No. 3871.

NOVEMBER 6, 1897.

The Bradshaw LectureON

PROGNOSIS IN HEART DISEASE.Delivered before the Royal College of Physicians of

London on Nov. 4th, 1897,

BY E. MARKHAM SKERRITT, M.D.,F.R.C.P. LOND.,

PROFESSOR OF MEDICINE IN UNIVERSITY COLLEGE, BRISTOL; SENIORPHYSICIAN TO THE BRISTOL GENERAL HOSPITAL ; FELLOW

OF UNIVERSITY COLLEGE, LONDON.

MR. PRESIDENT AND GENTLEMEN,-It is probably thewont of those upon whom from time to time devolves the

responsibility of delivering the lectures associated with thisCollege to select for their discourse matters to which theyhave devoted special consideration, or which are to theminvested with peculiar interest. Therefore when you, Sir,did me the altogether unexpected honour to invite me todeliver the Bradsha.w Lecture for the present year it seemedto me that I could but discharge the important duty withwhich I was entrusted by treating of some subject which hadbeen in the forefront of my observation and thought duringmy active professional life, and my choice fell upon a themewhich has also engaged the attention of those who havespoken with an authority to which it is not for me to aspire-one, however, which in its importance is always fresh, and isconstantly present to the practical physician, offering for hissolution ever-varying problems.The Father of Medicine has said, " The art of physic is of

great extent, life short, opportunity slippery, experiencefallacious, and judgment difficult." Still but too true of ourart as a whole, this applies with equal force to one at least ofits branches. Who is there that of his own experiencecannot say of prognosis in disease that "opportunity is

slippery, experience fallacious, and judgment difficult"? Andassuredly a full share of difficulty and fallacy surroundsthe subject which I have chosen for this lecture, foralthough in none of the ills which flesh is heir to is aknowledge of what the future has in store of greatermoment than in heart disease, yet in few things is the

possible margin of error so wide. It is not practicable withinthe time at my disposal to enter into a detailed considerationof the prognosis of heart disease in its various forms. Norshould I here venture to trespass upon ground which hasbefore been occupied by those with whom I could not presumeto compete. I propose rather to treat the subject from ageneral point of view and to discuss it in certain aspects andphases, having especial regard to the origin and nature ofsome of the uncertainties by which it is surrounded.The following factors enter into prognosis in heart disease.

First, an accurate estimate of the nature and extent of thechanges which have occurred in a given case-that is to say,a complete diagnosis. Next, a knowledge of its pasthistory with special reference to the causation of thecardiac trouble and the length of time that it has existed.Thirdly, an acquaintance with the course that may be runby a lesion such as is present. And lastly, a due weighingof the special features of the case in question.There is no need to argue at length the dependence of

prognosis upon diagnosis. If diagnosis is imperfect or

faulty or totally wrong prognosis will be correspondinglyerroneous. The foundation of prognosis is an accurate

appreciation of the changes produced by disease and of thepathological nature of the processes concerned-a know-ledge, that is to say, not only of what alterations haveoccurred in shape or size or structure or functionof an organ or part, but of how they have beencaused, and what is the ultimate history of the morbidagencies to which they are due. Where the heart is con-cerned error in prognosis may arise in connexion with eitherof these two factors; on the one hand, through mistake asto the actual physical condition of the organ; on the otherhand, owing to failure to realise what will be the resultantof the various forces which are rightly recognised as at work.And difficulty in these two directions tends rather to lieNo. 3871.

towards the extremes of age. In early life the discoveryof the lesion is usually easy, but there are wide possi-bilities as to its future course, while with advancingyears comes the time of degeneration, which in itsgravest forms often cannot with certainty be recognised.For youth is the period of acute inflammations-ofpericarditis and endocarditis- which are commonly dis-covered with ease by the skilled observer; but no wisdomwill avail to surely foretell the future whilst acute endo-carditis is running its course. Whether when the inflamma-tion subsides the roughened valve will be smoothed and thatunusual event occur, the disappearance of the murmur of £acute endocarditis ; or the morbid sound persist, but basedon so little actual valve change as to remain a murmur andnothing more ; or whether the lesion is destined to workhavoc with the heart and bring life to a speedy close,-allthis is beyond the reach of human foresight. Diagnosisis simple, definite prognosis impossible. Towards theother end of life the opposite tends to obtain. De-

generation has no distinctive physical signs ; and itoften cannot be said with certainty whether the haltingaction of the organ is due to change which is

organic and will remain or comes from simple andremediable weakness. Upon the view that is taken of thenature of the affection depends the prognosis that is given ;on the one hand, a grave forecast of increasingly impendingevil; on the other hand, it may be, the prospect of restoredpowers and lengthened years. But perchance the promise ofpeace and length of days is made to the man whose heart ischanging into fat, while the sword is hung over one whoseonly need is nourishment and rest.

It is important to recognise what is the position of phy-sical signs in heart disease-how far they can be relied uponas evidence of the nature and extent of existing morbidchanges and of their tendencies. Speaking of valvulardisease Markham says: " A too curious investigaticnof physical signs is apt here, as in the case of ailother diseases where physical diagnosis is concerned, tbmake the observer less attentive to the general signs andsymptoms than their real importance demands." AndWardrop egpresses his views in still stronger terms : " Howmany examples of erroneous prognosis do we not all meetwith? 7 And I am convinced that nothing has contributedmore to extend this humiliating catalogue than the intro-duction of auscultation." It is needless to say that thestethoscope does not merit such sweeping condemnation.And yet it cannot be denied that many of the errors made inthe prognosis of heart disease-and especially of valvularlesions-arise from too narrow a reliance upon its indications.The stethoscope will discover the " physical sign proper," the.murmurs, and therefore decide to which of the various classesof valvular defect any case belongs, and by placing it in this.category or in that determine what are the usual tendenciesof tbe affection. But here its function ends; beyond this itdoes no indicate what is in store for the particular patient.It is well known that the quality of a murmur is no guide tothe amount of valvular mischief which exists. For whilethe loudest murmur may remain for many years with quiteunimportant results the effects of a valvular lesion maysometimes be too grave for the production of a murmur atall. But we cannot adopt Latham’s dictum,3 that "as very general fact the loader the endocardial murmur theless is the amount of valvular impediment." There is intruth no rule in either direction, but each case stands byitself.A true estimate of the gravity of a lesion can only be-

gained by a general survey of the case in the broadestpossible light ; to determine, first, what has been its effectupon the heart itself, and then how far its influence hasextended beyond this organ. If it is found that a murmur ispresent-no matter at which orifice-and that there is nochange in that part of the heart upon which the strain firstcomes, and if it is also known that this murmur has existedlong enough for the effects of increased work to bemanifested, then it follows that the lesion is trivial andstationary and may remain so for an indefinite time. Onthe other hand, if hypertrophy or dilatation, or both, exist,their degree is a test of the actual interference with theheart in its work. Due weight is also given to thecharacter of the pulse and to symptoms such as.

1 Diseases of the Heart, second edition, p. 106.2 Diseases of the Heart, p. 283.

3 Diseases of the Heart (New Sydenham Society), p.275.T

1164 DR. MARKHAM SKERRITT: PROGNOSIS IN HEART DISEASE.

dyapnoea or palpitation or syncope, and to any evidence o:

interference with the pulmonary or the systemic circulationor of the presence of associated disease. It is, howevernecessary not only thus to check the special physical sign;of valvular disease, but also sometimes to estimate the valuEof symptoms by physical signs. When this happens it i,

usually in young patients who are far removed from th(class to which I shall next refer. A short time since I hadunder observation a young man who suffered from mostalarming cardiac symptoms, of which a very grave view hadbeen taken, frequent attacks of palpitation and dyapnocawith tendency to syncope being associated with a mitralsystolic murmur and a moderate amount of dilated hyper-trophy. Betweenwhiles, however, the heart was capable ofsteady and efficient contraction. It appeared to me that thephenomena were serious, out of proportion to the actualdegree to which the organ was affected, and that the outlookwas therefore favourable as to both the danger of theparoxysms and the prospect of ultimate improvement, andI am informed that time has shown the truth of thisconclusion.

C have referred to conditions in which the physical signsmay attract more attention than is their due. There is anopposite group, especially associated with advancing years,where they are apt to be by no means proportionate to thegravity of the actual state. In this case an intelligent con-sideration of the symptoms is essential, since they are ofgreater importance than the physical signs. For instance, aman beyond middle life, whose general nutrition is failing,auffers from shortness of breath and a tendency to palpita-tion. The heart’s action is found to be somewhat feeble,and that is all. And yet fatty degeneration exists, from whichthe patient may at any moment die.The importance of history, the second factor in prognosis,

is never underrated by the practical physician. By it aredetermined the origin of any morbid state, the length of timethat it has existed, and its tendency to development in onedirection or in another, and an accurate appreciation of theinformation which it conveys is of the greatest value. Wherevalvular defect is due to acute endocarditis it is importantto know whether there is a liability to a fresh onset ofthe malady in which it originated. For instance, whenendocarditis arises during the course of an acute I

specific disease such as scarlet fever, which usualiymakes one attack only, the prospect is better than in thecase of acute rheumatism, where recurrence is common, andoften lights up fresh endocardial inflammation. Or thehistory shows that a murmur may be due, not to endocar-ditis, but to weakness of heart following acute illness ororiginating in ansemia, in which event there is a reasonableprospect of cure. Or the course is perhaps preventable ormore or less removable, as when avoidable muscular strainproduces cardiac dilatation. Or it is a diathetic condition,suoh as gout, which can be kept in check, but not eradicated.Or the affection may originate in a persistent and irremediablecondition, as when dilated hypertrophy results from chronicBright’s disease or fiom the arterial degeneration of age. Inevery case a recognition of the cause of a cardiac lesion, andtherefore of the degree to which it may be influenced orremoved, enters into a rational prognosis.

It is difficult to over-estimate the value of a knowledgeof the length of time that a heart lesion has existed. I willillustrate this point M the case of acute endocarditis. It hasbeen pointed out tha% it is impossible to determine during anattack of this inflammation what will be its ultimate out-come. Walsh 4 says :

" Viewing all forms of valvular ixnpedi-ment as a single group, it is not possible to make anystatement of the least utility on the question of duration.Nay, even if any individual disease of the whole number beselected the extremes of brief and of protracted course arefound to lie so widely apart that it becomes practicallyuseless to strike a mean....... We must be content to registerthe unexplained truhh that all forms of valvular disease

may, on the one hand, prove the main instrumentsin mpidly killing, or, on the other, remain for a well-

nigh indefinite period subjectively latent." And with thisLatham’s testimony t.Ccords 5: "Such cases as have fallen inmy way have taught me that the period to which life maybe continued is very various. It may be a few months only, I

or a few years, or zs; may be for many years, even ten ortwenty or thirty. Of these facts I am certain, but I cannot

4 Diseases of the Heart, fourth edition, p. 292.5 Loc. cit., p. 2411.

array them numerically and statistically; and because Icannot I can determine no relative proportion between thosewho survive months and those who survive years, or those whosurvive few years and those who survive many, yet the factsare fure." Walsh is unable to account for so wide adivergence, but Latham’s explanation is as follows": " Whenthe heart is left in a state of unsoundness from past inflamma-tion two principal consequences are to be expected-eitherthere may be a renewal of inflammation in the unrepairedstructure, or this remaining as it was left may become theelement of further material changes in the whole organ.......The latter consist in alterations of bulk and size and shapeand capacity, no other causes being engaged in bringingthem about than those which are constantly at wOlk in thehealthy heart-namely, its own vital movements ; only theyare now at work with more or less energy than is eithernatural or healthy or they are at work without their naturaland healthy harmony."Considered from the point of view of pathological anatomy

the result in acute endocarditis may be as follows. First,resolution, with removal of the products of inflammationand consequent disappearance of all abnormal physicalsigns. I believe this to be one mode of terminationalthough this view is not universally held. Walsh says:"An indubitable endocardial murmur, holding on from thebeginning to the end of the acute disease, never, so far as Ihave known, totally disappears in after life." It will beallowed that murmurs are sometimes met with having allthe characters of those due to endocarditis, and thatthey may disappear with convalescence from the feveror comparatively soon afterwards. I have myself metwith what I have believed to be instances of this com.plete recovery. It has been urged that because themurmur does not persist therefore it cannot be due toinflammation. This important point is well argued byByrom Bramwell," who arrives at the conclusion in whichI have expressed my own belief. Latham,9 indeed,asserts that out of a series of 63 cases of rheumatic endo-carditis "peifect reparation occurred in 17; for in thesethe murmur ceased entirely." And Gibson 10 records therecoveries from mitral endocarditis as 25 out of 51. This isso large a proportion that the doubt arises whether in somethe murmur was not due to a cause other than inflammationof the endocardium. Resolution then being recognised asone mode of termination of acute endocarditis, undoubtedlya more usual result is the subsidence of inflammationbut the persistence of its products. The young con-

nective tissue growth in the affected portion of theendocardium goes through the same changes which occurin similar tissue elsewhere ; it matures into fibrous tissue,which as it develops tends to contract, and therefore thevalve-segments become more or less thickened, and perhapsdistorted to such a degree that their function is per-manently interfered with.

Pathologically, therefore, the result in all hearts thusaffected is the same-the persistence of the matured pro-ducts of inflammation. But the practical difference betweenone heart and another is great. In the one, perhaps, "a a littleridge on the surface of a valve, a little granulation on itsfree edge, a little thickening or shortening of a tendinouscord "-possibly so slight a change that, though per-manently marked by inflamation, the valve is practicallyperfect and no murmur exists, anyhow too trivial to giverise to definite interference with the function of the organ.fn the other the self-same morbid process results in somevalvular deformity, forming an obstacle before which theieart speedily fails. Pathologically identical, the outcome)f the same affection, clinically the position of these twolearts is widely different. "The renewal of inflammation inòbe unrepaired structure " may occur in one of two ways-dther by repeated attacks of acute inflammation similar tohe first or by the passage of endocarditis from the acuteorm into the chronic. Latham 11 says: "When acutebeumatism has been once suffered in early life there is aearful likelihood that it will be oftentimes suffered again.Moreover, the first attack is generally the type of every,ttack which is to follow ; they will all take the same course,nd involve the same structures. If the first involve theleart, so probably will they all."

6 Loc. cit., p. 296. 7 Loc. cit., p. 258.8 Diseases of the Heart and Thoracic Aorta, p. 373.

9 Loc. cit., p. 35.10 Reynolds’s System of Medicine, vol. iv., p. 462.

11 Loc. cit., p. 242.

1165DR. MARKHAM SKERRITT: PROGNOSIS IN HEART DISEASE.

I No one will dispute the liability of acute rheumatism to. recur. Yet in my own limited experience it is not very

exceptional for this fever to attack a patient in early life andi

not again, although many years may have elapsed. Forinstance, the other day I saw a man, aged twenty-seven years,who had suffered from rheumatic fever once only at the ageof three years; a loud aortic systolic murmur existed, butwithout symptoms. And exception may also be taken toLatham’s second point-that the first attack involving theheart all the later will probably do so too. For I do notthink that it is rare for acute rheumatism to recur withoutthe renewal of endocarditis. This is a point uponwhich it is not easy to speak dogmatically owing tothe difficulty in determining that the heart doesremain free from fresh inflammation. But it is fairto infer that this is so when the disturbance of the organ isnot out of proportion to the general symptoms of fever, andno changes can be recognised in the cardiac area eitherduring the acute stage or afterwards.Opinions differ as to the frequency with which acute

endocarditis passes into chronic inflammation. Latham 12says on this point: "This I believe to be a fact which, ifnot true in every instance, is true in the majority-namely,that after inflammation of the endocardium has ceased,whatever remnant of unsoundness is left it continues everafter without increase in its own kind. After the lapse ofyears the very appearance of all we find seems to testify that ithas long been stationary...... and when the results of clinicalobservation are compared with those of morbid anatomythey will be found to testify the same thing." This importantquestion is not adequately discussed by pathologists. You,Sir, point out the reason for this when you say :13 " Speci-mens of endocarditis in this early stage are frequent enough.But it is not easy to say what occurs next in the processbecause we do not have many opportunities of seeing theintermediate conditions between this which is found in casesof death from the acute disease which causes the endo-carditis and that advanced state of change in the valveswhich long afterwards proves fatal by disabling them. Itappears to us that in the interval between acute endo-carditis of rheumatic fever and the death long afterfrom valvular disease of the heart many frequentrepetitions of the inflammation must occur. Sometimeswe find inflammatory products of two distinct dates onthe valves, some recent, some older. But more usually achronic state of inflammatory irritation persists, slowlychanging the valve." Judging by clinical evidence my ownexperience points to the view that both these things happen.While in many instances there is only too good reason toconclude that the mischief is progressive, yet in some acuteendocarditis comes to a definite end and no further changetakes place in the tissue which has been the seat of inflam- 1mation. I have met with many cases in which no perceptible ialteration either in the character of the murmur or in the 1

general state of the heart could be detected at successive aexaminations, in some instances extending over a consider- E

able number of years. It is reasonable to conclude that rif the condition of the organ is thus stationary from the (clinical point of view it only remains structurally unaltered. EOn the other hand, instances are only too common in which s

it is plain that the valvular lesion is progressive, and where a

the obvious inference is that chronic endocarditis has r

carried on the work begun by the acute inflammation. tIt has thus been seen that the results of acute endocar- e

ditis, both pathologically and clinically, may vary within the iwidest extremes, and that no data exist by which it can be o

foretold during an acute attack what will be the ultimate i:

position of ’ any given case. How, then, will this e

most important question be answered ? 7 The problem twill be solved by time alone. Let me remind you of the o

statement which I have already made, that a knowledge of a

the length of time that a heart lesion has existed is of o

the greatest value in prognosis. Endocarditis must be hestimated by the results which it produces-the damage a;which has been done to the heart in a given time is a test of u

what will happen in the future ; and prognosis becomes a CI

problem in proportion. What, then, are the indications that lia condition is on the one hand grave in its tendencies and on irthe other unimportant ? The only test is the degree to which o1the heart has become secondarily affected, the evidence ftshowing that it is hampered in its work. The presence of a

- ————-—-———————————————————————— 12 Loc. cit., p. 274.

13 Wilks and Moxon: Pathological Anatomy, third edition, p. 134.

hypertrophy, the existence of dilatation, and their amount,signs of defect in the conduct of the circulation in the lungsor in the systemic circuit,-these it has before been said arewhat have to be sought. Let it now be supposed that thepatient comes under observation some considerable timeafter an attack of acute endocarditis-it may be twelvemonths or two years or longer-and that a murmur ispresent. Prognosis becomes, as has been said, a problemin proportion. If the heart is in a certain state at the endof a certain time, what will be its condition in six monthsor twelve months or in five or ten or twenty years And thelonger the interval that has elapsed since the acute inflamma-tion the more certainly can this question be answered. Ifin the same period one ípatient has arrived at the stage ofdropsical effusion, while another has a much enlarged heartwhich can still, however, overcome the obstacle to its work ;and another is unconscious of disease, and there is but slightincrease in cardiac size and strength ; and in yet another,no change whatever has occurred, the inference is plain thatas it has been in the past, so will it probably be in thefuture-disease that has advanced will continue to increase-that which has been quiescent will remain so still. And

through the whole series the foundation of prognosis istime-time and the changes which it has wrought.

I will conclude the consideration of the position of historyby reference to a case which well illustrates its importance.Nearly eight years ago I saw in consultation a patient whohad been informed that he was suffering from aorticaneurysm. The existence of disease had been discovered byaccident and had not before been suspected, the patientfeeling in his usual health. I found a most intelligent man,fully able to grasp the bearings of all that was said respect-ing his condition. The heart was enormously enlarged andhypertrophied ; the impulse was so forcible as to shake thechest-wall and could be plainly felt through the clothes.Although I was of opinion that the physical signs, intowhich I need not enter, did not justify the diagnosis ofaneurysm, yet they were not such as altogether to negativeits existence. But I was much struck with the pointalready mentioned-that the trouble had been discovered byaccident and not from symptoms complained of by thepatient, who was exceptionally intelligent and observantand had led an active life. It appeared to me that a lesionaccompanied by cardiac action differing so markedly fromthe normal, if of recent origin, could not arise withoutattracting the attention of the patient ; and on carefulinquiry it came out that the strong beating of his heart hadbeen noted in his early adult life ; and, further, that when hewas a little child his father once came into the nurserywhen the boy was undressed and observed somethingwhich led him to bring the family medical adviser,who examined the chest. I therefore concluded thatthe patient had grown up with the lesion that existed, sothat to him it gave no abnormal sign. It followed thataneurysm, which would be a recent development, did notexist. The prognosis attaching to the latter being thus setaside the question arose as to what the future had in store.On the principle which has been already discussed it wasargued that if compensation was so complete that the heart,although thus enormously enlarged, had been able through11 these years to do its work in such a way that an activeraan had no suspicion that it was otherwise than normal,there was no reason why it should not long remain equallyefficient. As a matter of interest, and as showing hownconclusive were the physical signs, I may add that as)pinions so divergent were given upon a subject of suchmportance the patient was examined in London by twosminent authorities, one of whom came to the conclusion,hat aneurysm existed, while the other agreed with my view)f the case. The patient, after hearing either diagnosis fullyargued by its supporter, made up his mind that the balanceIf evidence was against the existence of aneurysm, and laidois plan of life accordingly. This was nearly eight yearsgo. I have examined him at intervals since and have beenmable to detect any signs of advancing disease ; he is notonscious of any trouble ; he leads a busy and fairly activeife and looks the picture of health. I have gone thus fullynto this case because it is a forcible illustration of the valuef a knowledge of the past as a guide to the present and theuture. A most important decision turned upon the history,nd the result has proved that reliance was rightly placedpon its indications.An acquaintance with the course which is usually run by a

iven form of heart disease is one of the factors which haveT 2

1166 DR. MARKHAM SKERRITT: PROGNOSIS IN HEART DISEASE.

been enumerated as entering into prognosis. From what hasalready been said it will be plain that this knowledge oftencannot be applied with sufficient accuracy to be of muchvalue. It has been seen that in acute endocarditis it ispractically useless for determining what will arise in a

particular instance. Nor, viewing all forms of chronicvalvular impediment, in whatever way originated, is it

possible to make a statement with regard to any one ofthem that will necessarily hold good of a given case. Alesion that in one instance may end fatally within a fewmonths may in another be consistent with long life andpractically good health. It is, however, recognised that eachform of valvular disease has certain general tendencies andthat some of these are more serious than others. The relativegravity of valvular derangements is variously estimatedby different authorities. Walsh 14 places them in the followingdescending series: tricuspid regurgitation, mitral regurgita-tion, aortic regurgitation, pulmonary constriction, and aorticconstriction, tricuspid constriction and pulmonary regurgita-tion being too little known to be placed in position in the list.The worst results follow those lesions which directly obstructthe circulation behind them. Hence tricuspid regurgitationhas the first place, hindering as it does the return of bloodfrom the whole of the organs and tissues of the generalcirculation, the heart itself included. Similarly mitraldisease, the two forms of which come next in the series,causes obstruction to the passage of blood from the lungs.and consequently tends to produce the whole series ofpulmonary complications which are due to this back-pressure.On the other hand, lesions of the arterial orifices-the aorticand the pulmonary-so long as they exist alone, do notaffect the circulations behind them, protected as they are bythe auriculo-ventricular valves ; and the result turns thereforesolely on what effect is produced upon the ventricle itselfand how far there is interference with the supply of blood tothe artery. Apart from the liability to sudden death aorticregurgitation is much more serious than obstruction at thesame orifice because of the tendency to over-distension of theventricle during diastole. Of all valvular lesions aorticobstruction is the most favourable, the left ventricle fre-quently undergoing hypertrophy sufficient to overcome theobstacle at the orifice of the aorta. Pulmonary constrictionhas probably no more serious tendencies than aortic obstruc-tion. It is well known that the sufferer from certain formsof valvular disease is placed in a better position, especiallyas regards the prolongation of life, by having one or

more other forms of affection of the orifices added to thatwhich already exists. For instance, there is less liability tosudden death in aortic regurgitation if it is associated withmitral incompetence. Probably the regurgitation throughthe mitral orifice during the systole of the ventricle lessensthe amount of blood driven into the aorta, and therefore thequantity and force of that which distends the ventricleduring the succeeding diastole. Another familiar illustra-tion is afforded by the effect of tricuspid regurgitation inrelieving the pressure on the pulmonary circulation causedby mitral disease. It has doubtless fallen to the lot of mostto meet with cases in which urgent lung symptoms have beencaused by the position of the pulmonary circulation betweenthe obstruction to the onward flow due to affectionof the mitral orifice on the one side and the increasedvis a tergo of the hyp3rtrophied right ventricle on theother. When at last the tricuspid valve gives way partof the force of the hypertrophied ventricle is now expendedin returning blood into the auricle, and thus the tension inthe pulmonary circuit is lessened and the urgent lungsymptoms are relieved, though at great cost as regards thesystemic circulation.

I have before pointed out that the prognosis of chronicvalvular disease resulting from a non-recurrent specific feveris more favourable than that originating in acute rheumatism,inasmuch as further attacks of the latter may occur, bringingwith them fresh risk to the heart But the prospect is betterwhen the valvular change is due to the endocarditis ofrheumatic fever than if it results from inflammation that ischronic from the first. For while the former may remainquiescent unless the valve is attacked afresh during arecurrence of the fever the latter is commonly due to somepersistent cause leading to progressive inflammation with itsincreasing valvular deformity. An exemption may be madein the case of endocardial mischief arising in old people. Inmy experience it is here of little practical moment, slow in

14 Loc. cit., 392.

progress, and causing but slight disturbance in the functionof the affec’ed valve and altogether of secondary importanceto the degenerative changes in the vascular system generally,of which it is a pait.Time fails me to dwell upon the cause of chronic degenera-

tive changes occurring in the heart wall. When fattydegeneration-the most important of these-is once estab-lished it tends to increase owing to the persistence of itscause. Similarly no prolonged consideration can be devotedto the prognosis of hypertrophy and dilatation. Theirfate is bound up with that of their cause. As this is usuallypersistent and often progressive the secondary cardiac enlarge-ment is correspondingly permanent and tends to increase.The greater the hypertrophy in proportion to dilatation thebetter will the extra work be done and the difficulty be over-come. But only while the nutrition of the heart remainsgood. If the time comes that degeneration begins in thehypertrophied wall, the balance between work and power isdisturbed never to be restored. This is so commonly illus-trated in the late history of chronic Bright’s disease. Whenrenal inflammation becomes established in a patient whosenutrition is good the increased vascular tension is met byhypertrophy of the left ventricle, and the balance is thus sowell maintained that the heart carries on with ease thegreater work. But let the patient pass on to the time whenthe nutrition of the hypertrophied wall tends to fail ; thestrength of the heart is diminished while the calls upon itremain, and the symptoms of cardiac distress arise.The liability to sudden death is an important aspect of

prognosis. In the minds of the laity heart disease of everykind carries with it this awe-inspiring risk; and to informa patient that his heart is not sound is to condemn him toa life of miserable uncertainty. The physician, however,knows that this danger attaches chiefly to certain forms ofcardiac affection; it is therefore his duty to relieve thepatient of the dread of this accident in any case when it isnot likely to happen. Sudden death may occur in certainforms of chronic valvular disease, in dilatation, wheredegenerative changes exist, and from rupture of theheart or an aneurysm of this organ. It is well knownthat the lesion which carries with it by far the greatestrisk of sudden death is aortic regurgitation. It issaid by some authorities that this accident is liable to

happen even when there is comparatively little regurgita-tion. Walsh 15 quotes a case in which there were absolutelyno symptoms of disease, and there was neither hypertrophynor dilatation of the ventricle, and yet the patient droppeddown dead. He mentions, however, that the superficialpulses were markedly visible. In my own limited experienceI have not seen the tendency to fatal syncope unless theregurgitation is considerable and the ventricle is corre-

spondingly enlarged. It will be noted that in Walsh’scase, while the ventricle is said to have been normalin size and force, the superficial pulses were markedlyvisible. I have never met with the characteristic pulse ofaortic regurgitation when dilatation of the ventricle wasnot present, and on theoretical grounds it is not plain howa pulse indicating considerable regurgitation can exist whiledilatation is absent, since the ventricle has to contain anincreased amount of blood. Short of the existence of distinctsecondary dilatation I should regard a patient with aorticregurgitation as safe from fatal syncope. On the other hand,it must be borne in mind that many in whom aortic regurgi-tation and its accompanying changes are extreme die, notsuddenly, but by gradual increase of trouble. And, further,that there is less tendency to this mode of death when mitralregurgitation is added to aortic. One other valvular lesionsometimes ends abruptly, that is, mitral regurgitation. Thisdoes not often happen and is not to be feared unless com-pensation has failed. But that it may occur is impressed onmy mind by the memory of an occasion when I discussedwith a medical brother and the friends of the patient thecourse of life that should be followed, and death fromsyncope ensued within a short time of our leaving the house.The remaining varieties of valvular disease may be regardedas practically free from this risk. The same cannot, however,be said of dilatation, where the weak thinned wall sometimesunexpectedly ceases work.

It is, however, the degenerations which supply the majorityof the instances of sudden death. Angina pectoris is notablya malady which tends to terminate in the way underconsideration; ard in fatal cases some change in

15 Loc. cit., p. 394.

1167SIR R. T. THORNE: THE SOIL AND PATHOGENIC ORGANISMS.IK-

nutrition is practically always found - usually fatt;degeneration of the muscular substance, and especial],affection of the coronary arteries interfering with thlnutrition of the heart wall. Fatty infiltration, if excessivemay end in sudden syncope; this is much more likely thappen in the weak heart of true fatty metamorphosis. Buof all conditions the danger is most imminent when

degenerate htart has to face increased arterial tensionHere the type of cardiac action indicates the peril thathreatens. The pulse is quickened ; it may be irregular ancintermittent or fairly regular, and is often of good value, buits notable feature is high tension. The short and toneles;first sound of the heart is hurriedly followed by a ringingaortic sound. This kind of action marks a ventricle thaican barely hold its own until the strain is taken off by th(closure of the aortic valves, and it is plain that the patienilives on the brink of a precipice over which a trifling extrdemand upon the heart may at any time determine his fall.The last division of prognosis, which takes into considera

tion the special features of a given case, includes man)factors, such as social status, sex, temperament, and genera:habits, and the condition of other organs ; but their influencecannot be discussed in detail. Excepting the state of othe]viscera, perhaps the most important of these is position irlife. If the sufferer from cardiac trouble can be placed in anenvironment as nearly ideal as is attainable by the lavisrexpenditure of care and money his prospects differ muchfrom those of another who has to work for his breadin the station in life which he may chance to occupywhen the malady overtakes him. This is exemplifiedin the case of acute endocarditis. I hold stronglythat it is of the greatest importance to keep theheart as far as possible at rest for some considerable timeafter an attack of acute endocardial inflammation. Rest isthe first essential to the cure of inflammation and theremoval of its products. This is so obvious in the case, forinstance, of a joint that it is always recognised, and thesurgeon never grudges the time, however long, spent in theendeavour to secure a healthy limb. And it behoves the

physician to keep just as clearly in view the state of therecently inflamed valve. When the social position of a childsuffering from recent endocarditis will allow it is mypractice to enjoin the retention of the recumbent position forfrom three to six months. After this, if the murmur persists,the gentlest exercise is gradually allowed ; but for several yearsall violent exertion is forbidden. At the same time great atten-tion is paid to the general health. The intelligent cooperationof the friends, and as far as possible of the little patient,is needed to the success of this method. But where it hasbeen practicable I have seen reason to be well satisfied withthe result. In the case of older patients the treatment isapproximated to the above as closely as circumstances willallow. The prognosis of acute endocarditis much depends uponthis one question, whether or no the heart can for some timebe saved all but the "irreducible minimum " of work. Anytrouble and pains are well expended that will lessen the

prospect of valvular disease in after life.Contrast with this the case of the hospital patient.

The child or the young adult is treated for acuterheumatism accompanied by endocarditis, and the fever isquickly subdued. But the affected valve has not recoveredits normal condition, even if active inflammation has sub-sided ; it still remains a thickened and softened structure,ill fitted to withstand the pressure of the blood-stream. Thewhole future life may turn upon what the next few monthswill bring to this valve. And yet the exigencies of hospitalwork are such that the patient must be discharged whenconvalescent from the fever to take his chance with a stilldamaged valve. He receives excellent advice when heleaves; the boy must not do as boys are wont to do ;the older patient is warned against those things whichare placed in his way by his lot in life ; the wise counsel

iis not followed, and the still softened valve gives waybefore; the blood-current, or acute endocarditis becomeschronic inflammation, with its progressive increase of mis-chief. In heart disease there is more truth than is commonlythe case in the saying that there is one law for the rich andanother for the poor.In conclusion, I am constrained to put forward a plea for

mercy in the prognosis of heart disease. No one is exemptfrom the human attribute of liability to err. In the case ofthe physician this imperfection may be viewed in twoaspects-as it affects his own reputation and in its influenceupon the subject of his error. It is with the latter

that I am now concerned. The philosopher Baconmight well have had in view the prognosis of heartdisease when he counselled "not to engage a man’s self’peremptorily in anything, though it seem not liable toaccident, but ever to have a window to fly out at or a way toretire." " All must be familiar with instances of theoccurrence of the unexpected. I remember a man, fifty-nineyears of age, who was the subject of most pronouncedvalvular disease. When twenty years old be was warned thathis life was in danger and at the age of forty years wascondemned to die within the year. The other day I saw a,young man who had a mere suspicion of aortic obstruction ;.ten years before it was said that he might die at

any moment. Some twelve years ago I examined achild with marked mitral stenosis and dilated hyper-trophy-such a condition as might well have led toan early catastrophe ; she has grown into a well-developedyoung woman, who would not be suspected of the lesionshe carries. A lady, aged eighty-four years, has suffered fornearly twenty years-sometimes in a most alarming form-from all the symptoms of cardiac weakness commonlyassociated with fatty degeneration, and she still lives.The wider experience becomes the more does certainty

give place to probability, and it is wise to give due weight’even to possibilities. And especially should this be the casein dealing with disease of the heart, which carries with itto the sufferer the thought of constantly impending evil. Ithas been my lot from time to time to meet with those whohave been told, as has been proved without sufficient reason,that some grave cardiac lesion existed. To restore hope tolife, to give the patient to the full the benefit of such doubtas may attach to the nature of his condition and theuncertainty that too often attends the prediction of hisfuture, surely this is not only justifiable but also right, andthe lightening of the depressing influence of fear and dreadwill in itself tend to avert the danger that may threaten.For the imperfect and inconsequent manner in which this

lecture has been placed before you I crave your indulgence.I have touched only the borders of a subject whose im-portance deserves far abler treatment than it is mine tobestow.

Inaugural AddressON

SOIL AND CIRCUMSTANCE IN THEIRCONTROL OF PATHOGENIC

ORGANISMS.Delivered before the Midland Medical Society on Oct. 21st,

1897,BY SIR RICHARD T. THORNE, K.C.B.,

M.B. LOND., F.R.S.,PRINCIPAL MEDICAL OFFICER TO THE LOCAL GOVERNMENT BOARD.

MR. PRESIDENT AND GENTLEMEN,-It has long beenmatter of observation amongst those who are accus-

tomed to the investigation of causes of disease thatcertain infectious diseases tend to recur periodically,after intervals more or less long, in the same localities-whether these be houses, villages, or towns - undercircumstances that can hardly be explained excepton the assumption that the specific infections withwhich these diseases are associated have in such localitiescontrived to retain their vitality during the intervals and- tomaintain themselves outside the human body. Theseoccurrences stand in striking contrast with other prevalencesof the same diseases, often of equal virulence and extent,but which exhibit no tendency to recur ; and the questionnaturally arises how such difference in the behaviour ofdisease can be explained.

Similarly, there are individuals who, on a single exposureto an infection, do not fail at once to contract the disease inquestion ; whilst in contrast with these persons we know ofindividuals who are subjected to maintained risk and

exposure of precisely the same sort, and who seem from thevery first to possess a natural immunity against some