On account of the wide range of the gradations as regards the degree of

severity or mildness, of the diversity of symptoms referable to the

different {757} forms of disease of the heart with which the affection

may be associated, and of the varied disorders which may be

accidentally connected, the clinical picture of angina is by no means

uniform. There is, however, no practical advantage in making formal

varieties of the affection. Eulenberg makes four different types, their

differential characters being based on the different nerves supposed to

be especially affected, as follows: 1st, excito-motor cardiac angina;

2d, regulator angina; 3d, excito-motor sympathetic angina; and 4th,

vasomotor angina. Assuming that there is ground for these pathological

distinctions (which, to say the least, admits of doubt), in a practical

point of view they involve difficulties not compensated for by

important bearings on diagnosis and treatment. One point of

distinction, however, has important bearings--namely, the existence of

angina with or without organic disease of the heart. It cannot be

doubted that in the vast majority of cases angina is incident to some

form of cardiac lesion. That it may exist without any appreciable

lesion is admitted. The propriety of recognizing it as a functional

disorder rests on the latter fact.[5] Practically, the coexistence of

organic disease of the heart or otherwise, and, if organic disease

exist, its nature and extent, are points which it is important to take

into account in the diagnosis with reference to prognosis and

treatment.

[Footnote 5: Of 71 cases analyzed by Gauthier, in 3 only was the

affection to be regarded as purely functional. Vide Eichhorst.]

DIAGNOSIS.--The diagnostic points in cases of angina are the præcordial

seat of the pain, its radiations thence into the shoulder and upper

extremity, generally of the left side, the character of the pain, the

accompanying anguish and sense of impending death, the coexisting

disorder of the heart (which occurs as the rule), and the voluntary

immobility of the body. These are positive criteria which, if marked,

render the diagnosis easy and certain. The diagnosis is further

substantiated by finding the signs of organic disease of the heart,

especially if there be lesions at the aortic orifice or within the

aorta. Well-marked angina is in itself strong presumptive evidence of

organic disease of the heart. Not infrequently the existence of the

latter is for the first time discovered by an examination suggested by

the occurrence of an attack of angina. The cases in which the diagnosis

involves difficulty are those in which certain of the above-mentioned

diagnostic points are either wanting or not well marked.

The affections which may be mistaken for angina are gastralgia and

intercostal neuralgia. In gastralgia the pain is seated below the

præcordia. It may radiate in different directions, but does not extend

to the upper extremities, and is not accompanied by irregularity of the

heart's action. The patient writhes and changes the position of the

body in the effort to obtain relief. There is not a sense of impending

death. The paroxysms are of much longer duration than those of angina.

These differential points should suffice for the discrimination.

An acute attack of intercostal neuralgia does not differ so widely from

angina, but the differential points are generally distinctive enough

for a positive diagnosis. The pain in intercostal neuralgia is not

seated in the præcordia. It does not shoot into the upper extremities;

it is increased by the act of inspiration; the peculiar anguish of

angina is wanting; the action of the heart is likely to be regular; and

the diagnosis is confirmed by finding tenderness over circumscribed

areas in the intercostal spaces anteriorly, laterally, and posteriorly.

Cardiac lesions in cases of angina are to be excluded by finding no

physical signs of their existence. But it is to be remembered that

angina is not infrequently associated with lesions not readily

recognized by signs--to wit, obstruction of the coronary arteries and

fatty degeneration of the heart. Persistent feebleness of the heart's

action and symptoms other than angina {758} incidental thereto render

it probable that one or the other or both of these lesions exist. It is

probable that these lesions have been overlooked in examinations after

death in some of the cases in which angina has been reported as not

connected with any organic affection of the heart.

PATHOLOGY AND ETIOLOGY.--The paroxysms of angina have the distinctive

traits of neuralgic affections as regards the character of the pain,

its extension in the course of sensory nerves, the occurrence of

intermissions, the absence of fever, the functions of digestion and

assimilation remaining often unaffected, and the attacks not always

being referable to any exciting cause. The association of the

affection, as a rule, with organic disease of the heart is evidence of

course of some pathological connection. What is this connection? A

difficulty in answering this question arises from the fact that the

affection is associated not with any one lesion, but with different

lesions. It may be associated with obstruction (usually from

calcification) of the coronary arteries, with insufficiency of the

aortic valves, with rigidity from calcareous degeneration of the aorta,

with aortic aneurism, and with fatty degeneration of the heart, these

different morbid changes existing either singly or more or less of them

in combination. The question then resolves itself into another--namely,

What is the pathological condition common to these different lesions

which stands in a special etiological relation to angina? It is a

logical conclusion that the affection must depend upon some condition

which is common to these lesions. The association with the lesions is

too frequent to be explained by mere coincidence. The etiological

relation involves evidently a condition which exists only in a small

proportion of the cases of these lesions. This statement is a logical

deduction from the great infrequency of angina and the frequency of

these varieties of organic disease of the heart. I submit, as the most

rational theory, that the pathological condition on which the angina

depends is ischæmia of the heart. This theory is supported by the

frequency of the instances in which in cases of angina the coronary

arteries are obstructed; by the fact that not very infrequently this is

the only lesion found after death (two instances having fallen under my

own observation within the past year); by the association with aortic

insufficiency and rigidity of the aorta, lesions which interfere

materially with the supply of blood to the heart if it be admitted that

the blood is driven into the coronary arteries, not during the

ventricular systole, but by the recoil of the arterial coats in the

ventricular diastole; and by the association with fatty degeneration of

the heart when, owing to the weakness of the heart's action, the supply

of blood to the muscular structure of the heart must be diminished.

That the sudden withdrawal of a supply of blood to a part may occasion

neuralgia is shown by the intense pain in the limb which directly

follows embolism of the femoral artery. Moreover, general anæmia, as is

well known, favors the recurrence of neuralgia in various situations.

The cardiac nerves in which the pain is seated are doubtless sensory

fibres of the pneumogastrics. Their anatomical connections with the

brachial plexus will explain the extension of pain to the left upper

extremities. To account for the pain in parts which have no direct

connection with the cardiac nerves, it may be assumed that in angina,

as in other neuralgic affections, a centripetal influence conveyed to

the nervous centres may occasion pain referable to different

situations. This explains the shifting of pains which is one of the

diagnostic traits of neuralgia. The explanation of the disturbed rhythm

of the heart's action so often coexisting with the neuralgic pain is

not more difficult than in cases of functional disorder disconnected

from angina. For what is to be said of the rationale the reader is

referred to that portion of this article which treats of Functional

Disorders of the Heart.

{759} Angina, as a purely functional affection--that is, not

symptomatic of any organic lesion of the heart, and not due to any

structural change in, nor mechanical pressure upon, nerves--is obscure

as regards its pathology and etiology, but not more so than many other

neuralgic affections. As already stated, cases in which it is thus

purely functional are few in number--fewer even than has been supposed,

because there is reason to believe that lesions have been overlooked.

Moreover, cases which have been reported render it probable that in

some instances in which the heart has been found free from appreciable

lesions nerves entering into the cardiac plexuses may be the seat of

structural changes or may be subject to pressure from a morbid growth.

But there are cases in which no lesions are discernible during life,

and in which the existence of lesions is disproved by complete

recovery. The affection under these circumstances must be regarded as

purely functional. There is no positive knowledge of the etiology in

these cases. The affection has been attributed to gout, to hysteria, to

the action of cold, to the use of tobacco, and to other causes. These

causes may have a certain amount of agency, but there is an unknown

intervening link in their etiological connection concerning which, in

the present state of our knowledge, it is useless to speculate.

Age and sex have an undoubted influence in the etiology. The affection

very rarely occurs under middle life, and it occurs in men much oftener

than in women.

PROGNOSIS.--As a very rare exception to the rule, a single paroxysm

only may occur, the patient living for many years without any

recurrence. Recurring paroxysms sometimes are separated by long

intervals--weeks, months, and years. In the majority of cases, however,

paroxysms recur with more and more frequency and with increasing

severity. Under these circumstances death may take place after a long

period of suffering.

The liability to sudden death is an important point in the prognosis.

This may occur in the first paroxysm. An instance has fallen under my

observation within a few months, there having been no signs previously

indicative of disease of the heart. Calcareous obstruction of the

coronary arteries was the lesion found after death. A person subject to

paroxysms of angina must be considered as in more or less danger of

sudden death with the recurrence of each paroxysm. The physician should

be sufficiently impressed with the importance of this fact. While it is

doubtful whether it be the physician's duty to apprise the patient of

the fact, the danger should always be communicated to some discreet

relative or friend. To do this is a duty which the physician owes to

himself as well as to the patient. If he omit it, he exposes himself to

censure should sudden death unexpectedly take place. The mildness of

the paroxysms which have already occurred does not afford a positive

security against the liability to a severe and fatal paroxysm. But it

is a hopeful consideration that paroxysms may recur more or less

frequently for an indefinite period without proving fatal. At this time

I am cognizant of three cases in which paroxysms have recurred

frequently for several years, the patients, with that exception, having

had fair health. Let not the physician, therefore, predict with

positiveness that a patient with angina will die sooner or later in a

paroxysm. The uncertainty is a ground of encouragement as well as for

apprehension.

The coexistence of organic disease of the heart and the nature of the

cardiac lesions have a very important bearing on the prognosis. The

danger is in proportion to the importance of these. Recovery is never

to be expected when the affection is associated with well-marked

cardiac lesions, and there is always great danger in the recurrence of

paroxysms when the associated lesions are in themselves dangerous.

Lesions which give rise to free aortic regurgitation and to fatty

degeneration of the heart involve more or less {760} danger of sudden

death, irrespective of angina. It is evidence of greatly increased

danger if paroxysm of angina be superadded.

During a paroxysm of angina the immediate danger is to be estimated by

the symptoms denoting disturbance of the heart's action. The danger is

great in proportion as the action of the heart is feeble, irregular, or

intermitting. Per contra, the danger is less in proportion as the

deviation from the normal force and rhythm is small. It may be said

that there is no danger so long as the heart's action remains

unaffected, but the disturbance may be slight or wanting at the outset

of a paroxysm and afterward become fatally great.

A favorable prognosis may be entertained when there are no signs of

cardiac lesion, and when there is little or no disturbance of the

heart's action during the paroxysms. Let it be borne in mind that such

cases are exceptional and extremely rare. Let it also be borne in mind

that lesions especially apt to be associated with fatal paroxysms may

be latent--namely, obstruction of the coronary arteries and fatty

degeneration. The latter fact renders it proper that a favorable

prognosis should always be formed with a reservation, while the fact

that recovery takes place in a few well-marked cases of angina renders

it improper to withhold encouragement whenever lesions are not

discoverable and the paroxysms are not accompanied by alarming symptoms

referable to the heart's action. The long tolerance of the affection in

some cases is not to be lost sight of with reference to the

encouragement which may be fairly derived therefrom.

The immediate cause of sudden death in a paroxysm is probably an arrest

of the heart's action in diastole, or such a degree of diminution of

the force of its action that the accumulation of blood within its

cavities induces paralysis from distension.

TREATMENT.--It is important that a paroxysm of angina be treated as

soon as possible, not alone with a view to the relief of pain, but to

remove immediate danger. If the physician be present, an opiate in a

form to act promptly should be given either by the mouth or

hypodermically; the latter mode is to be preferred. Laudanum or a

solution of a salt of morphia is the most eligible form if given by the

mouth. If the heart's action be weak and irregular, a diffusible

stimulant is indicated. If at once available, chloric ether, Hoffman's

anodyne, and the compound tincture of lavender act efficiently. If

these be not at hand, an alcoholic stimulant should be given, diluted

but little, and the doses repeated at short intervals until the

paroxysm ends and the disturbed action of the heart has ceased. The

duration of paroxysms is generally so short that a physician is rarely

present unless they recur after brief intervals. A patient, therefore,

subject to angina should be provided with remedies and instructions as

to their use at the instant a paroxysm occurs. The amyl nitrite, first

recommended in this affection by Brunton, is a remedy of signal benefit

in some cases. From two to five minims may be inhaled at the

commencement of the paroxysm. It is especially indicated when the

characters of the pulse denote arterial tension. Caution is to be

exercised in its use if there be notable weakness of the heart's

action. Sinapisms, stimulating embrocations, and fomentations applied

to the chest have a certain measure of utility, but they should not

take the place nor delay the use of remedies which are more efficient.

A still more important object of treatment than relief in the paroxysms

is their prevention. During the intervals this object claims assiduous

attention. First in importance is the avoidance of all exciting causes.

Bodily exercise is to be kept within the limits required in order to

incur no risk of a paroxysm being produced. The same precaution applies

to mental excitement. Unhappily, this is not as easy as the avoidance

of muscular exertion. John Hunter's saying, that his life was at the

mercy of any scoundrel who chose to {761} insult him, proved a

prediction. He fell dead on receiving an insult from one of his

colleagues at St. George's Hospital. Sexual intercourse I have known to

prove an exciting cause. Excesses in eating and drinking are in this

category. The diet, however, is not to be reduced below the full

requirements for nutrition, and wine or spirits, as conducive to

digestion, are in some cases serviceable. The use of tobacco is to be

interdicted.

Coexisting affections which have no special pathological connection

with the angina may act as auxiliary causes, and therefore claim

attention. Gout is to receive appropriate treatment. Anæmia especially

is to be removed. This condition strongly conduces to the development

and the continuance of neuralgic affections. Chalybeate remedies and

the dietetic treatment are called for if this condition coexist. It is

a rational indication to supply the heart with good blood if it be true

that angina depends on an ischæmic condition of this organ.

Associated cardiac lesions are to be treated according to symptomatic

indications, as in cases in which angina does not occur. Digitalis may

be used under the proper restrictions. I have known this remedy to

prove highly useful in preventing the recurrence of paroxysms. Nux

vomica is sometimes useful as a cardiac tonic.

Various drugs have had repute as empirical remedies. Of these may be

mentioned the preparations of zinc, arsenic, the nitrate of silver,

phosphorus, the bromine salts, the iodide of potassium, and quinine.

There is no proof that these remedies have any special therapeutical

effect in this affection, but that they are sometimes useful there is

abundant testimony. Trial should be made of them, with proper care in

their administration. Electricity in the form of the induced and of the

constant current has been advocated as not only serviceable, but as

effecting in some instances a permanent cure.[6] Beard and Rockwell

have found general faradization useful in a few cases.[7]

[Footnote 6: Vide Eulenburg in _Ziemssen's Cyclopædia_, vol. xlv. p.

54.]

[Footnote 7: Vide _Medical and Surgical Electricity_.]

Exophthalmic Goitre (Graves' Disease; Basedow's Disease).

This affection is characterized by three striking symptomatic

events--namely, persistent increase of the frequency of the heart's

action, enlargement of the thyroid body, and protuberance of the

eyeballs. The name exophthalmic goitre relates to the last two of these

three events. It is defective, inasmuch as it does not include the

increased frequency of the heart's action, which is the primary one of

the three events, and the only one which is never wanting. As an

individual affection it was first described by Graves in 1835, although

cases in which these events were associated had been previously

reported. Parry collected 7 cases in which the affection of the heart

was associated with thyroid enlargement, and in 1 of these cases

exophthalmia existed. An account of these cases was published in 1825.

The name Graves' disease, proposed by Trousseau, has been adopted by

French, English, and American writers. Basedow's disease is the name

given to the affection by German writers. The affection was described

by Basedow in 1840 under the name Glotz augenkrankheit.

There are cases in which one of the events in this symptomatic triad is

wanting, the cases in other respects corresponding to the affection.

The exophthalmia is the event oftenest wanting, the goitre, the

functional disorder of the heart, and the associated phenomena being

the same as if protuberance of the eyeballs coexisted. In some

instances the goitre alone is wanting. The name exophthalmic goitre is

not strictly applicable to these cases, but that the affection is

essentially the same as when the three events {762} are present cannot

be doubted. It is a chronic affection, being in the great majority of

cases of long duration. Exceptionally, it is developed suddenly and

disappears after a few days. In these cases the affection has been

distinguished as acute, but its claim to be so called rests exclusively

on the shortness of its duration.

SYMPTOMATOLOGY.--Of the three cardinal events, the increased frequency

of the heart's action is the first in the order of time. This precedes

the other events usually for several weeks or even months. The

frequency varies in different cases within wide limits--namely, from 90

or 100 to 150 beats, and even more, per minute. There is notable

variation at different times in the same case. Generally, the frequency

is greatly increased by exercise and mental emotions. In other words,

irritability of the heart is in most cases a marked feature. As a rule,

there are none of the disturbances of action, in other respects than

frequency, which are found in cases of functional disorder not

associated with exophthalmic goitre. The action may be intermittent or

in other respects irregular, but in most cases the rhythm is not

disturbed. The patient is conscious of the heart's action, and is

annoyed by it, especially under any excitement; but there is not that

distressing sense of the disorder which is felt in the paroxysms of

palpitation with irregularity of action considered in the first

division of this article. At the outset and for a considerable period

there are no signs of any organic disease of the heart, or if the

latter be present the association is accidental; the disordered action,

as far as it relates to the affection under consideration, is purely

functional. At a later period there may be enlargement of the heart as

a result of long-continued increased activity of function. From the

first cardiac murmurs are generally present at the base and over the

body of the heart. These are blood-murmurs due to coexisting anæmia.

Following the increased frequency of the heart's action, after a

variable period enlargement of the thyroid body occurs. The enlargement

may be rapid, but in most cases it takes place slowly, and ceases when

it has reached a moderate degree. Cases are exceptional in which the

degree of enlargement is such as to occasion any obstruction to

respiration. Almost invariably both lobes of the thyroid body are

enlarged, but the enlargement is generally not equal on the two sides,

and, as a rule, it is greater on the right side. The enlarged lobes are

soft at first, afterward becoming hard. The subcutaneous veins over

them are often distended. Pulsation of their arteries is apparent to

the hand and to the eye. A systolic arterial blowing murmur and a

continuous hum are heard when the thyroid region is auscultated. In

some instances the murmur is like that of an aneurismal varix. As a

rule, murmurs are heard over the carotid artery and the jugular vein. A

thrill or fremitus is often felt by the hand placed upon the thyroid

body. The thyroid enlargement is due at first chiefly to dilatation of

the arteries and veins. Hyperplasia of the fibroid tissue occurs

afterward, and then the enlarged gland becomes hard to the touch. The

size of the enlarged thyroid body is often found to vary considerably

at different times--a fact attributable to varying degrees of the

dilatation of the vessels and of the consequent hyperæmia.

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