LECTURES ON ANGINA PECTORIS AND ALLIED STATES BY WILLIAM OSLER, M.D. FELLOW OF THE ROYAL COLLEGE”OF PHYSICIANS, LONDON PROFESSOR OF MEDICINE, JOHNS HOPKINS UNIVERSITY, BALTIMORE AUTHOR OF A PRACTICE OF MEDICINE LECTURES ON THE DIAGNOSIS OF ABDOMINAL TUMORS, ETC. NEW YORK D. APPLETON AND COMPANY 1897 CoprricHt, 1896, 1897, By D. APPLETON AND COMPANY. TO W. T. GAIRDNER, M.D., F.R. 8., REGIUS PROFESSOR OF MEDICINE IN THE UNIVERSITY OF GLASGOW. Dear Dr. Gairdner : Please accept the dedication of this little volume in token of the appreciation which your cis-atlantic brethren feel of the value of your life and work im our profession. . Sincerely yours, WILLIAM OSLER. NOTE. THESE lectures were delivered to the graduate class in medicine at the Johns Hopkins Hospital, and appeared in The New York Medical Journal, 1896, vol. lxiv. They are here republished with slight additions and corrections. CONTENTS. LECTURE I. History of the recognition of angina,—Heberden, Rougnon, Morgagni, —Literature.—Definition.—Forms of heart pain—Classification of the forms of angina. ~ Physiology and d pathology of the coro- nary arteries. , . ‘ . . . LECTURE Ii. ANGINA PECTORIS VERA. ETIOLOGY. GENERAL DESCRIPTION OF THE DISEASE. Incidence of the disease.—Station in life—Sex.—Age.—Epidemic in- fluences. — Heredity. — Gout. — Diabetes. — Syphilis. — Specific fe- vers.—Heart disease.-Locomotor ataxia,—General picture of the disease . > . . . . . . . . LECTURE III. ANGINA PECTORIS VERA, PHENOMENA OF THE ATTACK, Exciting causes.—Symptoms.—State of heart and pulse.—Pericarditis. —Respiratory features.—Gastro-intestinal symptoms.—Nervous and psychical symptoms . . . . . . . . . LECTURE IV. ALLIED AND ASSOCIATED CONDITIONS. I. Syncope anginosa.—II. The Adams-Stokes syndrome,—TH1. Angina sine dolore—IV, Cardiac asthma LECTURE V. PSEUDO-ANGINA PECTORIS, I, Neurotic group: (a) Hysterical and neurasthenic cases; (b) Angina pectoria vaso-motoria; (c) Reflex angina.—II Toxic angina: forms of heart painfrom tobacco. 1 es . . . . PAGE 20 45 67 86 a CONTENTS. LECTURE VI, THEORIES OF ANGINA, The importance of coronary artery disease.—Intermittent claudication. —State of the heart muscle in an attack.—Seat and cause of the pain.—Vaso-motor changes in angina,—Relations of spurious and trueangina . . . oe . . . * * LECTURE VII. DIAGNOSIS, PROGNOSIS, AND TREATMENT OF ANGINA, Anomalous cases of heart pain.—Elements in the diagnosis of true angina.—Differentiation of true and pseudo angina.—Prognosis, Treatment of angina pectoris vera.—Treatment of false angina. —Conelusion ». . 1 kw kkk kl APPENDIX, Nore A.—Rougnon’s claim . . : . . . . «“ B.—The case of Mr. Matthew Arnold . . . . . . “ C.—Retention of consciousness after apparent cessation of heart’saction =. 6 6 ww ww PAGE 111 131 157 158 160 But wel I woot thou doost my herte to erme That I almost have caught a cardtacle. The wordes of the Host to the Phisicien and the Pardoner.—CHAUCcER. LECTURES ON ANGINA PECTORIS AND ALLIED STATES. LECTURE I. History of the recognition of angina.—Heberden, Rougnon, Morgagni.—Lit- erature.—Definition.—Forms of heart pain.—Classification of the forms of angina.—Physiology and pathology of the coronary arteries. Tux history of the recognition of the disorder known as an- gina pectoris is connected with the names of three celebrated men—Heberden, Jenner, and John Hunter. On July 21, 1768, Heberden read, at the Royal College of Physicians, a paper entitled Some Account of a Disorder of the Breast, which was published in vol. it of the Medical Trans- actions of the College of Physicians, 1772. An extract from the original description must be quoted: “There is a dis- order of the breast, marked with strong and peculiar symp- toms, considerable for the kind of danger belonging to it, . . . The seat of it and sense of strangling and anxiety with which it is attended may make it not improperly be called angina pectoris. « Those who are afflicted with it are seized while they are walking, and more particularly when they walk soon after eat- ing, with a painful and most disagreeable sensation in the breast, which seems as if it would take their life away if it were to increase or to continue; the moment they stand still all this uneasiness vanishes. Tn all other respects the patients are at the beginning of this disorder perfectly well, and, in particu- 2 ANGINA PECTORIS AND ALLIED STATES, lar, have no shortness of breath, from which it is totally dif- ferent.” Subsequently, in the celebrated Commentaries upon which our grandfathers in the profession were educated, Heberden gave a fuller account of his experience with the disease. The name which he adopted can not be regarded as altogether sat- isfactory, since it was already in use in designating affections of the throat, with which its literal meaning—a strangling— is much more in harmony. In one sense, however, the term is fairly appropriate, since, as noted by Gairdner, the words anx- iety and anguish, expressive of two of the most prominent fea- tures of the disease, have a derivation from the same Greek word as angina. In 1773, John Hunter had his first attack, which was graphically described by his nephew, Everard Home: “ While he was walking about the room he cast his eyes on the looking- glass, and observed his countenance to be pale, his lips white, giving the appearance of a dead man. This alarmed him and led him to feel for his pulse, but he found none in either arm; the pain continued, and he found himself at times not breath- ing. Being afraid of death soon taking place if he did not breathe, he produced the voluntary act of breathing by work- ing his lungs by the power of the will.” In 1776 he had a second attack, and when convalescent he visited Bath. Here he was seen by his friend and pupil, Edward Jenner, of Berke- ley; and one of the most interesting and sagacious letters of that distinguished man was written to Heberden, giving his diagnosis of John Hunter’s case, and suggesting, for the first time, the probable association of disease of the coronary arteries with angina pectoris. The letter is worth quoting in full: * “ When you are acquainted with my motives, I * Baron’s Life of Jenner, London, 1827, HISTORY OF THE RECOGNITION OF ANGINA. 3 presume you will pardon the liberty I take in addressing you. I am prompted to it from a knowledge of the mutual regard that subsists between you and my worthy friend Mr. Hunter. When I had the pleasure of seeing him at Bath last autumn I thought he was affected with many symptoms of the angina pectoris. The dissections (as far as I have seen) of those who have died of it throw but little light upon the subject. Though, in the course of my practice, I have seen many fall victims to this dreadful disease, yet I have only had two op- portunities of an examination after death. In the first of these I found no material disease of the heart, except that the coronary artery appeared thickened. “ As no notice had been taken of such a circumstance by anybody who had written on the subject, I concluded that we must still seek for other causes as productive of the disease; but, about three weeks ago, Mr. Paytherus, a surgeon at Ross, in Herefordshire, desired me to examine with him the heart of a person who had died of the angina pectoris a few days before. Here we found the same appearance of the coronary arteries as in the former case. But what I had taken to be an ossification of the vessel itself, Mr. P. discovered to be a kind of firm, fleshy tube, formed within the vessel, with a considerable quantity of ossific matter dispersed irregularly through it. This tube did not appear to have any vascular connection with the coats of the artery, but seemed to lie merely in simple contact with it. “ As the heart, I believe, in every subject that has died of the angina pectoris, has been found extremely loaded with fat, and as these vessels lie quite concealed in that substance, is it possible this appearance may have been overlooked? The importance of the coronaries, and how much the heart must suffer from their not being able duly to perform their func- tions (we can not be surprised at the painful spasms), is a 4 ANGINA PECTORIS AND ALLIED STATES. subject I need not enlarge upon, therefore shall just remark that it is possible that all the symptoms may arise from this one circumstance. “ Ags I frequently write to Mr. H. I have been some time in hesitation respecting the propriety of communicating the matter to him, and should be exceedingly thankful to you, sir, for your advice upon the subject. Should it be admitted that this is the cause of the disease, 1 fear the medical world may seek in vain for a remedy, and I am fearful (if Mr. Tunter should admit this to be the cause of the disease) that it may deprive him of the hopes of a recovery.” In another letter * Jenner gives as his reasons for not pub- lishing his views earlier an anxiety lest they should be a source of annoyance to his friend Hunter. “ Soon after Mr. Paythe- rus met with a case. Previous to our examination of the body I offered him a wager that we should find the coronary arteries ossified. This, however, proved not to be exactly true; but the coats of the arteries were hard... . At this time my valued friend, Mr. John Hunter, began to have the symptoms of angina pectoris too strongly marked upon him; and this circumstance prevented any publication of my ideas on the subject, as it must have brought on an unpleasant conference between Mr. Hunter and me.” Te says that Mr. Cline and Mr. Home did not think much of his views. “ When, how- ever, Mr. Hunter died, Mr. Home very candidly wrote to me, immediately after the dissection, to tell me I was right.” The further details of Hunter’s remarkable case are always referred to. From 1785, when he had a severe illness, the at- tacks became increasingly frequent, and were brought on par- ticularly by exercise and by worry and anger; and, indeed, he was accustomed to say “ that his life was in the hands of any * Parry. An Inquiry into the Symptoms and Causes of the Syncope Anginosa, commonly called Angina Pectoris, 1799, HISTORY OF THE RECOGNITION OF ANGINA. 5 rascal who chose to annoy and tease him.” During the last few years of his life, though he did a large amount of work, the attacks seem to have been very frequent, and would come on after very slight exertion and while he was operating. As he had himself predicted, death came suddenly, in conse- quence of a fit of temper at a mecting of the governors of St. George’s Hospital, October 16, 1793. When contradicted flatly, he left the board room in silent rage, and in the next room gave a deep groan and fell down dead. The coronary arteries were found to be converted into open bony tubes, and the aorta was dilated. Attempts have been made by French writers to claim the priority in the description of the disease for Rougnon, pro- fessor of medicine in the University of Besancon. In a letter addressed to M. Lorry, dated February 23, 1768,* he describes the case and circumstances of the death of a Captain Charles. The patient had become asthmatic, and on walking fast had a sort of suffocation. Six weeks before his death he had com- plained to M. Rougnon of “ wne géne singuliére sur toute le partie antérieure de la poitrine en forme de plastron.” The attacks evidently occurred with great suddenness, and disap- peared with equal abruptness. The chief stress is laid upon the feeling of suffocation, but it is evident that associated with it there was pain of great intensity; “seulement une douleur gravative dans la région du caur, lorsqwil éprouvott ses suf focations.” Captain Charles died very suddenly, shortly after dining with his friends. The pericardium was fatty; the heart was large; there weré no valvular defects; the coronary veins were enlarged “ prodigiously ” ; no mention was made of the condition of the coronary arteries. RRougnon lays stress upon the obstruction in the lungs and excessive ossification of * Lettre a M. Lorry sur une maladie nouvelle, Besancon, 1768. 6 ANGINA PECTORIS AND ALLIED STATES. the cartilages. He confesses, however, that the condition was very puzzling, and the autopsy not at all satisfactory to his friends: “Jf, Charles est mort, disoient-ils, parce qu est mort.” I can not agree with Professor Gairdner, who says that “there was no trace of anything like a clinical description of angina pectoris in M. Rougnon’s letter.’ * The suddenness of the attacks, the pain in the region of the heart, the abrupt termination, and the mode of death—during exertion after a full meal—favor the view that the case was one of true an- gina. (Note A.) To Morgagni, not Rougnon, is due the credit of the first description of a single case. In the splendid section on aneu- rysm of the aorta, he describes angina pectoris accurately in Case V, referring to the paroxysms, the pain, the difficulty of breathing, the numbness of the left arm, and the effect of exer- tion. I read you here extracts from the case. “A lady, forty-two years of age, who for a long time had been a valetudinarian, and within the same period, on using pretty quick exercise of body, she was subject to attacks of vio- lent anguish in the upper part of the chest on the left side, ac- companied with a difficulty of breathing and numbness of the left arm; but these paroxysms soon subsided when she ceased from exertion. In these circumstances, but with cheerfulness of mind, she undertook a journey from Venice, purposing to travel along the continent, when she was seized with a parox- ysm, and died on the spot. I examined the body on the follow- ing day. . . . The aorta was considerably dilated at its curva- ture; and, in places through its whole tract, the inner surface was unequal and ossified. These appearances were propagated into the arteria innominata. The aortic valves were indurated.” He remarks: “The delay of blood in the aorta, in the heart, in the pulmonary vessels, and in the vena cava, would occasion * Lancet, 1891, i, p. 604. HISTORY OF THE RECOGNITION OF ANGINA. q the symptoms of which the woman complained during life; namely, the violent uneasiness, the difficulty of breathing, and the numbness of the arm.”—(Cooke’s Morgagni.) There are those, indeed, who regard Seneca as the first to describe the affection, in the remarkable account which he gives of his own disorder. With this view Forbes and Gaird- ner agree, but Parry and Stokes do not. I quote from Parry the following translation of part of Seneca’s graphic account: “The attack is very short and like a storm. It usually ends within an hour. I have undergone all bodily infirmities and dangers; but none appears to me more grievous. Why not? Because to have any other malady is only to be sick; to have this is to be dying.” Seneca states, too, that his physicians called the disease a meditatio mortis. , The literature of angina pectoris has become very volumi- nous. English writers have contributed most largely to the clinical description of the disease. Perhaps the two most valuable articles are lectures xxxvii and xxxvili in Latham’s Clinical Medicine, which you will find in vol. i of the New Sydenham Society edition of his works; and Professor Gaird- ner’s essay in Reynolds’ System of Medicine. The best recent expositions in French and German are to be found in Hu- chard’s Traité clinique des maladies du ceur, second edition, 1893, which gives a most exhaustive account of the. various forms of angina, and O. Rosenbach’s Die Krankheiten des Herzens, 1896. I pass about for your inspection a number of the monographs and journal articles which I have collected on the subject. Parry’s essay has become very scarce, but it is in all the larger medical libraries. Rougnon’s Lettre, pub- lished at Besancon, 1768, is still more rare. The copy in the Surgeon-General’s Library is the only one I have ever seen. I would ask you to look at the first part at least of these fly leaves, which I picked up in an old book shop a few years ago. 8 ANGINA PECTORIS AND ALLIED STATES, It is a letter to Dr. Heberden from a man who signs himself “Unknown,” descriptive of his own case. He had seen, in the Critical Review, an extract from Heberden’s original paper, and, recognizing his malady, he wrote in this letter one of the very best accounts which exists in the literature. It is particularly noticeable for two things: He clearly dissociated the pain of the attack from the angor or mental feature, and he first made use of the now hackneyed phrase describing the latter aspect as “an universal pause within me of the opera- tions of Nature.” Expecting a sudden death, he left orders that Heberden should examine his body. Within three weeks from the writing of the letter the dissection was made by John Hunter. Derinirron.—In the consideration of a disease it is well, if possible, to start with a clear understanding, or at least some concise statement, of its nature, and of the characters of the manifestations by which it is recognized. With some disorders this is a very easy matter. For example, insufficiency of the aortic valves is a clearly defined affection, with, it is true, a diverse etiology, a varied anatomical picture (from a trifling curl of the edges of a valve, to a clean shaving of a segment from the aortic ring); but with all its variations there are asso- ciated definite sequences and well-characterized signs. Angina pectoris is not a disease, but a syndrome or symp- tom group (without constant etiological or anatomical founda- tions) associated with complex conditions, crganic or func- tional, of the heart and aorta. Pain about the heart of an agonizing character, occurring in paroxysms, is the dominant feature of all varieties of the syndrome. Used to define we em- paroxysmal attacks of pain in the chest—breast-pang ploy the term generically, qualifying the varieties by such names as true, false, hysterical, and voso-motor. HEART PAIN. 9 Before passing to the discussion of the varieties of angina pectoris let. me refer briefly to the subject of Heart Patw.—Disturbance of sensation is a most incon- stant symptom of heart disease; the gravest. affections are often painless; the most trifling may present the features of an intense neuralgia; while a very limited lesion may have as its sole manifestation paroxysms of agonizing pain. The following abnormal cardiac sensations may be recog- nized: 1. Consciousness of the heart’s action; a fluttering, a sense of goneness, the indefinable uneasiness associated with palpita- tion, a sense of tension in the chest with gasping, all or some of which are common phenomena in emotional states, in indi- gestion, neurasthenia, and hysteria. 2. Pain—darting, stabbing, tearing or boring, dull and heavy, or acute and piercing, steady or paroxysmal—varying in grades of intensity and in duration, often transient and trifling, as in dyspepsia and the tobacco habit, more enduring and severe in hysteria and neurasthenia, and occurring in paroxysms of an agonizing, intolerable character in the forms of angina. It often radiates over the area of distribution of certain of the cervical and dorsal nerves. 3. There is an element peculiar to certain conditions of the heart, often associated with, but which can not itself be prop- erly characterized as pain—indeed, the patient often expressly states that it is not of the nature of physical pain—a sense of imminent dissolution, a mental anguish, which has been vari- ously expressed by patients and writers as a pause in the opera- tions of Nature, the very hand of death, angor animi, ete. This it is which constitutes the special feature in a majority of the cases of true angina. CLASSIFICATION OF THE Forms or Anctna Prcroris.—It may seem a refinement to subdivide and sort cases of a disorder 2 10 ANGINA PECTORIS AND ALLIED STATES. which is acknowledged to be only a symptom, or, as it has been expressed, a neurosal incident of cardio-vascular disease; but there are practical advantages which far outweigh any theo- retical objections—advantages of the very greatest moment in prognosis and in treatment. Following the work of Heberden, Parry, and others, there were cases reported as angina which did not belong properly to that category, and the disorder was confounded with cardiac asthma, which we now term cardiac dyspnoea. As early as 1812 J. Latham read a paper on certain symptoms usually but not always denoting angina pectoris (Medical Transactions, Royal College of Physicians). He remarks that when the ex- tremities are cold, the countenance is bluish or purplish, the pulse is rapid, and respiration is performed with difficulty and in an upright position of the body, the practitioner has usually concluded that the disease is angina pectoris. The class of cases which he described were evidently orthopnoea and car- diac dyspnoea, associated chiefly with affections of the abdo- men. THe calls the state angina notha, spurious angina, the first time, so far as I am aware, that the term was used in literature. Laennec recognized different degrees of intensity in an- gina, stating that it was “ far from possessing the degree of severity attributed to it by many authors,” and was evidently aware that it occurred commonly enough without indicating any serious disease of the heart or large vessels. “ Angina pectoris, in a slight or middling degree, is extremely common, and exists very frequently in persons who have no organic affection of the heart or large vessels.” * By far the most important contribution to the recognition of varieties of angina pectoris was made by Walshe, who, in ee * Forbes’s edition of Laennee, fourth edition, p. 650. pe FORMS OF ANGINA PECTORIS, 11 his text-book on Diseases of the Heart, described a pseudo- angina pectoris, occurring particularly in women, and in the subjects of hysteria, spinal irritation, and various forms of neuralgia. The recognition by Beau, Graves, Stokes, and others of the relation between the abuse of tobacco and attacks of angina led to the separation of the important group of toxic cases. Other forms of pseudo-angina which are described are those depend- ent upon reflex causes, and the vaso-motor type of Nothnagel. In any long series, the cases of angina fall into two groups: those in which there are signs of lesion of the heart or arteries, or of both, and those in which all symptoms of organic disease are absent. This was the important division recognized by Forbes into organic and functional angina—the angina pec- toris vera and the angina pectoris notha—the true and the pseudo-angina. In looking over the cases which form the basis of these lec- tures, I find that they fall into the following groups: (1) An- gina pectoris vera, and (2) angina pectoris notha, under which are grouped hysterical, vasomotor, and toxic forms. Tue Coronary Arrerres.—A few essential points in the anatomy and physiology of the heart may here engage our at- tention for a few minutes. The coronary arteries are the Abana and Pharpar of the vascular rivers, “lucid streams,” which water the very citadel of life. By means of these in- jected specimens, which I pass around, you may refresh your memories on their distribution. The arteries are, as you see, large in proportion to the size of the organ to be nourished. From the position of their origin it is evident that they must be subject to blood pressure during both systole and diastole. The left coronary is usually the larger, and divides into two main branches: the circumflex or posterior, which runs in the groove between the left ventricle and auricle, and the anterior 12 ANGINA PECTORIS AND ALLIED STATES, or descending ramus. Note particularly the branches of the latter vessel, which runs in the anterior interventricular groove. You will see a very large branch, which is given off to the anterior wall of the left ventricle, and several branches which pass deeply into the septum. This anterior branch is the important one in the morbid anatomy of the coronary arteries, since it is by far the most frequently found the seat of extensive sclerosis or of embolism or thrombosis. It may be called the artery of sudden death. From the date of Sir John Eric Erichsen’s observations on the subject (1842) to the present the effects of closure of the coronary arteries have been much discussed. A very good his- torical summary is given by W. T. Porter in the Journal of Physiology, vol xv, 1893. Tt is remarkable how discordant are the statements of different observers. As this author remarks, seldom have the results of physiological studies been more at variance; there is no statement which is not denied, no fact which is not disputed. More recently Porter has again gone over the whole question with a great deal of skill, and I will give you here some of his conclusions.* The frequency of the stoppage of the heart’s action is in proportion to the size of the artery tied. Ligation of the small- est artery, the arteria septi, does not cause arrest; of the next in size, the coronaria dextra, fourteen per cent. of the ligations were followed by arrest; then comes the larger descendens with twenty-eight per cent. ; and, finally, the circumflex, the largest artery of all, with sixty-four per cent. The effect of closure of the coronary arteries on the blood pressure within the heart is of great importance. After the tying of a single vessel there is a diastolic rise of pressure, which is not compensated for by any increase of pressure in ee * Journal of Experimental Medicine, vol. i, No. 1, 1896. THE CORONARY ARTERIES. 18 the coronary arteries; on the contrary, in them the pressure is falling, while that in the auricles is rising. It is known that the normal mean pressure in the auricles, and consequently in the coronary veins near their mouths, is very low. A rise of a few millimetres of auricular pressure might interrupt the entire coronary circulation. This is one of the most impor- tant points brought out by Porter’s researches, and I quote here a paragraph on this point: “It must be acknowledged, then, that a rising auricular pressure after ligation may at length put a stop to the whole blood supply of the cardiac mus- cle, and, as this rise is often occasioned by the closure of a single vessel, it is plain that the entire coronary circulation can, in fact, be interrupted by the ligation of one coronary artery.” It has been much debated whether the coronary arteries are really terminal or end arteries. Anatomically, it may be shown that they are not, since an injection liquid can be made to pass from one artery through communicating branches into the other. All are agreed, however, that the anastomosis is not sufficient to permit collateral circulation to keep a vascular area alive after the distributing artery is blocked. The effect of plugging of the artery is the production of what is known as an anzmic infarct, a well-recognized pathological condition, the consideration of which need not detain us. A very impor- tant matter relates to the effect of plugging of the coronary arteries upon the heart-beat; the contractions become of the type known as fibrillary, and it is difficult or impossible to get the organ to resume the ordinary co-ordinated beats, though experimentally this has been done, even after fibrillary con- traction has been established. The relation of coronary-artery disease to angina pectoris, which was suggested by Jenner, has directed the very particu- lar attention of writers to the changes in these vessels. It does 14 ANGINA PECTORIS AND ALLIED STATES, one good to look over the older literature, and to note the ac- curacy with which some of the cases have been recorded, par- ticularly by Morgagni. Parry, too, gives an interesting series from the older writers. The subject is so extensive that I can not enter upon it here in great detail, but I may, perhaps, bring it before you with sufficient emphasis if I speak of the common sequences in connection with illustrative cases. The coronary arteries are very subject to degenerative changes, particularly in persons who have passed the middle period of life. They may be affected alone or as part of a wide- spread disease of the vessels. For practical purposes we need not consider any other change than arterio-sclerosis in its vari- ous grades, from a trifling thickening to atheroma and rigid calcification. We must, however, recognize an affection of the orifices of the arteries, apart from the common degeneration of the trunks. A gradual narrowing of the orifice of a vessel may be quite as serious as extensive disease of the branches. There is a form of aortitis met with not infrequently in men between the ages of thirty and forty, who have had syphilis and who have worked hard and drank deep (devotees of Venus, Bacchus, and Vulean), in which the intima is swollen, almost corrugated, with fresh translucent areas of endarteritis. T skip all considerations of its anatomy. Three serious se- quences may follow: (4) Rupture of the aorta, sometimes only of the intima, as clean cut as with a razor, in half or a third of the circumference, sometimes with the formation of a dissecting aneurysm; (0) the slow development of the ordi- nary form of aneurysm of the arch; and (¢) narrowing of the orifices of the coronary arteries. Angina attacks, sudden death, and slowly developing myocarditis and its sequences are the possibilities in this third category. I pass around this fine plate of Corrigan’s, taken from the Dublin Journal, in which you see great swelling of the intima above the valves, due, as THE CORONARY ARTERIES, 15 Corrigan expressed it, “ to an effusion of organized lymph be- tween the lining membrane and the fibrous coat.” The pa- tient in this case, a man only thirty-nine years of age, suffered with severe attacks of angina. Let me illustrate by these specimens some of the more com- mon pathological conditions associated with disease of the branches of the artery. Here is an extraordinary heart, which illustrates how much of the coronary circulation can be cut off if the obstruction takes place gradually. The organ was taken from a man aged about thirty-six or thirty-seven, who had been an inmate for eighteen years of the Institution for Feeble-minded Children at Elwyn, Pa. He was a large, powerful imbecile, dumb but not deaf. THe was very good tempered, did a great deal of work about the farm, and fre- quently did very heavy lifting. He never had epilepsy; he was not known to be short of breath, nor had he complained or indicated in any way that he was out of health. One afternoon he had a sort of fit, the face became very much con- gested, and he died in about half an hour. There was nothing special found in the brain. The heart, as you see, is large, and weighed twenty ounces. There was general hypertrophy with dilatation. There was quite extensive fibroid myocarditis, particularly in the anterior wall of the left ventricle, at the apex, and in the lower portion of the septum ventriculorum; the valves were normal. But what I wish you to examine most particularly is the state of the coronary arteries, which are freely dissected out. The left vessel is almost obliterated, only a pin-point channel remaining, while of the right artery the main division passing between the auricle and ventricle is converted into a fibroid cord! Tt is much more common to find one artery extensively dis- eased, or even completely obliterated. Take, for example, this specimen, which was removed from a colored man, aged about 16 ANGINA PECTORIS AND ALLIED STATES. thirty-five, who had aortic insufficiency, with dyspnoea and cedema of the legs. He died suddenly, though he had for some weeks great dilatation of the heart and general anasarca. The aortic segments are curled and thickened, the ascending arch is greatly deformed, with a recent general endarteritis. There are a few calcareous plates. The right coronary artery is completely obliterated. There is no opening whatever on the aorta. The left vessel is dilated, and presents atheroma- tous patches. There are areas of fibrous myocarditis in the left ventricle, but in other respects the muscular substance of the heart does not look abnormal, and it is not fatty. Here is a much more common condition. In this anterior coronary artery you see a firmly adherent thrombus, which completely occludes the descending branch, to the lumen of which it is firmly attached. It was taken from a man about fifty years of age, who had mitral-valve disease and had a good deal of cardiac dyspnoea. Early one morning he was seized with severe pain about the heart and shortness of breath, and died in a very few moments. Both coronary arteries were thickened and calcified, and presented atheromatous plates, but no doubt the sudden death was due to the blocking of the anterior branch of the left coronary artery by the thrombus. When the occlusion has persisted for any length of time before death the condition of anzemic necrosis may be found. I am sorry not to have a fresh specimen to show you, but most of you have, no doubt, seen microscopic, if not macroscopic, examples. It is important in the dissection of the heart to slice carefully the septum and the wall, as these infarcts of the heart muscle are found in numbers directly proportionate to the care with which they are sought. We have not had any very large number of cases. They are much more common, I think, in hospitals with old chronic cases, or with which there are in connection large almshouses, as at the Blockley Hospi- THE CORONARY ARTERIES, 17 tal. I was much impressed at that institution with the num- ber of cases of anemic infarcts—many more than I saw at the Montreal General Hospital or have seen here. They occur most frequently in the walls of the left ventricle and in the septum, particularly toward the apex. When fresh they stand out beyond the level of the surrounding muscle, and are sometimes very firm, yellowish white, or even quite opaque white in color. With the fresh infarcts there may be old fibroid patches, into which ultimately these areas of anemic necrosis are transformed. To complete the series, I show you here sections of the de- scending branch of the left coronary artery, which you see is almost completely obliterated by an old, much-altered throm- bus. This case illustrates another sequence of slowly develop- ing coronary artery disease—namely, fibroid myocarditis at the apex, with weakening of the wall, and the gradual forma- tion of aneurysm of the heart. The specimen was taken from the body of a large, powerfully built man whose heart symp- toms developed with great abruptness, and who presented for many months an obscure train of symptoms pointing to serious disease of the myocardium. Autopsies on cases of angina pectoris are not common. The man with a fresh thrombus in the anterior branch of the left coronary artery probably died in a paroxysm of angina, but he had not had previous typical attacks. As I will tell you later on, the affection is rare in hospital practice so that we do not have opportunities of making the inspection of the bodies of persons who have died of the disease. And, lastly, a few words on the tnnervation of the heart, a cardinal point, inasmuch as the very essence of the angina par- oxysm must rest on some profound disturbance in the function of the nerves. The newer methods of investigation have added considerably to our knowledge of the distribution of the in- 18 ANGINA PECTORIS AND ALLIED STATES. trinsic nerves of the organ. Doubtless some of you have seen in the pathological laboratory Dr. Berkeley’s wonderful speci- mens illustrating the ultimate terminations of the filaments between and on the fibres.* In looking at them one realizes the truth of the remark of a recent author, that it is difficult to say in which the myocardium is richer, nerve elements or muscle fibres. Everywhere throughout the organ—in the tis- sues beneath the endocardium and pericardium, throughout the muscle substance, and about the blood-vessels—the nerves are in extraordinary profusion. The double nerve supply you know, from vagus and sympathetic, and the double function, the former controlling, checking, and inhibiting, the latter augmenting the force and hastening the frequency of the heart-beats. The researches of His junior and Romberg have shown that the ganglion cells of the heart, even those lying in the vagus branches, have the same origin as all other sympa- thetic cells. They differ in protoplasmic appearances and in other ways from the cells of the spinal ganglia. The rhythmic action of the heart is probably automatic, due to a power in- herent in the muscular fibres, though this point is still in dis- pute. Of the functions of the nerves we know a good deal, of the functions of the ganglia nothing. His and Romberg sug- gest that from them are transmitted to the central nervous sys- tem infinitely delicately graded, unconscious impulses, which regulate the circulation reflexly through the vagus and accel- erator. Of Kronecker’s co-ordination centre our knowledge is still very indefinite—indeed, its existence has been called in question. I have seen Kronecker perform the experiment, and certainly when the point in the dog’s heart is pricked—it is situated about the lower limit of the upper third of the ven- tricular septum—the organ becomes paralyzed in a state of fibrillary tremor, from which it does not recover. This point * Described in Johns Hopkins Hospital Reports, vol, iv, THE CORONARY ARTERIES, 19 is within the area of distribution of the anterior coronary artery, the vessel oftenest found plugged by thrombus or em- bolus in cases of sudden death. Do these cardiac nerves possess other properties? Have they also, with the special function, the endowment of receiv- ing tactile and painful impressions? Certainly the heart is not an organ of very acute sensibility. The most extensive lesions, inflammatory, degenerative, and neoplastic, may not excite a single painful sensation. Pericarditis of the most intense grade, with deep involvement of the myocardium, may give not the slightest indication of its existence. In experimental work, pinching of the heart muscle may excite reflex movements of the muscles of the body. There are a few interesting cases in the human subject in which the heart has been exposed by accident sufficiently to enable it to be grasped or touched. In the well-known. case which Harvey gives * of the young Viscount de Montgomery, in whom Charles I was so much interested, in consequence of a fracture of the ribs on the left side, with excessive suppuration, the heart was exposed, and from Harvey’s account was quite insen- sitive: ‘“ Nempe, in homine vivente et vegeto, citra ullam offensam, cor sese vibrans, ventriculosque ejus pulsantes vi- deret, as manu tangeret. Factumque est, ut serenissimus Rex, una mecum, cor sensu tactus privatum esse agnosceret. Quippe adolescens, nos ipsum tangere (nisi visu, aut cutis ex- terioris sensatione) neutiquam intelligebat.” There is one other point of great importance. Sensory- nerve endings have been demonstrated in the arteries by Thoma, and recently Smirnow + professes to have demon- strated similar structures in the connective tissues of the heart, he thinks the sensory-nerve beginnings of the depressor nerve. * Huercitationes de generatione animalium, 1651, p. 311. + Anatomischer Anzerger, 1895, LECTURE II. ANGINA PECTORIS VERA. ZTIOLOGY. GENERAL DESCRIPTION OF THE DISEASE. Incidence of the disease.—Station in life-—Sex.—A ge.—Epidemic influences. —Heredity.—Gout.—Diabetes.—Syphilis—Specifie fevers.—Heart dis- ease.—-Locomotor ataxia.—General picture of the disease. Incrpence oF THE Diszase.—As noted long ago by Sir Gilbert Blaine, angina pectoris is a rare affection in hospital practice. Gairdner criticises this statement rather sharply, and yet I think that a majority of hospital physicians would be found to support it. During the ten years in which I lived in Montreal, I did not see a case of the disease either in private practice or at the Montreal General Hospital. At Blockley (Philadelphia Hospital), too, it was an exceedingly rare affec- tion. I do not remember to have had a case under my per- sonal care. There were two cases in my service at the Univer- sity Hospital. During the seven years in which the Johns Hopkins Hospital has been opened, with an unusually large “ material” in diseases of the heart and arteries, and with many cases of heart pain of various sorts, there have been only four instances of angina pectoris. You will find the statement in Fagge’s Practice (third edition, vol. ii, p. 26) that “the writer has never seen classical angina in hospital practice.” On the other hand, an individual consultant may see within a year more cases than occur in all the hospitals of his town 20 ANGINA PECTORIS VERA. 21 within the same period. In corroboration of this striking con- trast between the incidence of angina pectoris in hospital and consulting work I may refer to the statistics of the Edinburgh Royal Infirmary, in which for the two years covered by the Hospital Reports, 1893 and 1894, there were five cases among a total of 8,868 medical cases. Compare with this the personal experience of the distinguished Edinburgh consultant, Dr. Balfour, who, in his recently issued work on The Senile Heart, gives an analysis of ninety-eight cases of angina pectoris seen within ten years. My individual experience embraces a series of sixty cases, forty of which may be regarded as true an- gina. The predisposing causes of angina pectoris vera are those of arteriosclerosis; that is to say, so intimately associated is the true paroxysm with sclerotic conditions of the coronary ar- teries that it is extremely rare apart from them. Men of mus- cular, even. athletic build, who have been devotees of Bacchus and of Venus, form perhaps the largest contingent. Gout, syphilis, and hereditary influence the causation only so far as they tend to cause sclerotic changes in the arteries; but it would be altogether too narrow a view to suppose that the setiology of the disease is identical with that of arterio-sclero- sis, The one is so common and the other comparatively rare even among the individuals most prone to sclerosis, that there must be a third element, an indefinite something, which yet escapes our knowledge, but which is the essential factor in the production of this terrible affliction. Sratron in Lire.—As Sir John Forbes remarks, it is an at- tendant rather of ease and luxury than of temperance and labor; on which account, though occurring among the poor, it is more frequently met with among the rich, or in persons of easy circumstances. It is remarkable how many prominent individuals have succumbed to the disease. We may say of it 22 ANGINA PECTORIS AND ALLIED STATES, as Sydenham did of the gout, that more wise men than fools are its victims. I do not know that any special occupation or profession predisposes to it, but the frequency with which physicians are attacked has been commented upon by several writers. In my list of sixty cases of all forms, there were thirteen medical men, eight of whom had true angina. This percentage is doubtless exceptional, and due, in part at least, to my nomadic habits, and wide acquaintance in the profession. Sex.—From the earliest description of the disease, the re- markable preponderance of males who are attacked has been noted. Heberden says: “I have seen nearly one hundred people under this disorder, of which number there have been three women” (Commentaries). The statistics collected by Huchard give in two hundred and thirty-seven cases of true angina only forty-two in women. Jn my own series of forty cases of true angina there was only one woman. Acr.—tThe age at which it is most common is that of ar- terio-sclerosis—after the fiftieth year of life. Of the forty cases on my list there were only four under the fortieth year. One of these, a man, aged thirty years, had had syphilis five years before; the other case, a woman, aged thirty-two years, had mitral-valve disease; the third case had terrible attacks of angina following chronic pleurisy. In the fifth decade there were thirteen; in the sixth, thirteen; in the seventh, nine; and of one case I did not get the exact age. The aver- age of the thirty-nine cases was about fifty-three years. Cases are reported in quite young individuals, even in children, but such are almost invariably the subject of chronic valvular dis- ease or of adherent pericardium. Epipemic, Iautative, anp Emorionan InFLUENCES.— Laennec was “ of the opinion that the prevalent type of disease influences its development,” and adds, “ I have some years met ANGINA PECTORIS VERA. 93 with it frequently, and hardly at all in others.” You will find reference in the literature to so-called outbreaks of angina which have been reported by Kleefeld * and by Gelineau.t I can not see that the cases recorded by Kleefeld have anything to do with angina pectoris. He describes the epidemic as a re- mittent fever with gastric complications, and much pain about the heart. Some of the cases were fatal, but no autopsies were made. Young persons, chiefly women and children, were attacked. Gelineau, surgeon to the French corvette L’Embuscade, reports a remarkable outbreak among the sailors during a pro- longed cruise in the Pacific. Scurvy had broken out and the men were much debilitated and anemic. They became sub- ject also to a severe dry colic. Following this there were many cases of angina. The first case was that of an old sailor, scor- butic and anemic, who while climbing the mast was seized with intense pain about the heart. Five days after, five other men were attacked in the same sudden way, and three days later, three more. Gelineau lays a good deal of stress upon tobacco as a factor in the causation of the pain, and also upon the debility following the scurvy, dysentery, and dry colic. The effect of imitation, that extraordinary occult influence so potent in many forms of hysteria, must, no doubt, be taken “into account. Perhaps the most notable instance is given by Dr. Taber Johnson in his report of Mr. Sumner’s case.* “T have observed a curious fact, which it may be interesting to refer to here. J mean the unusual number of patients suffer- ing from this disease, who, previous to Mr. Sumner’s severe illness, had never supposed that they had any disease of the heart. This fact has been referred to by newspaper corre- * Journal d. pract. Heilkunde, 1828, lvii. + Gazette des Hopitaux, 1862, xxxv. ¢ Boston Medical and Surgical Journal, 1874, 94 ANGINA PECTORIS AND ALLIED STATES. spondents—viz., that during the illness of Mr. Sumner, and especially since his death, instances of its occurrence have considerably increased, and especially among those who strongly sympathized with the late senator. This seemingly sympathetic cause of disease has been noticed in other cases. T have been consulted by as many as thirty individuals, since Mr. Sumner’s death, who imagined they were afflicted with his complaint. In some of these cases there was organic dis- ease of the heart, but in a majority of them there was no cardiac trouble at all. Two weeks after the autopsy in Mr. Sumner’s case, one of the physicians who assisted, a devot- edly attached friend of the deceased, died of angina pectoris. Tam informed that Dr. Hitchcock had but a few attacks, and that, prior to Mr. Sumner’s death, he had never been a suf- ferer from angina pectoris.” Dr. Johnson says that he himself suffered from two attacks very closely resembling, if they were not really, angina. One of these oceurred immediately after Mr. Sumner’s death, and Brown-Séquard, who was present, said the phenomena were undoubtedly those of a paroxysm of angina. Twenty-two years have passed, and, happily for himself, as well as for our brethren of the District of Columbia, Dr. Taber Johnson has now less mobile nerves. Tn Case X of my series of pseudo-angina the patient’s hus- band died suddenly in a paroxysm of true angina. Mental worry, severe grief, or a sudden shock may precede directly the onset of the attacks. In Case XXXVI, the parox- ysms came on after the shock of the announcement that a son had committed suicide. Hereprry.—True angina pectoris is an arterial incident, and since the members of certain families show a special tend- ency to arterial degeneration, it is not surprising to find cases in father and son, or in brothers, or even in representatives of ANGINA PECTORIS VERA. o5 three generations. There are remarkable instances on record. The first, and one of the most remarkable, is that reported by Dr. Robert Hamilton,* in which the father of the patient, a young man aged twenty-four, two brothers, and one sister were affected. In all, the disease developed in early life; in Hamilton’s own patient, at the twelfth year. It is quite pos- sible from his description that the disease may not have been angina pectoris, but spasmodic asthma associated with heart pain. The best-known instance is that of the Arnold family. Wil- liam Arnold, collector of customs of Cowes, died suddenly of spasm of the heart in 1801. His son, the celebrated Thomas Arnold, of Rugby, whose case J will narrate to you shortly, died in his first attack. Matthew Arnold, his distinguished son, was a victim of the disease for several years, and died suddenly in an attack on Sunday, April 15, 1888, having been spared, as he hopes in his little poem called A Wish— “the whispering, crowded room, The friends who come, and gape, and go; The ceremonious air of gloom— All, which makes death a hideous show! ” At the time of his death, the accounts which appeared in the Lancet and British Medical Journal were not clear as to the existence of attacks of angina. The various stages in the progress of his illness can be traced very well in his Zetters,+ in which you will find an account of numerous attacks from May, 1885, until the time of his death. (Note B.) In looking over the literature one finds occasional refer- ences to cases occurring in several members of one family. * Medical Commentaries, 1785, ix. + Letters of Matthew Arnold. Macmillan & Co., 1896. 3 96 ANGINA PECTORIS AND ALLIED STATES, Cazanave de la Roche* records three cases in one family—a sister, who was affected at the time of the report, and two brothers who had died of the disease. In Case XXIII on my list the patient’s father died of angina pectoris. Gout.—The relation of certain constitutional disorders to angina pectoris has been much discussed. The importance of gout as a factor was early suggested, and in this interesting little monograph of Butter’s, which I show you here—the first separate treatise on the disease—the author places the seat of the disorder in the diaphragm, and calls it diaphragmatic gout. The affection has also been termed asthma arthriticum. Nathaniel Chapman advocated strongly the arthritic na- ture of angina pectoris, and there can be no question, I think, that in a certain number of the victims gout plays an impor- tant role in inducing the arterio-sclerosis. I have been particularly interested in examining into this point in the cases which have come under my observation within the past four or five years. There are four cases at least of my series in which gout seemed to play a part. Dr. , of Virginia, seen April 3, 1894, a very robust, vigorous man of forty-eight, temperate, a hard worker, who had not had syphilis, and in whom the attacks were fairly characteristic, thinks that gout (which is in his family) is directly responsible for the attacks. Certainly, after using without benefit for many months the iodides and the nitrites, he obtained the greatest relief from a prolonged course of colchicum. It is now more than two years since I saw him, and he remains well. In another ease, a patient with attacks of angina pectoris sine dolore, there had been attacks of acute articular gout. In a third case, a man aged sixty-four, the upper half of the pinna of the lobe of the right ear was firm and calcified, * La Tribune médicale, 1895, p. 882. ANGINA PECTORIS VERA. OF and the same process was beginning in the left ear. There were no tophi, but the calcification was, to say the least, sug- gestive. A fourth case was that of a physician from North Carolina, aged forty-six, who had for many years attacks of gouty arthritis, chiefly in the big toe, less frequently in the ankles. There was a well-marked tophus in the right ear. Diaznetes.—The association of angina pectoris with dia- betes has been frequently noted. No instance has fallen under my personal observation. You will find the whole sub- ject very thoroughly discussed by Ebstein in a recent paper in the Berliner klinische Wochenschrift of last year (1895). Sypuitis is one of the potent factors in inducing arterio- sclerosis, and thus indirectly plays a réle in angina pectoris. Of the cases in my series, only four gave a history of syphilis. The instances of aortitis to which I have already referred, oc- curring in the third and fourth decades in men who have had syphilis, have worked hard, and have been heavy drinkers, are sometimes associated with severe attacks of angina. In Case I, Lieutenant X., aged thirty years, a robust, powerful man, had had syphilis six years before his visit to me. The secondary symptoms were slight, and he had not had very thorough treat- ment. A year before I saw him he began to have severe pains in the heart, recurring in paroxysms, and associated with pain down the left arm, and dyspnoea on exertion. There was no perceptible enlargement of the heart; there was a systolic murmur at the apex and a soft bruit at the aortic area, with- out special accentuation of the aortic second sound. The at- tacks had been of such severity that he had been off duty for many months. He improved very much upon the iodide of potassium, but still had attacks six months after I saw him, since which time I have not heard of him. Corrigan’s case, you remember, the illustrative plate of which I showed you at the last lecture, was in a young man, and belonged to this 98 ANGINA PECTORIS AND ALLIED STATES. group. The frontispiece in Balfour’s work on the heart (sec- ond edition) illustrates another case of the same kind in a still younger man, aged twenty-four years. The angina attacks were associated with an aortitis which narrowed greatly the orifices of the coronary arteries. Sprorric Frvers.—In connection with the specific fevers several writers have described angina-like attacks. Fraentzel, in his Vorlesungen tiber die Krankheiten des Herzens (Berlin, 1889), describes attacks of angina pectoris in the weakened and dilated heart following the infections, particularly ery- sipelas, typhoid fever, and pneumonia. J. W. Moore * has re- ported two instances of angina symptoms in connection with heart weakness during and after the specific fevers. In the epidemic of a remittent fever reported by Kleefeld (and al- ready referred to) the attacks of heart pain may have been of this character. I do not remember to have seen a case in which the attack developed during convalescence from one of the ordinary fevers. Among the many nervous sequela of influenza, few are more distressing than the attacks of severe cardiac pain. In some cases, indeed, the disease seems to have been the starting point of attacks of true angina. The frequency of the compli- cation in the practices of some physicians is remarkable. In a paper on The Action of Influenza Poison on the Heart, Cur- tin and Watson state that within two years they met with fully seventy cases of painful attacks about the heart. The il- lustrative cases in their paper + show that some of the attacks must have been of very great severity, but, in most instances, the duration of the disease was short and the cases evidently belonged to the category of pseudo-angina. I have seen but * Dublin Medical Journal, 1890, vol. Ixxxix. ¢ International Medical Magazine, January, 1893. ANGINA PECTORIS VERA. 29 two instances in which the attack seemed to follow directly upon the influenza. One is certainly pseudo-angina; the other proved to be the genuine disease. I saw on several occasions in Toronto a medical friend who, after a tolerably severe attack of influenza about three years ago, began to have attacks of agonizing pain about the heart. They came on without warning, the pain appearing in various parts of the chest, commonly under both shoulder blades, and espe- cially severe in both wrists. There was at first no irregularity of the pulse or difficulty in breathing; but in some attacks there were piping rales during expiration. At first these attacks were almost nightly; several times they ended in vomiting (preceded by profuse salivation), the passage of more or less flatus, and copious sweating. There was no mental anxiety whatever, ex- cept, as he expressed it, “the pain was so intense that J was afraid I would recover, in order to endure it again.” The pain in the arms was chiefly in the front of the wrists. The patient had not had any serious illness previously, had never had syphi- lis, had not been a heavy drinker, but had been a pretty heavy smoker. The attacks recurred with intensity throughout the early part of January. When I saw him there were no signs of cardiac disease. He had had a good deal of digestive disturb- ance. During the following summer and autumn he progres- sively improved, and I heard from him recently to the effect that now only in any extra strain, an in the attendance upon a difficult case of labor, does he feel any pain. He used the iodide steadily for some time without any special benefit. He at- tributes more benefit to lavage of the stomach with hot water night and morning. How far the influenza in this case was responsible for the attack is, of course, difficult to say, but when I saw him first he was very insistent that it was the cause of his whole trouble. From the rapid way in which the attacks have ameliorated and his present general condition there is, to say the least, a strong probability that it is functional and not associated with organic disease. The other case was that of the late chief justice of this State, who had, in the early winter of 1893, a very severe attack of 80 ANGINA PECTORIS AND ALLIED STATES, influenza with much fever and prostration. In the latter part of December he began to have pain about the heart in walking briskly up a hill. Then he had more severe attacks, but in the summer of 1894 he was better, and was able to take long walks. The attacks recurred about Christmas, 1894. I saw him on January 20, 1895. There was no enlargement of the heart, the sounds were clear, the second aortic a little accentuated. The only striking anomaly was a condition of trigeminal heart- beats—groups of three beats, with an interval, followed in regu- lar sequence. He improved very much through the summer of 1895. In October he had a severe shock on hearing of the sudden death from angina of his brother-in-law (Case XXXV on my list). He did not, however, have any recurrence until December. I saw him on January 5, 1896. The paroxysms had become more frequent and very severe. In the following week he died in an unusually prolonged attack. The onset of the angina corresponded with the period of convalescence from the influenza, which he always insisted had caused the attacks. Heart Disrasz.—Paroxysms of agonizing substernal pain, with radiation to the neck and arm, are rare in the ordi- nary forms of heart disease which we meet with in hospital work. Heart pain is common enough, and if we counted all such cases as angina we would not have to lay stress on the in- frequence of this syndrome in the wards. You remember the small boy in Ward F during the early part of this session, with greatly enlarged heart, probably from pericardial adhesions. Pain was the most distressing symptom of the case, but it had neither the intensity, the paroxysmal character, nor the ac- companiments which warrant the diagnosis of true angina. So, too, in the case of the old colored woman, at present in Ward O, with mitral-valve disease and extreme arterio-sclero- sis. I have pointed out to you that the attacks of sudden breathlessness and distress with transient pain, are of the na- ture of cardiac asthma, with which, as I will tell you later, angina pectoris is often confounded. Then, again, you have ANGINA PECTORIS VERA. 31 to bear in mind the common complaint of pain beneath the left breast in patients with chlorosis and various forms of anemia. Of valvular affections, aortic insufficiency is that with which angina pectoris is most frequently associated. Of the forty cases in my list three presented signs of this lesion. The subjects of the degenerative type of the disease, which de- velops in men after the fortieth year, are much more prone to angina than those in whom the insufficiency has followed en- docarditis. The younger the subject, the greater the proba- bility that the incompetency results from an acute aortitis, _as in Corrigan’s case, to which I have referred on several ocea- sions. Angina pectoris is excessively rare in mitral-valve disease. This is well illustrated by Nothnagel’s experience.* Of fifteen hundred cases of valvular disease of the heart seen in hospital and private practice, very many of which had symptoms of an- gina, there was but a single case in which the syndrome oc- curred in connection with mitral stenosis. Only one of my cases, a woman, had a mitral lesion. By far the most common heart disease with which angina is associated is chronic myo- carditis, the signs of which are often dubious. Cases of adherent pericardium and of aneurysm of the aortic arch may present the features of typical angina, more often, in my experience, of constant substernal pain or of cervico-brachial neuralgia. A majority of the subjects of angina present the signs of arterio-sclerosis, with accentuation of the aortic second sound and slight increase in the area of transverse heart dullness. Some of the most rapidly fatal cases are those in which the physical signs are very slight, or even absent. Of the cases on * Verhandlungen des Congresses f. innere Medicin, Bd. x. 82 ANGINA PECTORIS AND ALLIED STATES, my list, in four only was the physical examination negative; three presented apical or basic murmurs; of the remainder, all of whom showed signs of sclerosis of the arteries, nine had indications of myocardial changes. Locomotor Araxra.—Considering the close relationship of syphilis to this disease, in which also arterio-sclerosis is so common, it is not surprising that attacks of angina pectoris should oceur. No instance has fallen under my personal ob- servation. You know that aortic insufficiency is not rare in tabes. At Blockley the association was a matter of every-day comment, and in the physical-diagnosis class we would send to the out wards for the old tabetics to demonstrate the lesions of arterio-sclerosis, and if not of aortic incompetency, of the ring- ing metallic aortic second sound, which so often accompanied the dilated and rigid aortic arch. You will find the subject fully discussed by Leyden in the Zettschrift f. klin. Medicin for 1887, and since his paper there have been several less im- portant communications. Genera Picture or tHE Disease.—In any long series of cases of angina we can recognize four groups: I. Sudden Death, without other Manifestations of Angina Pectoris.—Much more true of angina pectoris is what Andral said of the fulminant form of cholera: it begins where other diseases end—in death. The affection has indeed been called by Sir Walter Foster a mode of death, which reminds one of the expression of the physicians who spoke of Seneca’s malady as a meditatio mortis. No inconsiderable proportion of sudden deaths in men of middle age and robust habits result from coronary-artery disease, from the rapid culmination, so to speak, of a condition which, in another (or on previous occa- sions in the individual himself), would have caused an ordi- nary attack of angina. Before all is over there may be a mo- mentary conscious agony expressed by a cry, but in other in- ANGINA PECTORIS VERA. 383 stances (and this is most frequently the case in the subjects of angina) the death is literally instantaneous; more rapid, per- haps, than that which occurs by any other mode. Of the fifteen deaths in my series, eight took place sudden- ly; in five, gradually by cardiac asystole; in one, I did not learn the exact mode of death; in another, the patient died of obstruction of the bowels. Of the eight cases, in five death was sudden, almost without warning, and not in a paroxysm — of angina. Mr. S. (Case XX VI) died on his doorstep; Mr. W. (Case XX VII) died as he was leaving a friend’s house; Dr. X. (Case VIII) died as he was walking from one room to another. He had had cardiac arrhythmia, Cheyne-Stokes breathing, and marked mental disturbance; Mr. E. (Case XXXV) died in- stantly on the edge of the bed as he was recovering from his first attack of angina, not having had pains for nearly twenty- four hours; Mr. R. (Case XI) fell over dead on attempting to get out of bed. The literature abounds in cases of this sort, and the proportion of the victims of angina who die abruptly is much larger than my figures indicate. Forbes mentions that of sixty-four cases sudden death occurred in forty-nine. Anatomically it has been shown that lesion of the coronary arteries is almost invariably present—either extensive arterio- sclerosis, embolism, thrombosis, or in rare instances the burst- ing of a small atheromatous abscess in one vessel, such as killed the celebrated sculptor Thorwaldsen.* An explanation of the awful suddenness—“ Life struck sharp on Death ”—is prob- ably to be found in the arrest of the heart in fibrillary con- traction, such as takes place experimentally in animals after ligation of a coronary vessel. Il. Death in the First Well-marked Paroxysm.—A man * Virchow’s Archiv, Bd. xxv. 84 ANGINA PECTORIS AND ALLIED STATES. in full health, in the prime of life, may be seized with a parox- ysm of angina, and die within a few hours. The cases in this category are not numerous. Perhaps the most remarkable one on record, which has become quite historic, is that of the cele- brated Dr. Arnold, of Rugby, who in the words of his distin- guished gon (also a victim of the disease), arose “ ... to tread In the summer morning, the road Of death, at a call unforeseen, Sudden.” The following is Latham’s account: * “