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·ANGINA PECTORIS

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·SCRIPT OF
ANGINA PECTORIS
A MOTION PICTURE
WPITTEN AND DIRECTED
BY
JOSEPH E F RISEMAN, BS., MD
Asrociato in Medicina Harvard Medical School Instructor in Medicine, Tufts Med cal
School Assoelale In Medical Research and Associale Visiting Physician
Bath Israel Hospital, Boston
PHOTOGRAPHED BY
THE HARVARD FILM SERVICE
HARVARD UNIVERSITY
A PRODUCTION OF THE
BETH ISRAEL HOSPITAL
EOSTOS NASS
LEED BY A GRANT FRO"!
BREWER AND COMPANY, INC
WORCESTER LASS

·COPYRIGHT 1943 BY
I E F. RISEMAN, BS, MD
(ALL RIGHTS RESERVED)
FIRST LIMITED EDITION
PUBLISHED SEPT 1943
PRINTED IN THE
UNITED STATES OF AMERICA

·FOREWORD The motion picture Angina Pectors and this booklet are intend. ed to present, in easily absorbable form, a Clinic on Angina Pectons The importance of the clinic method of presenting medical information is of recognized value, but the difficulties of assembling patients and material limits its use Motion pictures correct some of the difficulties associated with "Dry Chirucs,", and they have become a valuable method of disseminating medical knowledge Since a motion picture is portable, it makes a Clinic available to any one, anywhere, any time, it eliminates the difficulties and dangers of assembling patients on time for each presentation, it makes it possible to demonstrate a wealth of material collected, if necessary, from all parts of the globe, furthermore, errors, excess words, illegible charts, etc., can be eliminated in the cutting room As a result the motion picture method of presenting data is not only interesung but it makes it possible for the observer to absorb a considerable amount of knowledge with a minimum amount ol concentration, effort and reading The finished product may result, nowever, in such a wealth of material being presented in so short a penod of time that the observer is unable to absorb it at one sitting and must either see the picture again or have a means of referring to selected portions of it at his leisure This illustrated booklet was prepared to supply this need It is hoped that the booklet, combined with the motion picture, will aid the student in obtaining a sound understanding of the important facts about Angina Pectors and will serve as a useful review to those physicians whose busy lives make it impossible for them to read all the publications necessary to obtain this data The aspects presented are based pnmarily on work done at the Beth Israel Hospital of Boston They represent not theories or animal experiments but facts demonstrable by objective studies in patients with angina pectons I wish to acknowledge the valuable assistance of the following who worked without thought of time or remunerauon Dr Ellot L Sagall who helped in the preparation of the sets, Ms James Brewster ol the Harvard Film Service for his technical skill and wise counsel, Bliss Isabelle Len for her assistance in preparing the script, and Mr Howard D Brewer, president of Brewer & Company, Inc, for his interest in medical research and teaching and whose generous grant made thus presentaron possible IOSEPH E F. RISEMAN, MD Boston, Mass

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·CONTENTS Page LIST OF ILLUSTRATIONS ..... 13-17 PART 1 CLINICAL CHARACTERISTICS OF ANGINA PECTORIS 9. 23 The Standardized Exercise Tolerance Test 24 Color Plates ... 6. 25 The Typical Attack of Angina Pectoris 27 Frequency, Physical Build, Age at Onset 28 Blood Pressure. Electrocardiogram, Heart Size 29 Electrocardiogram During Attacks of Angina Pectoris 30 Diagnoshc Criteria of Angina Pectons 32 PART 2 PHYSIOLOGY OF ANGINA PECTORIS Studies on Narrowed or Occluded Artenes 35 36 Studies with Induced Anoxia 37 Theory of Referred Pain and Angina Pectons 38 Chnical Conditions Associated with Angina Pectoris 39 Physiology of Angina Pectoris-Summary Color Plates 40 .. 41 11 ·CONTENTS Page PART 3 PATHOLOGY OF ANGINA PECTORIS ...........4.4 45 Technique-Injection of the Heart 16 Color Plates 48-49 51 52 Technique-Opening the Heart Technique Concluded Characteristic Pathological Patterns Characteristic Pathological Patterns-Summary Color Plates 53 54 55 PART 4 59 60 61 63 64 TREATMENT OF ANGINA PECTORIS Criteria Used to Evaluate Therapy Color Plates Therapeutic Response of Individual Patients Nitroglycerin and other Nitrites Control Studies—Enteric Coatings Value of Theobromine Sodium Acetate Quinidine Sulfate Sedatives and Analgesics Atropine 65 66 67 68 70 Color Plates 72-73 Enteric Coated Potassium Iodide 75 76 76 77 Digitalis Surgery--Frequency of Operation Paravertebral Injection- Thyroid Denervation Total Thyroidectomy Plan for Treatment of Angina pectoris Treatinent-Summary 78 79 80 12 ·LIST OF ILLUSTRATIONS PART 1-CLINICAL CHARACTERISTICS OF ANGINA PECTORIS . Page Color Plate 1 Patient B. K.. 25 Color Plate 2 Patient BK During attack of Angina Pectors (unusually severe or "textbook" type) 25 Color Plate 3 Distribution of Pan in Angina 25 Color Plate 4 Clinical criteria diagnostic of Angina Pectoris 25 Color Plate 5 Excerpts from electrocardiographic tracing taken continuously during exercise, before, dunng and after precipitation of Angina Pectoris 25 Color Plate 6 Electrocardiogram of normal subject before and immediately alter exercise 25 . .. be Figure 1 Patient R S during attack of Angina Pectoris (usual response to attack) 23 Figure 2 The two step staircase in the cold room 24 Figure 3 Factors responsible for the variation in ability of patients with angina pectoris to exercise without inducing pain 24 Figure 4 The conditions ol the Standardized Exercise Tolerance Test 27 Figure 5 The sex distnbution of - 28 Figure 6 The physical build of 28 Figure 7 The age distributionc 28 Figure 8 The frequency of hypertension (blood pressure of 160/100 or greater) 29 Figure 9 The frequency of evidence of coronary artery disease the electrocardiograms of patients with Angina pectoris 29 Figure 10 The frequency of cardiac enlargement in patients with Angina pectoris 29 Figure 11 The frequency of pabents without hypertension, abnormal electrocardiograms or cardiac enlargement Figure 12 30 Method of measuring the heart rate and the blood pressure during exercise Figure 13 Method of recording electrocardiograns during 30 exerase Figure 14 Method of oblaining electrocardiograms during in- 30 duced generalized anoxemia 31 in . .. 4.. --04 ... 13 ·LIST OF ILLUSTRATIONS PART 2-PHYSIOLOGY OF ANGINA PECTORIS Page 44... Color Plate 7 Electrocardiograms in clinical and experimental coronary occlusion 41 Color Plate 8 Similarity of electrocardiograms in exercise and anoxia 41 Color Plate 9 Nerve supply to regions involved by the pain of Angina Pectoris 41 Color Plate 10 Diagramatic representation of nerve supply to heart 41 Vagus nerve (Yellow) Cardiac sympathetic nerves (Blue) Thoracic sympathetic nerves (White) Color Plate 11 Diagramatic representation of routes involved (red) in transmission of pain sensation from heart 41 Color Plate 12 Schematic representation of discrepancy between the Demand and the Supply of blood during exercise in patients with Angina pectoris 41 Figure 15 Figure 16 Figure 17 Figure 18 Figure 19 Figure 20 Figure 21 Figure 22 Apparatus used in producing anoxemia in the muscles of the forearm 35 Patient J M with angina pectoris and intermittent claudication on exertion 35 Examination of peripheral circulation in patient I M 36 Sutton and Lueth operation for experimental coronary constriction 36 Apparatus used to induce generalized anoxemia by re-breathing 37 Apparatus used for exercise with oxygen 37 Dissection of cardiac nerves 38 Schematic representation of balance between Supply and Demand with the normal subject at rest 39 Schematic representation of local (cardiac) oxygen debt of normal subject during exercise 40 "The steady state" after several minutes of exercise when the supply of blood equals the immediate needs 40 Recovery from exercise—The supply of blood is greater than the demands until the oxygen debt is cancelled 40 Figure 23 Figure 24 Figure 25 14 ·LIST OF ILLUSTRATIONS PART 3-PATHOLOGY OF ANGINA PECTORIS 4 FEVE . . Page Color Plate 13 Parry's book, title page Color Plate 14 Ag's heart with aorta, pulmonary artery and auncles removed to show the mouths of the 48 coronary arteries ........ Color Plate 15 The cannulae ted into the nght (red) and left (blue) coronary arteries 48 Color Plate 16 Apparatus used in injecting heart by method of Schlesinger 48 Color Plate 17 Steps in preparation of injection mass 48 Color Plate 18 Washing coronary arteries with saline 48 Color Plate 19 Simultaneous injection of night and left coronary arteries 49 Calor Plate 20 The first incision 49 Color Plate 21 The second incision 49 Calor Plate 22 The third incision 49 Color Plate 23 The fourth incision 49 Color Plate 24 The fifth incision 49 Color Plate 25 The bith incision completed (viewed from the inside of the heart) 55 Color Plate 26 The X-ray, dissected coronary vesels (viewed from the outside of the heart) and diagram of the coronary circulation 55 Color Plate 27 The normal circulation (colored X-ray) 55 Color Plate 28 Heart of a patent who died of coronary occlusion followed by myocardial infarction 55 Color Plate 29 Heart of a patient with Angina Pectoris showing one of the many patterns possible 55 Color Plate 30 lieart of a pauent with Angina Pectoris showing 9 old complete occlusions 55 Figure 26 figure 27 Figure 28 Figure 29 The first incision completed The second incision completed The third incision completed The fourth incision completed 51 51 $2 $2 ·LIST OF ILLUSTRATIONS PART 2-PHYSIOLOGY OF ANGINA PECTORIS ... Page Color Plate 7. Electrocardiograms in clinical and experimental coronary occlusion 41 Color Plate 8. Similarity of electrocardiograms in exercise and anoxia 41 Color Plate 9 Nerve supply to regions involved by the pain of Angina Pectoris 41 Color Plate 10. Diagramatic representation of nerve supply to heart 41 Vagus nerve (Yellow) Cardiac sympathetic nerves (Blue) Thoracic sympathetic nerves (White) Color Plate 11. Diagramatic representation of routes involved (red) in transmission of pain sensation from heart. 41 Color Plate 12 Schematic representation of discrepancy between the Demand and the Supply of blood during exercise in patients with Angina Pectoris 41 ... Figure 15 Apparatus used in producing anoxemia in the muscles of the forearm 35 Figure 16 Patient J M with angina pectoris and intermittent claudication on exertion 35 Figure 17 Examination of peripheral circulation in patient I M 36 Figure 18 Sutton and Lueth operation for experimental coronary constriction 36 Figure 19 Apparatus used to induce generalized anoxemia by re-breathing 37 Figure 20 Apparatus used for exercise with oxygen 37 Figure 21 Dissection of cardiac nerves 38 Figure 22 Schematic representation of balance between Supply and Demand with the normal subject at rest 39 Figure 23. Schematic representation of local (cardiac) oxygen debt of normal subject during exercise 40 Figure 24. "The steady state" after several minutes of exercise when the supply of blood equals the immediate needs 40 Figure 25 Recovery from exercise- The supply of blood is greater than the demands until the oxygen debt is cancelled 40 ·"IST OF ILLUSTRATIONS 63 Fage Cocond degree c! eftect of nutroglycerin Com. escn ci response of Group 1. Group 2. and GRLS 3 patents. E:ecce e response to nitroglycerin 2 cer se ci response to nitroglycerin Te causary for desintegration of erhene coated tablets 65 * Frequency of response to purines 66 PS Degree ct response to purines 66 FC Fercy ci response to quinidine sullato 67 F Degree ci response to quinidine sullato 67 - cukrauons et sedatives with other drugs are aroulable 66 1929 Framercy of response to sedatives 68 * Degree of response to sedatives 68 Pali Frequency of response to cobra venoin 69 42 Degree of response to cobra venom 69 2.5 43 Frequency of response to atropine sullato 70 Fire + Degree of response to atropine sultato 70 Fig. 45 As much as 35 drops of the salurated solution of potassium iodide may be necessary to equal 1 cc. cr 1 gram of the drug ngue 45 Frequency of response to potassium iodido 13 gm danly) 75 Fimmte 47 Degree o! response to potassium iodido (3 glo daily) 75 Figure 4 Frequency with which surgery was required in patents with Angina pectoris 76 Figure 49 Frequency with whuch surgery was portormed in patents with Angina pectoris 76 Figures 50 and 51 Results of surgery in patient RS 77 Figure $2 Results of total thyroidectomy in patients with Angina pectoris 75 70 ·LIST OF ILLUSTRATIONS PART 4-TREATMENT OF ANGINA PECTORIS Page Color Plate 31 "A tremendous number of methods of treatment have been advocated for Angina Pectoris" 61 Color Plate 32. The efficacy of over 70 different methods of treatment as evaluated by the Standardized Exercise Tolerance Test and clinical studies 61 Color Plate 33 Therapeutic agents of great value and the criteria used 61 Color Plate 34. Method of disguising medication to prevent recog. nition by the patient during evaluation studies 61 Color Plate 35 The frequency with which patients respond to therapy (Groups 1, 2 and 3) 61 Color Plate 36 Nitroglycerin prevents the electrocardiographic changes during exercise 6) Color Plate 37 The most effective Xanthines (uncoated and enteric coated) 72 Color Plate 38 Uncoated and enteric coated purines 72 Color Plate 39 Comparative degree and duration of effect of Nitroglycerin and Theobromine Sodium Acetate (uncoated and enteric coated) 72 Color Plate 40 Enteric coated potassium iodide 72 Color Plate 41. Value of quinidine sulfate in Angina Pectoris 72 Color Plate 42, The lack of effect of cobra venom on the electrocardiogram during exercise 72 Color Plate 43. The effect of Digitalis on the electrocardiogram during exercise 73 Color Plate 44. Comparative value of medical and surgical procedures 73 Color Plate 45 Schematic representation of treatment of Angina Pectoris by decreasing the demand for blood 73 Color Plate 46 Schematic representation of treatment of Angina Pectoris by increasing the coronary blood supply 73 Color Plate 47 Schematic representation of Angina pectoris by interrupting the sensory nerves 73 73 Color Plate 48 The "routine treatment" of Angina pectoris 16 ·REFERENCES PART 1 CLINICAL CHARACTERISTICS OF ANGINA PECTORIS Heterden, W Some Account of a Disorder of the Breast Med Trans Coll. Phys London, 1768 Pisenan Joseph EF and Stern, Beatrice A Standardized Exercise Tolerance Test for Patients with Angina pectoris on Exertion Amer Jour Med Sci 188, 646, 1934 Fiseman, Joseph E F and Brown, Morton G An Analysis of the Diagnostic Criteria o! Angina Pectoris Amer Ht four 14, 331, 1937 Riseman, Joseph E F The Relation of the Systolic Blood Pressure and Heart Rate to Attacks of Angina Pectoris Precipitated by Elfort Amer Ht lour 12, 53, 1936 Riseman, Joseph EF, Waller, John V and Brown, Morton G The Electrocardiogram During Attacks of Angina Pectoris Its Characteristics and Diagnostic Significance Anes Ht Jour 19, 683, 1940 Pothschild, Marcus A and Kissin, Milton Induced General Anoxema Causing S-T Deviation in the Electrocardiogram Amer Ht Jour 8. 745. 1933 Levy. Robert L, Baruch, Alvar Lund Bruern, Howard G Effects of Induced Oxygen Want in Patients with Cardiac Pain. Amer Ht Jour 15, 187, 1938 Surrell, CT. Nims, MG and Josephson, CI The Induced Anoremia Test Amer H1 jour 23, 306, 1942 Patterson, James E, Clark, Thomas Wand Levy. Robert L. A Comparison of Electrocardiographic Changes Observed During The "Anoxemia Test" On Normal Persons and on Patients with Coronary Sclerosis Amer H: Jour 23 837 1942 PART 2 PHYSIOLOGY OF ANGINA PECTOAIS MacWilliam, I A, and Webster, WJ "Some Applications of Physiology to Medi. cine, Sensory Pheromena Associated with Delective Blood Supply to Working Muscles Brit M ILS1, 1923 Lew13 T Pickering. CW and Rothschild, P: "Observations upon Muscular Pain in Intermittent Claudication" Heart 15359, 1931 Lewis T Pain in Muscular Ischemic Its Relation to Anginal Pain" Arch Int Med 43713 1932 Suron DC and Lueth, Harold C Pan Arch In: Med. 45, 827, 1930 Blugart Herrman L Holl. Hebbel E, Londowne, Muton and Schlesinger, Monroe Experimental Studies on the Effect of Temporary Occlusion of Coronary Areries in Producing Persister Electrocardiographic Changes Amer Jour Med Sa 194, 193, 1937 Rothschild Mircus A and Kissin fillon Anginal Syndrome Induced by Gradual Cereral Anodesia Proc Soc Exp Biel Med 29, 577, 1932 Remar losers E Fard Browa, llorton G The Efect of Oxygen on the Exercise Tolerance of Patients with Arg.na Pectoris Aner Ht. Jour 18, 150, 1939 Heas H On Disturbances of Sensat.on with especial Reference to the pain of Visceral Disease Brain, 161, 3893 Bran, 17339, 1694 Brain. 19 153 1895 Keete Ches'er S and Resnik, William H Arging Pecotis Arch Int med 41, 769, 1929

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·Part 1
Clinical Characteristics
of
Angina pectoris

·REFERENCES PART 3 PATHOLOGY OF ANGINA PECTORIS Parry. C H "An Inquiry into the Symptoms and Causes of Syncope Anginosa Commonly called Angina pectoris" London 1799 Schlesinger, Monroe ] An Injection Plus Dissection Study of Coronary Artery Occlusions and Anastomoses Amer Ht Jour 15, 528, 1938 Blumgart, Herrman L, Schlesinger, Monroe and Davis, David Studies on the Relation of The Clinical Manifestations of Angina Pectoris, Coronary Thrombosis and Myocardial Inſarction to the Pathological Findings Amer Ht Jour 19, I, 1940 PART 4 THERAPY OF ANGINA PECTORIS Riseman, Joseph E F Summary of Ten Years Objective Study of Treatment in Angina pectoris New Eng Jour Med (in press) Riseman, Joseph E F and Brown, Morton G Medicinal Treatment of Angina Pectoris Arch Int Med 60, 100, 1937 Brown, Morton G and Riseman, Joseph EF The Comparative Value of Purine Derivatives in the Treatment of Angina Pectoris lour Amer Med Assoc 109, 256, 1937 Riseman, Joseph E F and Brown, Morton G The Duration of Attacks of Angina Pectoris on Exertion and the Effect of Nitroglycerin and Amy! Nitrite New Eng jour Med 217, 470, 1937 Riseman, Joseph E F and Linenthal, Harry The Prolonged Use of Enteric-Coated Tablets of Theobromine Sodium Acetate in the Treatment of Edema and Angina Pectors New Eng Jour Med 224, 933, 1941 Freedberg, A Stone, Riseman, Joseph EF and Spiegl, Erwin D Objective Evrdence of the Efficacy of Medicinal Therapy in Angina Pectoris Amer Ht Jour 22, 494, 1941 Freedberg, A Stone, Spiegl, Erwin D and Riseman. Joseph E F Octy! Nitrite in the Treatment of Angina Pectoris Amer Ht Tour 22, 519, 1941 Levy, Robert L. Bruenn, Howard G and Williams. Norman E The Modifying Action of Certain Drugs (Aminophyllın, Natrites, Digitalis) Upon the Effects of Induced Anoxemia in patients with Coronary Insufficiency Amer H: Jour 19, 639, 1940 Williams, Norman E, Carr, Henry A, Bruenn, Howard Gand Levy, Robert L Further Observations on The Eflects of Certain Xanthine Compounds in Cases of Coronary Insufficiency. As Indicated by the Response to Induced Anoxemia Amer Ht Jour 22, 252, 2941 Blumgart, Herrman L. Riseman, Joseph E F Davis, David and Berlin, David D Therapeutic Effect of Total Ablotion of Normal Thyroid on Congestive Heart Failure and Angina Pectoris Arch Int Med 52, 165, 1933 Riseman, Joseph E F The Treatment of Chronic Heart Disease by Tota! Thyroid. ectomy Jour Med Soc New Jersey, July, 1936 20 ·PART 1 CLINICAL CHARACTERISTICS OF ANGINA PECTORIS In 1768, William Heberden presented before the College of Phy. sicians, in London, a treatise entitled "Some Account of a Disorder of the Breast (Frontispiece) This begins as follows "There is a disorder of the breast, marked with strong and peculiar 1mplonis, considerable for the kind of danger belonging to it, and not extremely rare, of wlueb I do not recollect any mention among medical andbors The seat of it, and sense of strangimg and anuely with #bich it is attended, may make it not improperly be called Angina Protoris." She The patient presented in plates 1 and 2 is 65 years of age has had angina pectors for six years Like most patients with this condition, she is perfectly comfortable between attacks (Plate 1, page 25) On exertion, however, and occasionally on emotion or even while at rest or during sleep, she may develop the characteristic symptoms which we call angina pectons (Plate 2. page 25) As will be shown, allacks of angina can be precipitated by having pabents repeatedly mount a two-step staircase. During such cpisodes this patient illustrates dramatically the typical clinical characteristics of this condition First-the allacks are obviously uncomfortable (Plate 2, page 25). Second-the discorniort is located in the anterior chest and inner aspects of the arms Third--the attacks are most commonly precipitated by exertion Fourth--they are sudden in onse! The pain in this parent did not develop until about 10 seconds belore she was forced to stop Filth-the attacks are short in duration The attack photographed corresponds closely to the description given in most textbooks, in fact this is the reason that this parhcular patient was selected The severity of the pain in this individual and the seventy of this patients reaction to attacks, however, are distinctly unusual In the allack photographed pain was precipitated by 21 trips over the two step staircase performed in 1 minute and 38 seconds the attack lasted 1 minute and 42 seconds The more common appearance of the attacks as they occur in over 95% of parents 15 shown in ligure I (Figure 11

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·Plate 1-Patent BK
Plate 2 Textbook" attack of angina
pectoris
DIAGNOSTIC CRITERIA
S
2. Als
3. GiF FORT
4. 1. NOUCES
$. TORT DURATION
Fla'o 3 Distribution of pain in angina
Plate 4_Clinical criterio diagnosis of
angina pectoris,
sec 0 LIGIERES
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تلال
5
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i ze 3 Cont nous electrocard ograms
ang aca art
Plate Continuous electrocardiograms of
normal during exercise
25

·THE STANDARDIZED EXERCISE TOLERANCE TEST a It is important to realize that our knowledge of angina pectoris rests almost entirely upon what patients are able to describe to us about their sensations Furthermore, so far as we know, this condition exists only in human beings Therefore, it is necessary to study angina pectoris not in laboratory animals but in patients. The fact that most patients develop attacks on exertion makes it possible to study angina pectoris objectively in the laboratory. Such studies have been carried out since 1932 at the Beth Israel Hospital of Boston As part of this work, attacks have been precipitated by having the patient exercise in the presence of a physician (lig 2) These studies have been carried out in a room equipped with a refrigerating unit to maintain constant temperature of 45 to 55 degrees This cold room is necessary, for when (Figure 2) the various factors influencing the amount of work which can be done before developing an attack were measured, it was soon found that some patients with angina can exercise almost indefinitely at room temperature, whereas, they develop attacks rapidly on exercise in the cold (lig 3) It was also found that a heavy meal will decrease the amount of work which can be done before pain. Excitement or emotion also increases the ease of precipi- FACTORS INFLUENCING tating attacks It exercise is ABILITY TO WORK repeated or continued, we find that in some patients one at: tack builds up a slight immunity, while in others the first attack predisposes to a second episode Similarly, medication may influence the ease of precipitating pain As a result of these studies, the Standardized Exercise Tolerance Test (Figure 3) was developed This test reproduces in the laboratory the conditions responsible for the majority of attacks in daily life and makes it possible to study angina pectoris objectively without relying on the patients observations for our basic knowledge The standardized conditions used in these tests are as follows (lig 4) The temperature of the room is inaintained between 45 and 55 +50 +50 PERCENT CHANGE IN LIL -50 ae سلااسات OSR wo -50 24

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·THE STANDARDIZED EXERCISE TOLERANCE TEST a It is important to realize that our knowledge of angina pectoris rests almost entirely upon what patients are able to describe to us about their sensations Furthermore, so far as we know, this condition exists only in human beings Therefore, it is necessary to study angina pectoris not in laboratory animals but in patients. The fact that most patients develop attacks on exertion makes it possible to study angina pectoris objectively in the laboratory. Such studies have been carried out since 1932 at the Beth Israel Hospital of Boston As part of this work, attacks have been precipitated by having the patient exercise in the presence of a physician (fig. 2) These studies have been carried out in a room equipped with a refrigerating unit to maintain constant temperature of 45 to 55 degrees This cold room is necessary, for when (Figure 2) the various factors influencing the amount of work which can be done before developing an attack were measured. at was soon found that some patients with angina can exercise almost indefinitely at room temperature, whereas, they develop attacks rapidly on exercise in the cold (fig 3) It was also found that a heavy meal will decrease the amount of work which can be done before pain Excitement or emotion also increases the ease of precipi. gi FACTORS INFLUENCING tating attacks If exercise is ABILITY TO WORK repeated or continued, we find that in some patients one attack builds up a slight immunity, while in others the first attack predisposes to a second episode Similarly, medication may influence the ease of precipitating pain As a result of these studies, the Standardized Exercise Tolerance Test (Figure 3) was developed This test reproduces in the laboratory the conditions responsible for the majority of attacks in daily life and makes it possible to study angina pectoris objectively without relying on the patient's observations for our basic knowledge The standardized conditions used in these tests are as follows The temperature of the room is maintained between 45 and 55 +50 +30 PERCENT CHANGE HEIL ul.lar SONY Geon wzo -50 (hg 4)

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DIAGNOSTIC CRITERIA
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·THE TYPICAL ATTACK OF ANGINA PECTORIS ... degrees Fahrenheit The exer- SUDDEED TRCISE cise is carned out at least one or two hours after a light meal, and the patient rests for one- LOW TEMPERATURE 45-5S'E. half hour after coming to the ONE HOUR AFTER LIGHT MEAL laboratory. No medication is KC RECEXT ATTACK given for at least 12 hours belore the test XO MEDICATION Only one *FAMILIARITY WITH TEST measurement is carried out on any given day, and no work is THESE COAL CONDITIONS performed if the patient has ex- GIYE.COM0 RISOLTS... perienced an attack on the way (Figste 4) into the hospital, except in those individuals who always experience many attacks every day Since excilement frequently induces attacks, it is necessary to minimize the emohonal factor, famliarity with the test brings this about The attack shown in patient RS (hg 1. page 23) does not correspond closely to the usual textbook description but it is absolutely typical of the usual attacks as they occur in daily life in the vast majority of patients The patent shows no expression of severe discomfort, although he prefers to remain perfectly quiet. There is no lear of impending death and no pollor, flushing, lanting, perspirauon or vomiting as has been described by some authors Although the patient feels that the arrack has persisted for some minutes, actual measurement shows that it was about 38 seconds in duration The characteristic regions in which pauents feel the pain are as follows (Plate 3, page 25) The anterior chest is always involved in an area limited by the antener axallary lines on the sides, the suprasternal notch above, and the epigasinum below The region beneath the sternum is the most common location Radiation of the pain occurs in approximately 60% of patients The most common region to which the discomfort travels is the left arm, along the inner aspect of the bzceps, the elbow, the forearm, the wrist, and the little and ning fingers In some patients at as relented to similar locations in the nght arm The upper back, in the region of the spine, is commonly involved, although the pain here is not disturbing to the patent Rarely, it radiates to the neck or to other regions such as the lower jaw ·FREQUENCY, PHYSICAL BUILD, AGE AT ONSET It has been said that the usual patient with angina is short and stocky, of the so-called vascular build, and that they show abnormalities in the electrocardiogram, blood pressure or heart size The frequency of the different physical characteristics as actually found in a group of 100 of these patients is as follows NE FREQUENCY Heberden stated: "I bare seen nearly a bundred people under this disorder, of which inniher there bave been three women." More recent studies show that it is 3 to 4 times as common in men as women (hg 5) 金鱼 in (Figure 5) ITSIZE: WILD PHYSICAL BUILD While it is true that the majority of patients are stocky, obese, or "vascular", there are striking exceptions to this rule It is obvious that the build of the patent is of no aid in establishing the diagnosis (hig 6) (Figure 6) AGE AT ONSET Angina pectoris may occur at any age, but it is not common in patients under 40 About 80% of patients are between 45 and 65 years of age when the symptoms first become evident (fig 7) (Figure 7) 28 ·BLOOD PRESSURE, ELECTROCARDIOGRAM, HEART SIZE BLOOD PRESSURE. Since one-half or the patients have normal blood pressures it is obvious that hypertension is not an important iactor in the diag- DOSIS O! angina pectoris (lig 8) (Figure 6) TIG ELECTROCARDIOGRAM Similarly, only one-half of the patients show evidence ! heart disease in the standard electrocardiogram This is somewhat surprising in view of the lact that these patients all have heart disease, but the heart has many areas which are silent electrocardiographcally {{g 9) (Figure 9) HEART SIZE Only onetourth of patients with angina pectons show cardiac enlarge ment, even when the measurements are made by X-Ray. This is in sharp contrast to the lindings in other forms of heart disease such as congestive clure (lig 10) (Flat 10) ·ELECTROCARDIOGRAM DURING ATTACKS OF ANGINA PECTORIS cise ELECTROCARDIOGRAM, BLOOD PRESSURE, and HEART SIZE. Onc-fourth of the patients with angina show no abnormalities in electrocardiogram, blood prcssure or heart size, cven though the discaso may be advanced and the symptoms soverc (fig. 11). It is important to realize that abnormalitics in electrocardiogram, blood pressure or hoart Bizo aro evidence of (Figure 11) cardiac damage and are not cvidence of heart pain. Since the attacks come suddenly, without warning, and are of short duralion, it is obvious that opportunities to make measurements during spontaneous attacks are rare The heart rate and the systolic blood pressure can be obtained during exerquite readily by a special technique (fig 12) Such observations show no constant relationship between the heart rate or the height of the blood pressure and the onset or precipitation of the attack (Figure 17) A fow observers have been fortunate enough to obtain electrocardiograms during spontaneous altacks The short duration of the pain, and the time necessary for thic technical procedure of taking such tracings, suggests that these clectrocardiograms were obtaincd toward the end or oven after the acuto discomfort The Standardized Exercise Tolerance Tcst makes it possible to take electrocardiograms continuously before, during and (Figure 13) after the attack (fig 13) 30 ·ELECTROCARDIOGRAM DURING ATTACKS OF ANGINA PECTORIS The electrocardiogram taken continuously during the precipitation of an attack practically always shows characteristic changes, especially in the precordial lead. (Plate 5. page 25). These changes begin shortly after the onset of exercise and increase slowly, reaching a maximum at the time when the patient is forced to stop because of pain. The changes consist of a deviation, usually a depression, of the S-T seg. ment as can be seen by comparison with the tracings taken at rest. Thereafter, they either subside rapidly or show further progression, especially in the height of the T waves While changes in the T waves may occur during the attack, they are more common during recovery from the pain and the exertion The marked S-T changes found in patients with angina after exertion are not common in normals, but they do occur (Plate 6, page 25) Changes in the T waves, however, are quite frequent In our experience the electrocardiogran after exercise is of little practical value in the diagnosis of angina pectoris (Figure 14) It has also been found that patients with angina pectoris may show these S-T and T changes when breathing a low concentration of oxygen (higs 14 and 19) Many patents al 10 show such changes. however, while on occasional normal individual may show abnormalies which are indistinguishable from those observed in patents with angina It is obvious, therelore that such changes are of little diagnoste value ·ELECTROCARDIOGRAM DURING ATTACKS OF ANGINA PECTORIS ELECTROCARDIOGRAM, BLOOD PRESSURE, and HEART SIZE. One-fourth of the patients with angina show no abnormalities in electrocardiogram, blood pressure or heart size, even though the disease may be advanced and the symptoms severe (fig 11) It is important to realize that abnormalities in electrocardiogram, blood pressure or heart size are evidence of (Figure 1) cardiac damage and are not evidence of heart pain, Since the attacks come suddenly, without warning, and are of short duration, it is obvious that opportunities to make measurements during spontaneous attacks are rare The heart rate and the systolic blood pressure can be obtained during exercise quite readily by a special technique (lig 12) Such observations show no constant relationship between the heart rate or the height of the blood pressure and the onset or precipitation of the attack (Figure 12) A few observers have been fortunate enough to obtain electrocardiograms during spontaneous attacks The short duration of the pain, and the time necessary for the techncal procedure of taking such tracings, suggests that these electrocardiograms were obtained toward the end or even after the acute discom. fort The Standardized Exercise Tolerance Test makes it possible to take electrocardiograms continuously before, during and (Figure 13) after the attack (lig 13) -- 30

·Part 2
Physiology
of
Angina pectoris

·DIAGNOSTIC CRITERIA OF ANGINA PECTORIS Obviously, there is little in the physical examination, X-Ray, blood pressure, or electrocardiogram which is of value in the diagnosis of angina pectoris By observation of patients during attacks, the important diagnostic characteristics were found to be (Plate 4, page 25) The attacks are sudden in onset with little or no premonitory symptoms. 2 The discomfort is in the anterior chest Radiation of the pain is important if it occurs, but it may be absent 3. The discomfort is vague in character and difficult for the patient to describe 4 Exertion is the most common precipitating cause, although it may also occur on emotion 5 The attacks are short in duration According to the patient they rarely last longer than 15 to 20 minutes Practically all patients show all five clinical characteristics Difficulties in diagnosis arise mainly because of the inability to obtain a clear cut description of the patient's symptoms Under such conditions, observation of the patient during a typical attack may be of considerable value in diagnosis Heberden's classic description includes the five characteristics which recent experience has shown to be of diagnostic value (frontispiece) "Those, who are afflicted with it, are seized, while they are rolkmę, nn) more particularly when they walk soon after catmg, wtb o pamful and most disagreeable sensation in the breast, which seems as of 11 would take ther life away, of it were to increase or to continue: the moment they stand still, all thus uwasımess tandsbes." 32 ·PART 2 PHYSIOLOGY OF ANGINA PECTORIS There is considerable evidence in the literature that attacks of angina pectoris occur when the heart muscle receives an insufficient amount of oxygen or blood or both This anoxemia or ischemia theory is consistent with more of the known clinical facts concerning angina pectors than is any other concept Furthermore, it makes many characteristics of the disease more understandable There is considerable experimental evidence in favor of this theory Lewis showed that muscular exercise. in the absence of an ade. quate blood supply, causes pain in the muscles used We can occlude the blood supply to the arm of a normal healthy subject by inflating a blood pressure cuff to a level greater than that of his arterial blood pressure (hg 15) If the muscles of the forearm are then exercised, the available oxygen dissolved in the tissues 15 soon used up, and the subject experiences first fatigue, then pain in those muscles involved This pain rapidly in- Creases (Figaro 15) in severity and continues even though exercise is stopped As soon as the tourniquet is released however, fresh blood enters the arm and the pain disappears immediately in The clinical counterpart of this expenment 18 seen patients who have arteriosclerosis involving the arteries of the heart and also those of the legs On exercise, such patients may develop not only angina pectoris but also pain in the call muscles (hg 16) This condition called intermittent claudication' is fairly common among elderly indivi. duals even in the absence of angina pectors Figure 15)

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·STUDIES WITH INDUCED ANOXIA changes are associated with an insullicent supply of oxygen to the heart muscle Their occurrence may be of value in establishing the diagnosis of myocardial infarction. Another line of evidence in favor of the anoxema theory was presented by Rothschuld and Kissinin 1932 who showed that altacks of angina pectors could be precipitated in some patients at test by having them breathe low concentrations oxygen (ug 19) The apparatus consists of a spirometer, such as an ordinary basal meta- {Figure 19) bolism machine, connected in series with a reservoir of about 20 hters, and a motor blower to insure circulation As a result of this re-breathing, the oxygen content, as determined by analysis, is decreased to as low as 8 or 10%. Under these conditions, some but not all patients with angina develop pain Electrocardiograms taken during such experiments (Plate 8, page 4?> moy show changes in the S-T segment and the T wave identical with those observed in the same patent dunng spontaneous attacks of angina or during attacks induced by exerase. These changes ate similar to those lound in some patients with coronary occlusion Such studies indicate that attacks of angina are associated with myocardial anoxia regardless of whether they are produced spontaneously. by exercise, or by generalized anoxemia - The opposite of this type of experiment has been performed by Riseman and Brown in 1939 (hig 20) Their investigations show that exercise while breathing pure oxygen enables patients with angina to do mote work without pain than is possible under the usual standardized conditions, even though handicapped by the OPPOTHUS (Purus ·STUDIES ON NARROWED OR OCCLUDED ARTERIES ar- The presence of teriosclerosis in the legs is indicated by the absence of palpable puisations of the dorsalis-pedis and the posterior-tibial arteries and also by the relatively cold temperature of the feet This can be demonstrated by the sense of touch More accurate measurements with a dermatherm show that the temperature (Figure 17) of the great toe is considerably less that that of other parts of the body. such as the thumb (hg 17) T In 1930, Sutton and Lueth showed experimentally the relationship of anginal pain to narrowing of the coronary arteries In these experiments an animal anesthetized, the heart was exposed, and a ligature passed about one of the coronary arteries (fig 18) After recovering from this operation, they could occlude the artery (Figure 19) at will by gentle traction This constriction caused discomfort in the chest and left paw The clinical condition "coronary occlusion" simulates this experiment In this condition patients suddenly develop pain in the chest which is similar to their anginal attacks but is much more severe and continues for several hours Post-mortem examination of such individuals usually reveals that one of the major arteries of the heart has become completely occluded so that the cardiac circulation is restricted similarly to the artificial restriction in the experimental animal (see was part 3) Electrocardiograms taken during experimental coronary occlusion in dogs or coronary thrombosis in man (Plate 7, page 41) may show S-T segment and T wave changes similar in character but more pronounced than those seen in attacks of angina pectoris These 36 ·CLINICAL CONDITIONS ASSOCIATED WITH ANGINA PECTORIS quate blood flow, or regurgitation of such a degree that during diastole a portion of blood flows back into the heart rather than through the coronary vessels Abnormal rhythms, especially if the rate is rapid, may result in poor circulation Under such conditions, the increased work of the heart together with the poor blood flow, may result in myocardial anoxia and angina pectoris In anemia, the decreased number of red blood corpuscles results in a decreased supply of oxygen to the heart in addition, the heart has to work harder to supply the necessary oxygen As a result, inany elderly patients with anemia experience heart pain In exophthalmic goiter, the tissues of the body, including the heart, require an increased amount of oxygen and the heart beats laster As a result, a lew patients develop angina Similarly, some patients with congestive failure, clthough complairung primarily of dyspnea, may experience a feeling of pressure, choking, squeezing or pain in the anterior chest or arms. Patients with emphysema or asthma also complain of symptoms simulating angina pectons in these individuals the abnormality of the lungs prevents adequate oxygenauon of blood when the patient exercises EXERCISE, IN NORMALS angina pectoris can be The mechanism of sumarized and illustrated by the Law of Supply and Demand as it applies to the coronary circulation In the normal in- DEMAND SUPPLY dindual and in most patients with angina pec PANATTACK foris the Supply of blood through the coronary F.ro ) vessels is adequate for the needs or Demands c! the myocardium when the subject is at rest (hg 22) FA NO 39 ·THEORY OF REFERRED PAIN AND ANGINA PECTORIS The theory of referred pain as presented by Head in 1893 explains why patients, who exercise with their legs, experience pain in the anterior chest and inner aspects of the arms The usual distribution of pain in angina pectoris (Plate 9. page 41) is innervated, in the chest, by the eighth cervical, the first second, third, fourth, and fifth thoracic nerves The sensory innervation of the inner aspect of the arm is derived from the eighth cervical, the first and second thoracic nerves The anatomic nerve supply to the heart 13 well known An actual dissection of these nerves shows that it is a most complex network (hg 21) The cardiac nerve supply consists of fibers from the vagus, which unite with the cervical sympathetic, and the thoracic sympathetic chain and ganglia (plate 10, Functionally, the sympathetic nerves connect (Figure 21) with the ganglia of the eighth cervical, the first second, third. fourth and fifth thoracic nerves Impulses which arise in the heart travel up the sympathetic nerves to the nerve roots in the dorsal ganglia and spinal cord The sensation of pain set up by these impulses is felt not in the organ actually involved, but in the areas innervated by the peripheral nerves arising in the same segments of the spinal cord (Plate 11. 123 page 41) page 41) Thus, the sensations set up in the heart by anoxemia are experienced as pain in the anterior chest and inner aspects of the arms The anoxemia-ischemia theory helps considerably in understand. ing why angina pectoris is associated with certain diseases For example, it is most commonly found in elderly individuals of the arteriosclerosis age group Syphilis of the aorta and mouths of the coronary arteries may also be a cause of inadequate coronary circulation Similarly, some patients with disease of the aortic valves may complain of angina pectoris In these patients, examination of the valves may reveal a degree of stenosis so great as to prevent an ade- 38 ·CLINICAL CONDITIONS ASSOCIATED WITH ANGINA PECTORIS quate blood flow, or regurgitation of such a degree that during diastole a portion of blood flows back into the heart rather than through the coronary vessels. Abnormal rhythms, especially if the rate is rapid, may result in poor circulation Under such conditions, the increased work of the heart together with the poor blood flow, may result in myocardial anoxia and angina pectons In anemia, the decreased number of red blood corpuscles results in a decreased supply of oxygen to the heart In addition, the heart has to work harder to supply the necessary oxygen As a result, many elderly patients with anemia expenence heart pain In exophthalmic goiter, the tissues of the body, including the heart, require an increased amount of oxygen and the heart beats faster As a result, a few patients develop angina Similarly, some patients with congestive failure, although complaining primarily of dyspnea, may experience a feeling of pressure, choking, squeezing or pain in the anterior chest or arms. Patients with emphysema or asthma also complan of symptoms simulating angina pectors in these individuals the abnormality of the lungs prevents adequate oxygenation of blood when the pauent exer. cises EXERCISEZIN NORMALS angina pectoris can be The mechanism of summarized and illus. trated by the Law of Supply and Demand as it applies to the coronary circulation, In the normal in DEMAND SUPPLY dividual and most NO patients with angina pec- PAIN, ATTACK toris the Supply of blood through the Coronary vessels is adequate for the needs or Demands of the myocardium when the chant : in 273 ·PHYSIOLOGY OF ANGINA PECTORIS-SUMMARY On exercise, however, the heart must work EXERCISE IN NORMALS harder and, therefore, the Demands of the myocardrum increase In response to this increased demand, the Supply of blood through the coronary arteries also increases, but lags behind (hg 23) As a result, a slight relative anoxia of the myocardium exists for SUPPLY DEMAND Na PAINI ATTACK (Figure 23) several minutes until the EXERCISE IN NORMALS balance is re-established NN (fig 24) With cessation of work, the opposite takes place The Demand is decreased to the resting level, and the coronary blood Supply soon decreases also to a degree sufficient for the body at rest (figs 25 and 22), OEMAKO SUPPLY NO PAINT ATTACK (Figure 24) The situation is quite different in angina pecto EXERCISE IN NORMALS 12, page DEMAND ris Here, when the Demands are increased by exercise, the coronary circulation is not able to increase (Plate 41) This discrepancy between the Demands for blood and the Supply of blood causes marked myocardial anoxia and ischemia As a result, the patient experiences heart pain SUPPLY NO SAIN, ATTACK (Figure 25) This is referred to the chest and arms 40

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Plate X-Similarity of electrocardiograms :
exercise and aroxe.
Flate 7 --Electrocardiograms in COTOTY
occlusion
Plate 10 - The cardiac nerves
Fla:e 9-Sensory nerve distribution in
angina pectoris
EXERCISE ANGINA.
DEM
NO
PAIN ATTACK

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·Part 3
Pathology
of
Angina pectoris

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·PART 3 PATHOLOGY OF ANGINA PECTORIS Parry's Book on angina pectoris published in 1799, includes a tromscript of a letter from Dr Jenner This teads in part as follows (Plate 13, page 48) "? nos making a transterse sectron of the beart pretty near tla base u ben my knife struck against sometbrug so baril and gritty as to notch it. I uell remember looking up to the ceiling u bich t'as old and crumbling, conceiling that some plasster bed fallen dou'n, But on a further serulin) the real cause appeared, Ile coronaries were become bony canals ” Recent work on the anatomy and pathology of the heart has confirmed the findings of Jenner The coronary circulauon is not easy to see in the gross specimen. It consists of the left coronary artery which divides into the left anterior descending branch and the left circumflex branch There is also a right Coronary artery If we remove the aorta, pulmonary artery and the auncles we can see the mouths of these vessels coming of the aorta just at the base of the cusps of the aortic valves (Plate 14, page 48) The simplest method of studying the coronary arleries is to open the lumen of each vessel with a fine pointed scissors. The objections to this method are that it may dislodge fresh Occlusion and, lurthermore, it is not suitable for studying vessels smaller than 1 millimeter in diameter According to a second method, the vessels are cut across at frequent intervals and then probed This has the saine drawbacks as the previous method Hearts have been injected with various radio-opaque materials and studied by X-Ray The vessels appeas to Toss each other, however, and adequate study is dificult A simple practical method which corrects these dilticultes was devised by Schlesinger in 1939 This method combines the use of Injection, X Ray. and Discection By means of it we can study the entire course of each blood vessel down to 40 micra Areas of obstruction or narrowing 100 small to be seen by other methods of study are readily observed, and the presence of anastomotic circulation is easily recognized. This method has given us considerable information about the pathology of angina pectors The method can be used in the routine examination of all post-mortem material The technique is simple 45 ·TECHNIQUE-INJECTION OF THE HEART Glass cannulae, connected to short lengths of rubber tubing and metal adapters, are carefully inserted into the mouths of the coronary arteries and tied into place securely (Plate 15, page 48) A bath of warm isotonic salıne is prepared by mixing one part of 18% salt solution with 19 parts of hot tap water (Plate 16, page 48) A heating unit and thermostat adjusts the temperature of this bath to 45 degrees centigrade The heart is suspended in the bath, and a thermometer is inserted into one ventricle While the heart is being warmed, the injection mass can be prepared (Plate 17, page 48). One and one-hall grams of agar-agar are weighed out, using an ordinary balance This is placed in a pyrex container which can be covered To this is added 100 cubic centimeters of a 30 per cent solution of lead acetate in water 70 cubic centimeters of a 12 per cent solution of anhydrous sodium phosphate is added and mixed by shaking. This results in the precipitation of the insoluble and radio-opaque lead phosphate Phenolsulfonphthalein is added as an indicator With a graduated pipette, enough ten percent sodium hydroxide is added, with shaking, to neutralize until the first pink color appears Finally, dıştılled water is added to bring the total volume up to 200 cc Usually, 10 to 20 cubic centimeters are required agar is brought into solution by heating over an open flame Boiling is continued for 10 minutes The mixture froths vigorously, and frequent shaking is necessary to prevent its boiling over The hot injection mass is then filtered through a double layer of gauze into narrow mouthed 50 cc centrifuge tubes Finally, the injection mass is colored by the addition of dyes fuchsın is added to give a red color and methylene blue for blue The tubes are stoppered and shaken thoroughly to ensure mixing The agar- A flask weighted with lead is filled with saline from the bath The injection mass is kept warm to prevent solidification of the agar Both cannulated arteries are connected to the flask which in turn is connected to a mercury manometer With a cautery bulb the pressure in the system is raised to 200 millimeters of mercury This forces saline into the arteries and removes the residual air and blood (Plate 18, page 48) The containers of colored, radio-opaque mass are now fitted with two hole rubber stoppers so that pressure can be applied above the fluid and the mass forced out The containers are connected to the 16

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Plate 18 --Washing coronary arteries
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Fla'a 19-Injecting the coronary arteries
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·TECHNIQUE-OPENING THE HEART manometers, and also to the heart in such a way that the blue mass can be injected into the left coronary and the red mass into the right (Plate 19, page 49) The manometers are joined so that the pressure is the same throughout the system The valve to the saline is shut off and the valves to the arteres turned on The pressure in the system is raised to 200 millımeters of mercury This inects the mass into both arienes simultaneously at identical pressure The red mixture fills the right coronary artery, the blue mass fills the leit The cannulae are then clamped off, and in order to harden the agar-agar injection mass the heart is placed in a bath of ice and salt solution for about 10 minutes The injected heart is then unrolled by a series of incisions, so that the vessels lie in one plane The first incision starts in the pulmonary artery and divides the pulmonary valve (Plate 20, page 49) It also cuts the right ventricle to the apex just to the right of the interventricular septum This results in the opened right ventricle lying to your left, IVALI CUTI an (Future 26) INT Vertar CUTZ NA hamrat while the left ventricle remains intact (lig 26) The second incision starts in the aorta between the two comnulated vessels and extends into the base of the interventricular septum (Plate 21, page This again divides the pulmonary artery (hg 27) The interventricular septum is now removed in one piece as close as possible to the walls of the left ventricle 49) {Figure 3?) 51 ·TECHNIQUE CONCLUDED (Plate 22, page 49). A scalpel is best for this procedure This partially opens the left ventricle (fig. 28). vament mniu The fourth incision starts in one of the pulmonary veins It cuts the aortic ring and the anterior cusp of the mitral valve (Plate 23, page 49) This unrolls the left ventricle. (fig 29) CUT 3 REXONE INTERYETT SEPTUN SEPTUN (Figure 28) TAK san ONIT NEONAT The fifth and final in. cision goes through the suvena cava, the aortic ring again and the tricuspid valve (Plate 24, page 49) This permits the right ventricle to be unrolled completely (Plate 25, mits CUTA INTERYEXT SEPTUM Page 55) LIE STAR (Figure 29) The heart has now been opened without having cut any of the major vessels Furthermore, all the vessels now he in one plane An X-ray of the unrolled heart is now taken Using the X-ray as a guide, the vessels are carefully dissected By studying the X-ray together with the dissection, tiny areas of narrowing and obstruction not recognizable by other methods of study can be detected readily From the X-ray and the dissection, a colored diagram is made. This diagram, together with the X-ray, are permanent records (Plate 26. The myocardial tissue can be examined microscopic and then discarded, page 55) 52 ·CHARACTERISTIC PATHOLOGICAL PATTEPUIS From a careful study of the X-ray, the dissection and te de gram, the course of the coronary circulation during life com te vi ized THE NORMAL CIRCULATION Plate 27. page 55, shows a normal heat obtained from man 63 years of age with no cardiac disease who died c! intestina! obstruction following operation in the normal heart, the injection comment Nows smoothly through the entre length of the blood vessels both left and night. There is no obstruction, delay, or any evidence ol collateral or anastomonic circulation This normal pattern is quite different from those seen in coronary artery disease MYOCARDIAL INFARCTION The heart shown in plate 28, page 55. was obtained from a man 50 years of age with angina for only 11 days before the onset of myocardial infarction which resulted in death The left anterior de scending artery shows an area of narrowing but no obstruction near its origin The lelt arcumflex shows a similar area of arteriosclerosis with a thrombus completely occluding its lumen The right coronary artery and distal portion of the left descending are normal The left circumflex, however, fills poorly beyond the occlusion There are no adequate anastomoses As a result, the circulation was unable to compensate for the sudden occlusion of the left circumflex artery An infarct developed in the area nounshed by this vessel, and the patient died of a ruptured myocardium ANGINA PECTORIS -One Pattern A third heart (Plate 29, page 55) was obtained from woman 60 years ol age who had angina pectoris for 5 years. At post morlem it showed one of the many patterns possible in this condition There was an old complete occlusion of the right coronary artery near its mouth This prevented the red mess from going further There was marked ortenosclerosis of the left arcumflex and lefi descending arteries resulting in narrowed tortuous lumens, and there was a second old occlusion in the lelt descending artery in response to these narrowings and occlusions a neh anastomotic network was built up during hie so that the circulation to the right side of the heart was maintainer from the left coronary artery This anastomotic circulation was ade. quate to maintain lile for several years despite occlusions of two of the ma'n coronary arteries The coronary circulation was impaired, howcver, so that the myocardium sultered from ischemia, and the patient expencrced angina pectonis ·TECHNIQUE CONCLUDED 49), (Plate 22, page A scalpel is best for this procedure. This partially opens the left ventricle (fig. 28). Turhaut LIFT minicu The fourth incision starts in one of the pulmonary veins It cuts the aortic ring and the anterior cusp of the mitral valve (Plate 23, page 49) This unrolls the left ventricle (fig. 29) CUT 3 LENOYS ETC RYTUT SEPTUM SEPTUN (Figure 28) The fifth and final in. cision goes through the suvena cava, the aortic ring again and the tricuspid valve (Plate 24, page 49) mits the right ventricle to be unrolled completely (Plate 25. YETT This per- CUTA INTERYENT SEPTUM $220TAI page 55) (Figure 29) The heart has now been opened without having cut any of the major vessels Furthermore, all the vessels now he in one plane An X-ray of the unrolled heart is now taken Using the X-ray as a guide. the vessels are carefully dissected By studying the X-ray together with the dissection, tiny areas of narrowing and obstruction not recognizable by other methods of study can be detected readily From the X-ray and the dissection, a colored diagram is made This diagram, together with the X-ray, are permanent records (Plate 26. page 55) The myocardial tissue can be examined microscopically and then discarded 52

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Plate 26 The complete preparation.
STOMOSIS
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Plate 27-ormal circulation
Plate 28 Myocardial irfarction.
RC
Fiata --A-910 festorus
Plate 30-Ann Deioni

·CHARACTERISTIC PATHOLOGICAL PATTERNS_SUMMARY ANGINA PECTORIS_Many Old Occlusions A fourth heart (Plate 30, page 55) obtained from a man 53 years of age, shows how extensive occlusions and anastomoses can be. The left circumflex artery had an old occlusion near its mouth. The first branches of the right coronary and the left descending arteries were also occluded There was an old occlusion of the left descending artery and also of its second major branch A fresh thrombus, the cause of death, was found in the right coronary artery and there was an old occlusion near this point Anastomoses had developed beyond these occlusions so that the branches received blood from the major vessels A seventh occlusion failed to stop the circulation The flow of blood must have been reversed in some of the terminal branches, for they received blood from the opposite sides of the heart An eighth occlusion, in a branch of the left descending also caused reversal of the flow of blood A ninth occlusion was found in another terminal branch The remainder of the vessels were killed by mass from both the right and left coronary arteries Despite these 9 old occlusions, this patient with angina pectoris was active in business up to 22 hours before death. There was only one, small, old infarction An analysis of the variations in the circulatory pattern lound in coronary artery disease shows the following First, complete occlusion of one or more of the major vessels is a common occurrence Second, these occlusions do not prevent longevity and physical activity, providing an adequate collateral circulation develops Third, angina pectoris occurs when following coronary occlusion the collateral circulation is not adequate to Supply the Demands of the myocardium during exercise 54

·Part 4
Treatment
of
Angina pectoris

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·PART 4 TREATMENT OF ANGINA PECTORIS A tremendous number ol methods of treatment have been advocated for angina pectoris (Plate 31, page 61) According to the published reports, each of these methods makes the patient Inore comfortable Little exact or comparative information of their effect has been available, however Since, so far as we know, angina pectoris exists only in humans the benefits of therapy must be evaluated not in laboratory animals but in patients. The value of any method of treatment can be measured objectively by the Standardized Exercise Tolerance Test For example, the value of nitroglycerin can be demonstrated as follows The amount of work which a patient can do without medication before developing pain is found by repeated tests under the usual standardized conditions of cold, food, and so forth which have been found to give constant results The patient then places a tablet under his tongue and waits a measured length of time for it to take effect The test is then repeated. By means of a counter and stop-watch, we again measure the amount of work which he can do By this method we can demonstrate that most patients after nitroglycerin can do more work, without pain, than was possible without medication Obviously, since most patients with angina develop their attacks on exertion, any treatment of value must enable the patient to perform more work belore developing pain. This objective method of study makes it possible to evaluate the effect of treatment without being in. iluenced by the impression of the patient or the physician This objective method of study has been used in the Angina Clinic of the Beth Israel Hospital of Boston since 1932, the results have proven of value in the clinical management of patients Up to the present time the ellicacy ol over 70 dillerent methods of treatment have teen tested and compared (Plate 32, page 61) A group of about 20 methods have been found of great value, others have been of slight or only moderate value, while despite the claims of the manufacturers, many are of little value

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·VARIATIONS IN THERAPEUTIC RESPONSE OF INDIVIDUAL PATIENTS THE NITRITES Generations of patients and doctors can testify to the value of nitroglycerin lor decreasing the length of attacks It is also helpful in preventing attacks For example, studies in one patient (hg 30. 200 center curve) showed him able to do 20 per cent more work of exercise is started 1 minute alter nitroglycerin After 2 minutes he can do 40 per cent more work After 3 minutes. 60 per cent more Shortly after this, however, the ellect diminishes rapidly and dis- 10 o appears within 10 minutes Ex- MIIUTES AFTER DITROGLYCERIE perience shows that this a moderate response to mtroglycerin (Figure 30) Other patients show far more stnking benefit They can do at least 100 per cent more work for at least one half hour after taking nitroglycerin (lig 30. top curve) A third group of patients show no response to this therapy (hg 30, bottom curve) The response to nitroglycerin can be used to determine the procability of a patient's response to other forms of treatment (Plate 35, PER COIT CHANGE IN ITI IS page 61) For example, one group of patients is able to perform approximately 100 per cent more work when given nitroglycenn When given othe drugs. they show a definite increase in exercise tolerance and, more important, practically complete disappearance of attacks in danly lite This group consists of a little less than one-third of the patients A second group is able to do approximately 50 per cent more work a'ter nitroglycerin When these patients are given other medicanon they show a definite decrease in frequency of attacks in daily lite but attacks are not likely to disappear entirely This group includes one third of the patients A tard group is unfortunate for they show no response to nitroglycerin or any of the usual methods of treatment This group includes 40 per cent of patients It is thus possible to dinde patients with angina pectoris into three groups on the basis of their response to therapy That these results are due to actual changes in the heart and not to psychological influence can be shown by taking electrocardiograms during and following exercise (Plate 36, page 61) Under ordi- 63

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·CONTROL STUDIES-ENTERIC COATINGS THE PURINES use According to animal experiments and electrocardiographic Theobromine and studies in patients, these drugs are vasodilators theophyline which are obtaned from cocoa or tea are relatively insoluable They can, however, be joined with many other substances to lorm loose chemical combinations which increase their solubility and ellectiveness Many of these have been prepared and are available for The comparative value of 18 different xanthine derivatives have been measured and demonstrated by the Standardized Exercise Tolerance Test A lew are o considerable value Many widely advertised brands, however, are o! little value In order to control these studies, and to eliminate the psychological factor, the response has been compared to that obtained following sodium bicarbonate or lactose prepared to resemble the medication being studied (Plate 34, page 61) The response to medication when disguised by dipping in tincture cudbear served as an additional control Electrocardiographic studies further differentiate between active and inert therapy The most effective of these xanthines are Theobromine Sodium Acetate, Theophylline Sodium Acetate, and Theophylline Calcium Salicylate (Plate 37, page 72) All the yanthines when given in suficient dosage cause gastric distress but this can be prevented by encasing them in an enteric coaung which enables them to pass through the stomach intact and disintegrate in the small intestine (Plate 38, page 72} patients absorption takes place in 4 to 6 hours (hg 33) It must be remembered therelore, that it is the tablet given belore reuring which 15 elective in the early morning In most JOURS HOUA 1719 270 33) ·NITROGLYCERIN AND OTHER NITRITES nary conditions, the patient illustrated shows definite changes in the S-T segment of the electrocardiogram at the time when an attack is precipitated by exercise When nitroglycerin or other effective vasodilators are given, the patient can perform a greater amount of work than is otherwise possible At the same time, the electrocardiographic changes ordinarily observed either do not occur or are markedly diminished Nitroglycerin can be absorbed readily by the mucous membrane under the tongue Since the duration of attacks is short, the medication must be absorbed within a period of a few seconds For this reason, the more soluble hypodermic tablets are preferable to tablet triturates A properly prepared tablet should dissolve in water at room temperature in about 1 minute The toxic or untoward effects of nitroglycerin are seen more commonly in young individuals than in those with arteriosclerosis They are due to vasodilation and consist of a burning and flushing of the face, together with headache, and occasionally faintness, if there is a marked fall in blood pressure In most instances 1/200 grain of nitroglycerin is as effective as larger doses and is less likely to give untoward effects Nitroglycerin is RESPONSE TO MEDICATION FREQUEXCY our most valuable drugs (figs 31, 32) It is clinically effective i in 60 per cent of patients (Groups 1 and 2) It is of low toxicity and low in cost Its use 60 before work results in an aver- NITROGLYCERIN age increase in exercise toler- GROUP 1 GROUP 2 GROUP 3 ance of about 120 per cent in The optipatients of Group 1 100 100 mum dose is 1 200 grain, but 1.400 every hour is of consider- (Figure 31) able value in some patients one of Ô RESPONSE TO MEDICATION DEGREE L over Amyl Nitrite can be used by inhalation It is an effective nitrite but offers no particular advantage nitro glycerin and is more costly The same is true of Octyl Nitrite which also is given by inhalation Erythol-tetranitrate and Mannitol Hexanıtrate are considerably less effective So. dium Nitrite is of little or no value PER CENT INCREASE IN C.LT 50190 XITROGLYCERIX CO20 NS020 GROəm (Figure 32) 64 ·QUINIDINC SULFATE QUINIDINE SULFATE Quinidine has not been used sufficiently in angina RESPONSE TO MEDICATION FREQUENCY pectons Experierce in over 100 patients has shown that this drug is clinically effective, low in toxicity in patients with angina, and low in cost The administration of the sulfate QUINIDINE in doses of 5 grans four GROUP 1 GROUP 2 GROUP 3 times a day helps approximately 44 per cent o! patients (ligs 36-37) What is more important is that it is often of (Figure 35) value in patients not benefitted by the xanthines Its use results in an increase in exercise tolerance of about 50 per cent RESPONSE TO MEDICATION DEGREE PER CENT INCREASE IN E QUINIDIHE fo ticos WAO hom (Figure 39) Objective evidence of the value of quinidine com be obtained from the study of the electrocardiogram during work (Plate 41, page 72) Alter quinidine is given, exercise fals to induce the S-T segment changes usually seen when no med.cauon is administered Quindine also cautes prolongation of the Q-T interval (the duration from the beginning of the QRS to the end of T) This spearhic effect shows that quinidine acts fo: about 6 hours alter administration ·VALUE OF THEOBROMINE SODIUM ACETATE page 72). The efficacy of these preparations can be illustrated by comparing them with nitroglycerin (Plate 39, Adminis tration of nitroglycerin before exercise enables patient, S W., to do over 75 percent more work than is otherwise possible This response reaches its maximum in 3 minutes and is gone in 20 minutes. The effect of Theobromine Sodium Acetate is equally striking. although somewhat less pronounced Fifteen minutes after the administration of a capsule or a tablet, this patient can do 57 per cent more work than was possible without medication This effect persists for about 3 hours The therapeutic action of RESPONSE TO WEDICATION TRAUENCY the enteric coated tablet is more delayed and also more prolonged The enteric coat. ing prevents absorption for about 4 to 6 hours, but its 46 therapeutic effect continues PURINES for almost 10 hours Follow GROUP) GROUP 2 GROUP 3 ing its use, this patient is able to do about 50 per cent more 50 work than was otherwise possible (Figure 34) RESPONSE TO MEDICATION DEGREE IC 033 MI The purines are of value in about 45 per cent of the total number of patients (ngs 34, 35). 85 per cent of those in group 1. but only 12 per cent in group 3 The average increase in exercise tolerance following the use of the purines is approximately 50 per cent PURINES < 150 INCREASE COD07 PER CENT NUCO FTCOOM (Figure 35) 66 ·SEDATIVES AND ANALGESICS COBRA VENOM RESPONSE TO MEDICATION FREQUENCY The use of cobra venom as an analgesic deserves special mention Many patients to whom the drug is given develop a marked de. crease in attacks of poun in daily life and are able to do considerably more work under standardized conditions Furthermore, this drug is of value in many patients who do not respond to other availacle medications (lig: 41, 42) 67 COM YDLOM GROUP 2 GROUP 3 GROUP 100 50 GO (Figure 41) PER CENT INCREASE IN CIT. donos con There are two draw- RESPONSE TO MEDICATION - DEGREE backs to its general use First, the drug must be injected intramuscularly every day for at least a week before an effect is obtanned, and it must be COULIYOION conunued indefinitely at least tvice weekly to maintain an eliect Many patients are unable to continue this form of treatment because of inconvenience and cost The 12.10 (2) second drawback is that it acts solely as an analgesic The lack of vasodilatıng ction can be stown hy electrocardiographic studies (Plate 42, page 72) If we compare the electrocardiogram with the patient standing at rest with that taken during an attack, we see the typical S-T deviation Cobra venom causes no change in the electrocradiogram at rest After exertion, howcver, although the patient does not experience pain, the electrocardio gram is soll typical of angina com Cobra venom is ol value for symptomatic reliel even though there is no basic cord:cc improvement In selected cases it may obviate the necessity for surgery AN ·SEDATIVES AND ANALGESICS SEDATIVES The sedatives have a definite place in the treatment of angina pectoris, both alone and in combination with other drugs Many such combinations are available on the market (fig 38). TE SOUVE 6. (Figure 36) RESPONSE TO MEDICATION FREQUENCY The beneficial results of the sedatives are probably due to a decrease in emotional activity which results in a decreased frequency of attacks As many patients state it SEDATIVES makes the pain easier to bear" GROUP 1 GROUP 2 GROUP 3 The sedatives most commonly used are the bromides and the barbiturates, especially pherobarbital (Figure 30) The opiates are extreme RESPONSE TO MEDICATION DEGREE ly valuable Since they are habit forming. they are best reserved acute exacerbatons of the disease - for SEDATIVES An increase in exercise tolerance following the use of these drugs is not common, but does OCCUT some patients who are helped by few other drugs (figs 39, 40) in (Figure 40) 68

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·ATROPINE THERAPY ACTING ON THE AUTONOMIC NERVOUS SYSTEM Therapy which acts on the autonomic nervous system includes atropine, physostigmine, and carotid sinus stimulation All these are of some value in angina RESPONSE TO MEDICATION FREQUENCY g I ATROPINE GROUP 1 GROUP 2 GROUP 3 (Figure 43) Only a few patients respond to atropine, but this drug is of importance because it is of benefit to some persons in group 3 (tigs 43- 44) RESPONSE TO MEDICATION DEGREE 150 PER CENT INCREASE IN E.T.T. ..50 100 ATROPINE co coaព URODAM (Figure 447 Caroud sinus pressure and physostigmine, both of which stimulate the vagus nerve also have a beneficial effect in some patients 70 ·OGU SURC. DRUGS DIGITALIS IN L.Lt AFTINE DIGITIUS KROV oor HÍ CENT INCREASE IN EU F 005 toons woon DS ITACIONES Flate 43-Digitalis may be injurious in angina pectons Plate 44 - Comparative value of medical and surgical procedures TREATMENT OF ANGINA TREATMENT OF NONAT 3.0 NITRITES DORIS MA QUINDI DEMAND $U??18 11 IL SUPPLY OLMAR NG PAN ATTACK ATTACK 1 Fla'e 45-Methods of decreasing demand 1.3 angina pectoris Plate 46-Methods of increasing supply angina pectoris TREATMENT OF ANGINA PATIE273 VITK AISIRA PURINES · 100DIDIC ATROPINC LE 31 SEDATIVES NO RESPONSE GROUP GROUP 2 GROEP . SYMP $CNG rivius : No PAIN ER 7 Syntimatte rolief without Plate 48the routine treatment ·O Plate 37-The most effective purines Flate 33 -Uncoated and enteric coated purines 69 PER CERT CHANGE IN LIL INKIDE NOURS ATTER MEDICATİOL. ate 39 —The value of theobromine sodium acetate Plate 40—Enteric coated potassium iodide privatnim TOIR YEROX L. AFTEN COINA VERON ممال COBRI YAHOM AT IEST ifth 1 titatis EJ, 2 TRITS ATTACK ATTACI Plate 41-Value of quinidine sulphate in angina pectoris Plate 42-Symptomatic value of cobra venon 72 ·ENTERIC COATED POTASSIUM IODIDE IODIDES The iodides are of undoubted value in those lew cases of angina secondary to thyro. toxicosis or syphilis The doses commonly used, however, have proven of little value in the usual case of angina pectors It frequently requires as much as 35 drops of the saturated solution to equal I CC or 1 gram of drug, hence 15 drops 3 times a day is really (Figure (5) a small dose (ng 45) Larger doses, one gram 3 or 4 times daily, have been found to be of greater value in a few cases, especially those in Group 3 who are RESPONSE TO MEDICATION - TASQUENCY 1.0 GM. @ 13 POTASSIUM IODIDE GROUP 2 GROUP 3 GROUP (Figure 45) unhkely to be helped by other medication In order to avoid gastric d:stress, this is best given as an enteric coated tablet (figs 46-47), (Plate 40, page 72) RESPONSE TO MEDICATIOX DEGREE 1.0 GM. PCR CENT INCREASE IN ST. 50 POTASSIUM IODIDE OCOR LOCOS waCOSO T

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·PARAVERTEBRAL ALCOHOL INJECTION-THYROID DENERVATION hali refused operation when the risks and likelihood of beneht were explaned to them As a net result, surgery was performed in only seven per cent of the patients with angina who came to the hospital for treatment The results in patient RS who was incapacitated by angina pectoris for over 6 years illustrate the effect of surgery on the sympathetic nervous system (hg 50) His exercise tolerance was 17 to 20 trips, and his pain was experienced in the second interspace on the left and along the inner aspect of the left arm After paravertebral alcohol BEFORE OPERATION E.T.T. 17-20 3 MONTHS AFTER PARAYERTEBRAL ALCOHOL INJECTION E.T.T. 13-26 NEURITIS IB MONTHS AFTER ET.T. 20-21 (Fr. 53) injection the seventy of the attacks decreased strikingly They were limited to a small area encircling the left wrist His abihty to work, however, was not increased Simultaneously, he developed a severe neundis whuch persisted for over a year Belore the neuritis subsided completely the anginal syndrome returned in its original location and severity Eighteen months after (hg 51) because of continucuon of his 18 MONTHS AFTER E.T.T. 20-21 DENERVATION THYROID 3 WEEKS POST OP. E.T.T. 16 5 WEEKS POST OP. LIT. 16 (Figure 5>> ·DIGITALIS-SURGERY-FREQUENCY OF OPERATION DIGITALIS The digitalis bodies deserve special mention, for these drugs are frequently harmful to patients with angina pectoris This can be shown objectively by electrocardiograms and exercise tolerance studies For example, when no medication was given, patient ML developed an attack on performing 40 trips, and the eletrocardiogram shows the typical S-T depression (Plate 43, page 73) When these studies were repeated after digitalization, the electrocardiogram taken at rest showed no striking changes On exercising, however, the patient developed a severe attack after 28 trips The electrocardiogram shows a marked depression of the S-T segment This striking decrease in exercise tolerance was accompanied clinically by a corresponding increase in the frequency and severity of attacks in daily life SURGERY ANGINA MILD BEFORE AXGINA MILD TREATMENT AFTER There are numerous reports in the literature on the surgical treatment of angina pectoris Obviously, evaluation of the results of surgery is just as unreliable as the purely clinical evaluation of medical therapy Experience at the Beth Israel Hospital indicates that in 46 per cent of patients with angina, the symptoms even without treatment are so mild that TREATMENT 30% UNGIA) SEVERE DESPITE TREATMENT POOR ONITION ( UOMEO SURGICAL RISKS (Figure 185 7 surgery is not indicated (fig 48) In another 24 per cent, the response to medical treatment makes surgery unnecessary This leaves 30 per cent of pahents in whom the symptoms were severe despite therapy (hig 49) Since angina pectoris is the result of an aging process, it is not surprising that onehalf of these are poor surgical risks Of the remainder, SURGERY REFUSED (Figure 49) 76 ·PARAVERTEBRAL ALCOHOL INJECTION—THYROID DENERVATION half refused operation when the risks and likelihood of benefit were explaned to them As a net result, surgery was performed in only seven per cent of the patients with angina who came to the hospital for treatment The results in patient R S who was incapacitated by angina pectons for over 6 years illustrate the effect of surgery on the sympathetic nervous system (lig 50) His exercise tolerance was 17 to 20 trips, and his pan was expenenced in the second interspace on the left and along the inner aspect of the left arm After paravertebral alcohol BEFORE OPERATION E.LT. 17-20 3 MONTHS AFTER PARAVERTEBRAL ALCOHOL INJECTION ET.T. 13-26 NEURITIS 18 MONTHS AFTER ET.T. 20-21 (Figure 50) Injection the severity of the attacks decreased strikingly They were limited to a small area encircling the left wrist His ability to work, however, was not increased Simultaneously, he developed a severe neunts which persisted for over a year Before the neunus subsided completely the anginal syndrome returned in its onginal location and seventy Eighteen months aller (lig 51) because of continuation of his 18 MONTHS AFTER E.T.T, 20-21 DENERVATION THYROID 3 WEEKS POST OP. ET.T. 16 $ WEEKS POST OP. ELT. 16 (Figure 51) ·TOTAL THYROIDECTOMY angina, thyroid denervation was performed He was more comłortable after this operation His exercise tolerance remained the same, but the pain was less severe and was limited to the left arm Five weeks later, however, the symptoms returned Sympathetic nerve surgery, therefore, results in symptomatic relief without any increase in ability to work -200 The most striking results which we have observed were 400 400 obtained by Total Thyroidectomy 300- - 300 (iig 52) This procedure lowers the metabolism and thereby de- 2004 creases the work of the heart Those patients whose basal 100 100 metabolic rates were decreased by 20 to 30 per cent showed an -0 20-30 12-17 6-9 average increase in exercise PER CENT DECREASE IX B.M.R tolerance of nearly 400 per cent They were also practically free (Figure 52) from attacks daily life Patients who showed a moderate fall in basal metabolism showed proportional improvement, while those who showed little change in meta, bolism had no clinical improvement and no appreciable increase in exercise tolerance PER CENT INCREASE IN E.T.T. in We have seen that few patients require surgery In suitable cases, however, the beneficial response to total thyroidectomy may be marked and the untoward effects negligible The comparative effect of medical and surgical therapy can be illustrated as follows (Plate 44, page 73) Following the use of the purines, patients in Group I show an increase in exercise tolerance of 70 per cent The use of quinidine results in a 75 per cent increase in exercise tolerance Nitroglycerin causes an increase of 120 per cent Cobra venom enables patients to do about 150 per cent more work Although the patient may be more comfortable following paravertebral alcohol injection, there is usually no appreciable increase in ability to work The same is true following denervation of the thyroid gland After total thyroidectomy on the other hand, the average increase in exercise tolerance of all patients studied was 180 per cent 78 ·PLAN FOR TREATMENT OF PATIENTS WITH ANGINA PECTORIS THE ROUTINE TREATMENT OF ANGINA PECTORIS Treatment must be individualized Specilc emotional or exertional factors responsible for attacks can be eliminated in many cases. In others hyperthyroidism, anemia or arrythias may be corrected with benefit in most patients, medication is necessary. As a result of measuring the value of 70 different therapeutic agents, it is possible to present a practical plan of therapy using those preparations most likely to be of value in the largest number of cases (Plate 48, page 73) The punnes, if given in adequate doses, are most likely to be of beneht These will help about 43 per cent of all patients, 85 per cent of Group I, 50 per cent of Group 2. but only 12 per cent of Group 3 ! medication is of value, it will be evidenced within a week by complete or almost complete disappearance of attacks in daily life. Any improvemen short of this is not due to the medication used. Il no satisfactory response is obtained, it is advisable to administer quinidine sulfate as the next drug most likely to be of benefit Sixty per cent of all patients are helped by either the purines or quinidine This includes all patients in Group 1, 70 per cent of Group 2, but only 24 per cent of Group 3 The treatment of the remaning 40 per cent of patients, especially those in Group 3, is the present problem and recent studies have concentrated on a search for therapeutic agents which will help this group Atropine sulfate, though not as valuable as the purines or quinidine, may help 10 per cent of such patients in Groups 2 and 3 The sedatives. phenobarbital or codeine sulphate, will help other patients in Group 3 and, of course, gre of value as an adjunct to other therapy in all patients There remains about 20 per cent of patients, two-thirds of whom are in Group 3 who respond to none of these medications In patients with severe angina, it is advisable to use combinations of medication Such treatment should begin with a period of complete bed rest Adequate sedatives, either barbiturates or opiates, should be given This may be combined with small frequent doses of nitroglycerin 1 400 every hour In some instances, it may be advisable to give an active punne in addition, and, if necessary, quinidine sulphate. This regime will result, usually, in complete disappearance of pain, unless there has been a recent coronary occlusion or there is a strong emotional element Cobra venom is advisable at the symptoms return when the pabent is allowed up and about again If this lals to give reliel, surgery should be considered total thyroidectomy in suitable cases, sympathetic nerve surgery in others

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·TREATMENT—SUMMARY In summary, since angina pectoris occurs when the Supply of blood is inadequate for the Demands of the heart, treatment may take 3 general forms, The first consists of decreasing the Demand for blood by rest, sedatives, or if necessary, decreasing the metabolic needs ol the body by total thyroidectomy (Plate 45, page 73). The second method of treatment consists of increasing the supply of blood by the use of drugs such as nitroglycerin, the purines, and quinidine sulphate (Plate 46, page 73) The third type of therapy (Cobra Venom and Sympathetic Surgery) should be used only where it is impossible to readjust the balance between Supply and Demand by the above methods (plate 47, Here, the underlying physiological mechanism responsible for the attacks is not altered, but the procedure interrupts the sensory nerves so that pain is not experienced. page 73) The aims of treatment in angina pectoris are First, relief of discomfort, Second, prolongation of life and prevention of myocardial infarction, and, Third, economic rehabilitation of possible, or at least prevention of cardiac invalidism The plan of treatment just outhned. together with a thorough understanding of the patient and his condition, goes a long way towards fulfilling these aims 80

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