis. Thethreshold for pain has been lowered by theremoval of anxiety and consequent overactionof the sympathetic nervous system. On theother hand, patients cease to experience effortangina after sustaining a myocardial infarct,presumably because the pain-producing area hasnecrosed.An objection to the term.' precordial ' is that,

whereas true anginal discomfort is often sternal insite, it is usually felt across the upper chest, orarises in areas to which the pain may spread. Ihave known anginal pain arise in the left wrist orboth wrists; in the left arm or both arms ; in theback or nape of neck; though in alnmost every caseit was also experienced across the upper chest.The pain may spread to the throat, especially to theleft jaw, and even the left side of the face and tothe left eve and behind the ear. When this painspreads from the upper sternum to the right armit is almost proof of coronary occlusion. Veryrarely is pain felt in the right arm in cardiacneurosis, but it must be remembered that anginalpain may on rare occasions be described only inthe right upper chest and right arm.When angina is due to syphilitic occlusion of the

mouths of the coronary arteries (in contradistinc-tion to the usual atheroma extending along thecoronary vessels), the pain on effort tends to lastlonger, is not soon relieved by rest, is often morespasmodic, and is associated with nocturnalparoxysmal dyspnoea and angina decubitus.These nocturnal symptoms are the outcome of themechanical effect on the coronary flow, relative topressure from a dilated aorta in recumbency. Itmust be remembered, however, that syphilis doesnot always.cause dilation of the aorta. Incident-ally, in syphilitic angina it is much more im-portant to treat the heart before the syphilis, forsyphilitic tissue is better than none.

DiagnosisThe diagnosis can frequently be made from the

description of the symptoms alone. Clinicalexamination may not reveal any significant sign inthe heart, arteries or blood pressure. There maybe no evidence of cardiac failure. Radioscopy hasfrequently revealed a normal size and contour ofheart, and aorta, in undoubted cases. Electro-cardiography may not reveal any sign of a patho-logical kstate of the heart muscle until permanentocclusive changes arise. In doubtful cases it isadvisable to repeat electrocardiography im-mediately after exercise or after inhalation of IOper cent. oxygen, thereby provoking precordialpain. By these tests, which should be accom-plished within three minutes of the onset of pain;one may observe an alteration of the complexesin the electrocardiogram, revealing signs of tem-porary muscle defect. Injections of adrenalin willprovoke angina but the concomitant risk ofventricular fibrillation forbids its use as a test.Confusion sometimes occurs in the interpretationof an inverted T-wave in lead i in hypertensivepatients. Intravenous injections of potassiumsalts will cause the T-wave to become upright inpure hypertension, whereas they will accentuatethe inversion in coronary occlusion. Unfortunatelythis procedure is not without risk, since potassiumsalts given intravenously slow the conductionmechanism of the heart.

I would refer briefly to those unfortunatepeople with para-oesophageal hernia. This hiatushernia provokes three types of symptoms: chieflygastric, occasionally respiratory, and not in-frequently precordial pain simulating angina. Thecommon occurrence of pain with flatulence aftermeals, the persistence of the pain or discomfort atrest, and the daily recurrence over long periodswill suggest this abnormality. To add to theconfusion I have found that nitroglycerine will giverelief by its antispasmodic effect on oesophagealtissue, in the same way as inhalation of octyl-nitrite.

PrognosisI believe that patients without true pain,

especially where there is no spread to the neck andjaw, or where the discomfort is mainly one-sided,and particularly those who can walk off theirsymptoms and have no sense of constriction orsuffocation, have a more favouable prognosis.

Spasmodic angina, though little understood,sometimes has a favourable prognosis, especiallyin the emotional type where effort does not playso important a part. Vasodilators are not alwayssuccessful in its treatment, and then the symptomsrun their course.Angina of old age does not appear to alter the

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course of the natural span of life, possibly becauseof the development of multiple anastomoses in thecirculation of the myocardium.A patient with angina very rarely dies in the first

attack ; he may live, with recurring attacks, fori S years or more. Death is usually associated withcoronary thrombosis, not necessarily occurring atprecisely the same time as the vascular clotting,for other factors come into play, such as ventricularstandstill and fibrillations, contingent upon in-volvement of the conducting mechanism associatedwith coronary spasm. Such spasm no doubt attimes may be widespread involving coronaryarteries without marked atheroma. The prognosisis influenced to a large degree by the mental re-actions of the patient to his complaint, by thecare taken in regard to habits and diet, and by thehistory of thrombotic attacks.

TreatmentThere are few conditions where advice is so

strongly needed about general hygienic measuresand regulation of the patient's life. For prophy-laxis he must take fresh stock of himself and,according to the severity of his symptoms, limit hisactivities, especially those associated with over-strain.

At the outset it is best to explain to the patient-that, with age, there is a lessening of cardiacreserve, and this takes the form of warnings thathe is overstepping the boundaries of his heart'scapacity for work ; that if he limits his physicaland mental effort he will be freer from the pain ordiscomfort, and he will need to live within thelimits of his tolerance. ' Regular habits ' and' going slow' should be his watchwords. Heshould take longer over his dressing in themorning, not hurry over his breakfast; it mayeven be necessary for him to get up half an hourearlier. Then he should rest before and aftermeals. We often hear the patient's story of painafter breakfast when effort is needed to catch the-train or bus, and how much more distress there isif he has to walk against a cold wind. He muststop when pain arises, and must curtail his futureefforts to a point short of the production of thispain. It is wise to try and break the habit of thispain-producing effort, for by walking slowly thepatient may be able to live for years without re-quiring va'sodilators; and, when he finds freedomin this way, there may appear in time less tendencyto pain.

If any special effort is required, or if he knowsthat a certain effort must be made which usuallybrings on his pain, a tablet of nitroglycerine shouldbe chewed a few times and allowed to be absorbedfrom under the tongue just before such an effort.The nitroglycerine is more rapidly effective taken

in this way than when swallowed. For a longeraction which need not start so quickly it is betterto swallow the nitroglycerine. The tablets shouldbe fresh. Patients are sometimes afraid of takingthese tablets, either because they producethrobbing in the head and slight giddiness orheadaches in those with so-callad hypotension, orfrom a fear of drug taking. As a rule by redutcingthe dose one can discover the requisite amount torelieve the symptoms without causing unpleasanteffects. It is wise to start with a small dose, es-pecially for patients with the minor manifesta-tions; even I/200 gr. may be found efficacious.Larger doses, say, I/ISo gr. or I /ioo gr., may benecessary later.Food must be carefully chewed; the stomach

cannot take over the duty of the teeth. In-digestible food must be avoided. By the age a mandevelops angina he should know what disagreeswith him. Small meals at short intervals should betaken rather than larger meals at longer intervals.

Avoidance of gastric and colonic distension isvery important. Much has been written about theharmful effects of alcohol and tobacco. If alcoholsuits the patient, a moderate amount of it, par-ticularly in the evenings, does no harm. Cassidv6declares that tobacco has little if any effect oncoronary disease, but he admits that cigar smokinghas been known to induce intermittent claudica-tion. It is therefore wisest to prescribe modera-tion in smoking and avoidance of inhalation.Vasoconstriction can be caused by nicotine, andsome anginal subjects do get pain after cigarettesmoking. We cannot altogether exclude thepsychological effect where the patient has beenforbidden this luxury and fears the consequenceof indulging it.

I am not convinced of the efficacy of nicotinicacid. Experimentally, a high dosage is requiredto promote vasodilation of the coronary vessels,and then tingling and pricking sensations becomevery unpleasant. Nicotinamide produces lessside-effects but probably also less vasodilation.The same may be said of testosterone therapy;

great claims were made in the United States ofAmerica, but they have not been confirmed inthis country. Vitamin E has also recently been invogue but without convincing testimony.We should also resort to psychotherapy, which

can do much for a hypersensitive patient ; he mayeven lose his angina for a time.

Cardio-omentopexy has gone out of favour,though some good results were recorded, pre-sumably by supplying fresh channels from thevascular tissues of the omentum to the surface ofthe heart.

Thyroidectomy is now little heard of in thetreatment of angina. A series of cases published

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some years ago gave promising results, presumablyby lowering the basal metabolism. In a propor-tion of the cases thyroid feeding became necessaryowing to the development of myxoedema, whichhas also been known to provoke angina.

I am investigating the effects of propyl-thiouracilbut have not yet given it an extensive enough trial.

Cervical sympathectomy has given good results.It was once believed that abolition of the pain inangina might place the patient in a more seriousstate, since he would make an effort, possibly witha fatal result, if he did not have the warning pain;this theory is no more accepted. Smithwick'soperation, by which the lumbar and dorsalsympathectic ganglia are removed, is of chief valuefor the hypertensive patient with vasomotor angina.

Khellin,7 an Egyptian drug produced by ex-traction of the seeds of a plant (ammi visnaga)which grows on the shores of the Mediterranean,has been used for centuries as an antispasmodicin the treatment of renal and ureteral colic.Chemical analysis has shown it to be a di-methoxy-methyl-furano-chromone belonging to the samegroup as the coumarines. Khellin causes a pro-longed relaxation of all the visceral smoothmuscles, especially the ureters, but it was not untilI945 that it was discovered that khellin acts as acoronary vasodilator without affecting the bloodpressure. The drug can be obtained in thiscountry from British Drug Houses as a tincture,and i dr. should be given three times a day; upto 3 dr. can be given as a single dose. Khellin alsohas a beneficial effect on bronchial asthma by in-ducing relaxation of the bronchial muscles.

Since infection appears to play a part in coronarydisease, eradication of a toxic focus, if possible,should always be advised. Gall-bladder lesionsare commonly associated with angina; both heartand gall-bladder are innervated by the vagus; andRae Gilchrist8 believes that cholecystectomy isjustified in many cases with obvious gall-bladderdyspepsia. A patient with angina usually under-goes such an operation well if a skilled anaesthetistis employed.

Coronary ThrombosisEtiology. Coronary thrombosis develops usually

after the age of fifty, but i i cases have been re-corded between the ages of twenty and thirty, tenof which were in males. There was no syphiliticinfection in these ;- a raised blood pressure wasfound only in one, and signs of arterial diseasewere absent, apart from coronary atheroma.Miller and Woods9 reported one additional casein this country, in a patient aged twenty-two.

SymptomsThe pain of coronary thrombosis is not always

precordial, for it arises not infrequently in theepigastrium, suggesting acute dyspepsia, gall-bladder trouble, or a perforated peptic ulcer. Inmany cases, however, it is definitely felt over theheart, in the left mammary area, or in the mid-line,and it tends to spread to the shoulders, jaws, .arms,back and nape of neck, just as in angina pectoris.Shock and circulatory collapse may be the onlysymptoms and signs of infarction, in which casesevere pain may come oh at a later stage.There are at times prodromal symptoms of

indefinite pains under the sternum or of aching inthe left arm; these may exist for as long as I4days before the attack, and are probably due to asmall subendothelial haemorrhage in a coronaryvessel leading later to thrombosis.

Frequently the first attack has been un-recognized and called dyspepsia or pleurodynia,and has been so slight that the patient has not evensought medical advice. Careful questioning mayelicit the previous history of precordial discomforton effort.

In contradistinction to angina of effort, thepatient with thrombosis tends to be restless in anattack. He may move about, trying to secure acomfortable position. I have known a patient toget out of bed and, on her knees, bend forward onthe floor, in a partially successful attempt to obtainsome measure of comfort. In the early stagesthere are commonly nausea and dyspnoea.

It has been stated that even where there is nopain there is always dyspnoea. This is not quitetrue. I have certainly encountered severe painwithout respiratory distress.

SignsThere is evidence usually of the various degrees

of shock, many very severe with pallor, sweatingand vomiting.The pulse varies according to the pathological

upset in the myocardium and conductingmechanism. One expects to find a weak pulse andlowered blood pressure; yet occasionally thepulse may be normal, and the condition of thepatient fairly good. The pulse, which is usually ofpoor volume, may become slow by damage to theauriculo-ventricular bundle or to the sinus node,producing a wandering pace-maker, or it may berapid from auricular or ventricular tachycardia.The abnormalities in auricular rhythm arise es-pecially when the auricular branches of thecoronary vessels are involved. Premature beatsare commonly encountered.

It has often been stated that the blood pressurefalls rapidly in coronary thrombosis; this is truein many cases, but sometimes it takes 12-24 hoursbefore it drops. I have known a very dyspnoeicsweating patient with chest pain have a blood

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pressure of I70 systolic, and be-in consequence notrecognized as a case of coronary thrombosis. Theblood pressure in this case dropped to 120 andI15 mm. Hg. in 24 hours.

Electrocardiography in difficult cases can givethe clue to the diagnosis usually in the threecommon leads, but occasionally only in the fourthlead. The electrocardiogram can be more easilyinterpreted a few days after the initial attack.

Pulmonary congestion must be looked for, andinquiry made about nocturnal wheezing, as thisportends left ventricular failure. Attention shouldbe paid to the development of an evanescent peri-carditis and slight pyrexia with leucocytosis, es-pecially on the third or fourth day, accompanied bya raised blood sedimentation rate.

Recurrent precordial pains following a coronarythrombosis suggest weakening of the cardiacmuscle and the development of an aneurysm. Thiscan be seen by radioscopy, sometimes in an obliqueview, as a prominent immobile area.

PrognosisPatients occasionally die suddenly in a first

attack, but usually they either succumb during thefirst few weeks or make a good recovery tor awhile.

Untreated cases seem to develop angina ofeffort more readily than those adequately treated.The amount of shock is a guide to prognosis.Though the pulse may be good and the condition

of the patient fairly good, death may ensue in ashort time from further occlusion.

Clots forming on the endocardium over the in-farcted area are responsible for emboli causingocclusion both in systemic and pulmonary circuits,for both ventricles can become involved with oneinfarct.

Fibrillation carries with it a graver prognosis.

TreatmentThe most essential treatment of coronary

thrombosis is rest in bed and alleviation of the painand shock. For rapid relief of pain there isnothing so good as an intravenous injection of$ gr. of morphine or omnopon. This is supple-mented by hypodermic injections, and as much as! gr. of morphine may be found necessary, andmorphine may be repeated every few hours insmaller doses. Omnopon also contains papaverine,-which relieves spasm of unstriated muscle, butthe amount present is too small to be significantlyeffective; ioo mg. of papaverine is a useful dose.Dilaudid has ten times the analgesic action ofmorphine, but the duration of freedom from painis not so long. This drug should be used wherethere is idiosyncrasy to morphine. Sometimesthe dilaudid provokes nausea and vomiting, and

then codeine phosphate, i or 2 gr., should be tried.If 2 gr. does not relieve the pain sufficiently, nosuc.cess will be attained with larger doses. Hyper-duric morphine is also useful for prolonged action.Physeptone is under trial. This new drug (dl.2 di-methyl-amino 4; 4 diphenyl-heptone-5 onehydrochloride) has spasmolytic and analgesicproperties, making it particularly suitable for re-lief of pain of visceral origin. It may be ad-ministered by mouth or by subcutaneous, intra-muscular, or intravenous injection. Weight forweight it is equal to morphine in its analgesicaction; io mg. of physeptone produces an effectabout equal to that of - gr. of morphine, withrelief of pain for three or four hours; 30 mg. ofphyseptone may be required for severe pain.The hypnotic effect and side-effects are less thanthose of the opiates. The relief of pain alsocombats shock.

Inhalation of oxygen may be necessary. Thefunnel method is wasteful. The B.L.B. mask iseffective but can be trying to a restless dyspnoeicpatient; in which case the nasal catheters on aspectacle frame are best. The oxygen tent issomewhat alarming to the patient and presentsdifficulty in nursing; it takes time to install andneeds careful maintenance to prevent suddenlowering of oxygen concentrations..Of the anticoagulants, heparin has the dis-

advantage of having to be given intravenously andrequires laboratory control by the blood coagula-tion time. Dicoumarol can be administered bymouth, but again needs control by estimation ofthe prothrombin level. It is slower in action thanheparin and probably safer. Both may, fromoverdosage, suddenly cause haemorrhage invarious parts of the body as a result of severehypoprothrombinaemia. The risk is particularlygreat with a patient suffering from coronary arterydegeneration, where there is liability to subintimalhaemorrhages. I consider the use of this drug iscontraindicated where there is concomitant hyper-tension. From experiments carried out by Peterset al. (1946)10 it was estimated that the embolismor mortality rates were considerably reduced.One should aim at giving dicoumarol on al-

ternate weeks, in sufficient doses to lower theprothrombin level below 50 per cent. to 6o percent. On an average the dosage employed isapproximately ioo mg. a day; patients naturallyvary with their reactions and some require asmuch as I50 mg. a day. I have known the pro-thrombin level to return to normal in seven daysfollowing the cessation of the administration of thedrug. It must be borne in mind that the effectsare cumulative with sudden development ofsevere hypoprothrombinaemia; hence the advocacyof using alternate weeks for the administration

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of dic zum.arol, as a safeguard in prolonged therapy.Of coronary vasodilators the nitrites lower the

general blood pressure ; this must be avoidedwhen dealing with coronary thrombosis. Papa-verine hydrochloride has little toxic effect andapparently is not habit-forming. I have used itwith apparent success but have not yet been ableto obtain the synthetic compound, eupaverine,which is said to have a greater antispasmodiceffect. The dose of papaverine i's usually ioo mg.two or four times a day. It has practically nonarcotic or depressing effect on the circulation.Aminophyllin is one of the xanthine groups;

it has popularity as a coronary vasodilator, andMcMichael"' has urged its use as an augmentor ofcardiac output in left ventricular failure; he hasproved this effect by catheterization of the rightauricle. This drug is very effective in reducingvenous pressure. Certainly patients with leftventricular failure improve after administration ofaminophyllin when given either by mouth orparenterally, preferably the latter. There isevidence to show, however, that it should not beused in coronary thromBosis during the period ofshock, since it may produce a fall in blood pressureand tachycardia. Intravenous administrationshould particularly be avoided where a lowering ofblood pressure may produce ill effects.

Ventricular tachycardia, strangely enough, ap-pears to be promoted by digitalis therapy. Unlessthere are signs sufficiently significant of cardiacfailure, digitalis should not be prescribed. Somecardiologists say it should always be avoided, es-pecially since recent investigations have providedevidence that there is increased coagulability ofthe blood after digitalis therapy.

Quinidine is the best drug to restore normalrhythm when auricular fibrillation develops, and itshould be combined with digitalis when accom-panied by congestive failure. It should not beused if a conduction defect is present; it retardsimpulse formation at the sino-auricular node,

slows conduction, and lengthens the refractoryperiod, but it prolongs the prothrombin time.

Extra-svstoles can usually be abolished by givingquinidine, 3 gr. a day, or papaverine, IOO mg. threetimes a day.

Mercurial diuretics may be found more bene-ficial than digitalis in congestive failure, providedthe kidneys are not diseased. The drug should beadministered cautiously; because sudden deathhas taken place after larger doses, especially wherethe kidney tubules are degenerated.The patient should be kept. in bed for a month

in mild cases, or six weeks in more serious cases.Bed-pans are usually essential. Occasionally thepatient Qannot manage a bed-pan, and then thebest procedure is to bring the level of a commodein line with the bed. The patient slips his legsoutside the bed and is easily lifted on to thecommode. Returning to bed offers no greatdifficulty.

After the patient is allowed up, he should staythree months away from his usual work.

SummaryThe common causes of precordial pain are dis-

cussed with special reference to left-sided infra-mammary pain, true angina and coronarythrombosis.The aetiology, diagnosis, prognosis, and treat-

ment are dealt with in respect of each disease.

REFERENCESi. MENDLOWITZ (I945), Amer. Heart Journal.2. PARKINSON, J. (I941), 'Effort Syndrome in Soldiers,'

British MIedical Journal, April I2, I, p. 54 .3. LEWIS, T., The Soldiers Heart ' and The Effort Syndrone.'4. British Encylopaedia of Medical Practice, 9, 627.5. Campbell, M., Communications to British Cardiac Society.6. CASSIDY, M. (I946), ' Harveian Oration on Coronary Disease.>7. KHELLIN (1946), British Heart Journal, 8, No. 4, 171.

Ammi Visnaga in the Treatment of the Anginal Syndrome.'Anrep, Barsoumn, Kenawy and Misrahy.

KHELLIN (I947), Lancet, April 2I, p. 557. 'TherapeuticUses of Khellin," by the same authors.

8. GILCHRIST, RAE, Personal communication.9. MILLER and WOODS (I943), British Heart Journal, April.

io. PETERS, et al. (I946), Journal Amer. Medical Association, 130,398. 'The Action of Theophylline-ethvlene-diamine.'

I i. McMICHAEL (I946), British Heart Journal, 8, No. 4, 235.

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