Anatomical charateristics, causes and pathology, symptoms, diagnosis and Prognosis, homeopathic treatment of Endocarditis and Myocarditis….

) New Remedies, 2nd Ed. Dose: the first dilution has been found most useful. Asclepias syriaca, as you will observe from the provings, will likely prove of service in endocarditis from renal affections, or from a retention of scarlatinal poison. Dose: the tincture, a few drops, in water. Baptisia will prove in your hands an unrivalled remedy in endocarditis during or following typhoid or other low fevers, especially when you have present its well known characteristic symptoms. Dose: the first decimal dilution, in drop doses. Cactus grandiflorus will never fail you, in the severest cases of the acute form, if that peculiar symptom, “Sensation of constriction of the heart, as if from a band around it, preventing movement,” is present. No other remedy equals it in controlling the severe nervous palpitations common to the disease. I get the best effects from the 1st dil. Cimicifuga must not muscular structure, would be chiefly indicated.

Definition – Anatomical Characters – Causes and Pathology – Symptoms – Physical Signs – Diagnosis – Prognosis – Treatment.GENTLEMEN : I shall, in this lecture, take up one of the most important of the inflammatory affections of the heart; more important than pericarditis, because of the serious valvular lesions which it usually leaves.

An inflammation of the membrane which lines the cavities of the heart, and is duplicated to cover the valves, is called endocarditis. It is not more than fifty years since this disease has been clearly described and recognized, but clinical experience has demonstrated that it is by no means infrequent. In the majority of cases it occurs as a complication of acute rheumatism. The inflammation may be acute, subacute, and chronic, but these distinctions are not of practical value.


This inflammation is said to be confined, in the vast majority of cases, to the membrane lining the cavities of the left side of the heart. The lining membrane of the right auricle and ventricle is rarely inflamed, and when inflamed it is also present on the left side.

All portions of the endocardial membrane of the left side are not equally subject to inflammation. You must bear in mind that it generally attacks the membrane covering the valves and lining the orifices, and that it is in these situations that it leaves the most troublesome results. There are two reasons for the tendency to attack these localities. 1st. The membrane here is most exposed to the blood-currents; the valvular portion is in constant motion, and is almost constantly in a tense or strained condition. 2nd. The membrane is here underlined by fibrous tissue, and not, as in other situations, in close proximity to the muscular walls of the heart.

Flint believes there are grounds for believing that the foetus in utero is subject to endocarditis, and that the inflammation is then limited to the right side. He believes the malformations found in infants – cyanosis, etc. – may thus be accounted for.

In the occasional instances in which death has occurred during the inflammation, there has been found (a) redness from vascular injection, (b) alternations in the membrane itself, and (c) the presence of inflammatory products.

(a) Redness, due to endocarditis, is caused by injection of the vessels which ramify in the areolar tissue beneath the membrane, but it is not always found, and may disappear as a post-mortem change. But the redness, when found, is not always a proof of inflammation, for it may be the effect of the imbibition of haematin dissolved out of the red globules of the blood which the cavity contained after death. This redness from imbibition, however, is distinguished from that due to inflammation by these differences: (1) It is not an arborescent, but a uniform redness, and when examined with a lens, injected vessels are not visible; (2) It has a deeper and darker color than inflammatory redness; (3) It is not more likely to be limited to the valves and orifices, and is more conspicuous in the arteries than in the cavities of the heart. Moreover, in redness from imbibition, the membrane preserves its normally firm, polished appearance.

(b) Alterations in the membrane itself are much more indicative of inflammation than redness. These changes are: “loss of the smooth, polished appearance which the membrane has in a healthy state; instead of which it becomes opaque, rough, velvety, and felt-like; more or less swelling and softening; and brittleness of the subjacent areolar tissue.” (Flint.)

(c) The presence of inflammatory products will prove to you conclusively, if present, that endocarditis has existed. You remember that the endocardium, unlike other serous membranes, is not a shut sac, wherein inflammatory products may be collected and retained. Such products may be washed away by the currents of blood and carried along with the circulation. Another difference is that the free surface of the endocardium is in contact with the blood itself, and that while the fluid detaches and removes morbid products, it may also furnish deposits by yielding a portion of its fibrin; which undergoes coagulation.

These products of inflammation, then, may be derived from two sources, namely: the exudation of lymph, and the coagulation of fibrin from the blood. The extended lymph occurs on the free surface of, as well as beneath, the endocardium. That on the free surface, if not washed away, forms layers, as in pericarditis. The roughness of the exuded lymph attracts – as it were – fibrin from the blood, as the threads did when passed through the arteries in Dr. Simon’s well known experiments. When we consider that in acute rheumatism the fibrin of the blood i in excess, we can see how the tendency to fibrinous depositions is greatly increased in endocarditis from that cause.

Various morbid growths are to be enumerated as the result of endocarditis. They are commonly called vegetations, and are found either at the base or the free extremities of the valves. They occur in the form of small granular masses, or beads, from the size of a pin’s head to a millet seed, studding the margins of the curtains of the mitral valve, and fringing the crescentic extremity of the fibrous portion of the segments of the valves of the aorta.

Virchow denies the occurrence of the exudation of lymph in endocarditis. He charges the formation of excrescences and membraniform layers wholly to proliferation or morbid growth, and the coagulation of coagulated fibrin from the blood within the cavities of the heart. Flint, however, believes that morbid growths may have, as a nucleus, the true vegetations or exuded fibrin, to which may be added the coagulated fibrin from the blood.

Other morbid changes may occur, namely: loss of substance by ulceration and erosion; perforation of the valves; lacerations; and even gangrene. Among the rarer occurrences are adhesions of the valves of each other, or to the walls of the heart.

The remote effects of endocarditis will be considered in future lectures, when we come to consider the Organic Diseases of the Heart. I will only say here, that in a very large proportion of cases, valvular lesions, involving either obstruction or regurgitation, or both, owe their origin to the anatomical changes which occur as a result of endocarditis. It may be months or years before serious structural changes obtain; but you should carefully watch your patients who have had this disease, and be on the look-out for the first symptom of organic affection, for it is rare that they are escaped altogether.


Endocarditis is rarely an idiopathic affection. Like pericarditis, it is usually associated with acute articular rheumatism. It differs, however, from the former, in occurring independently of that affection, and is a comparatively rare affection as occurring in other pathological connections. When the two diseases occur together, the combined affections are designated endo-pericarditis.

Of 474 cases of rheumatism, collected and analyzed by Fuller, endocarditis existed in 214, the ratio being 1 to every 2.25 cases. Of 204 cases, endocarditis existed in 138, pericarditis in 19, and endo-pericarditis in 38. Bamberger says endocarditis occurs in 20 per cent. of all cases of rheumatism.

The connection of endocarditis with acute rheumatism is the same as that of pericarditis. It is not developed as a metastasis, but depends upon the same morbid condition that causes the rheumatic affection.

Endocarditis may become developed in connection with renal disease, owing to the analogy of structure between the endocardium and the serous membranes. (See Pericarditis.)

It is said that in non-rheumatic endocarditis the aortic valves are more likely to be the seat of inflammation than the mitral; the reverse being true, as has been seen, of rheumatic endocarditis.

Endocarditis and pericarditis are frequently associated. Fuller says that in 204 cases, analyzed by him, this combination existed in 38. Either affection may take precedence in point of time.

Endocarditis is sometimes associated with pleurisy or pneumonia. It is less frequently associated with these affections than pericarditis. Endocarditis is occasionally developed in connection with the eruptive and continued fevers, and with that morbid condition known as pyaemia, but its occurrence in these connections is rare. It may also be produced by injuries of the chest; but cases of traumatic endocarditis are rare.

The experiments of Richardson, made by injecting into the peritoneal cavity of a dog a solution of lactic acid, containing ten per cent of the acid, seems to show that lactic acid, when absorbed into the blood, will cause endocarditis.

In about twelve hours after the operation, the symptoms and physical signs of endocarditis appeared. Richardson regarded his experiment as proving synthetically that rheumatic endocarditis is produced by a similar agent. In rheumatism the morbid conditions are supposed to be caused by the presence of lactic acid in the blood.


Endocarditis may give rise to immediate pathological results which are important, namely: emboli, or plugs, consisting of detached vegetations, or excrescences, which, propelled with the current of blood into the arteries, are at length arrested in their course in trunks too small to permit their future progress, giving rise to arterial obstruction and diminished supply of blood to certain parts. For a further consideration of this subject, see Valvular Lesions.

“The solidified products in cases of endocarditis, namely: fibrin and lymph, are, to a greater or less extent, disintegrated by the blood-currents, and carried into the circulation, either in solution or suspended in the form of minute particles. It is supposed that the comminuted solid deposits, transported to different organs, and becoming arrested in the capillary vessels, may give rise to vascular obstruction and secondary inflammation in these organs. The kidneys and spleen are most likely to be the seat of disease thus induced. These effects are primarily mechanical; but it is highly probable that morbid changes in the blood itself are sometimes induced by the admixture of the liquid products of endocardial inflammation. It can hardly be otherwise if, as is not improbable, purulent matter is occasionally formed on excoriated or ulcerated surfaces, which are in some instances observed after death in cases of endocarditis.” (Flint.)

The formation of large masses of fibrinous coagula in the cavities of the heart belongs to the immediate pathological effects of endocarditis. It is supposed that these antemortem clots are the formations called by the older writers, polypi of the heart.


The symptoms of endocarditis are less distinctive even than those of pericarditis. Occurring generally in connection with acute rheumatism, its symptomatic indications are merged in those of the latter affection. In a large proportion of cases, there are no symptoms which attract attention to the heart as the seat of any disease. Examination, however, with a view to determine the presence, or otherwise, of phenomena which point to endocarditis, may elicit symptoms which are of importance in the diagnosis. These symptoms consist of pain referable to the heart, symptomatic fever, and excited action of the organ, or palpitation. Symptoms arising from obstruction to the passage of blood through the orifices of the heart, do not belong properly to the symptomatology of endocarditis, but are due either to lesions resulting from endocardial inflammation, or to accidental events, such as the formation of coagula. (Flint.)

Pain is very rarely a prominent symptom, and, as in other serous inflammations, is sometimes altogether absent. Even when it is present it is not easy to refer it to endocarditis, except by taking into account other symptoms, and especially the physical signs. The pain is generally dull and obtuse, rarely sharp or lancinating. A feeling of uneasiness hardly amounting to pain, is sometimes referred to the praecordia. The suffering which patients endure from the pain in the joints is so much more severe, that they will not be likely to mention the uneasiness in the heart unless you question them closely. If the pain in the region of the heart is so severe and acute as to cause complaint, the probabilities are that pleurisy or pericarditis is present, rather than endo-carditis.

The fever is not of any importance, for it is not distinctive of this disease.

Palpitation in endocarditis may arise indirectly from excitation of the muscular structure of the heart. The action of the heart may be irregular, as well as unnaturally excited.

The pulse may not correspond with the action of the heart, for while the latter may be acting with increased force, the pulse may be weak.

If you observe these symptoms occurring during the course of acute rheumatism, you may safely suspect the presence of endocarditis, and you should resort to physical examination without delay.


Increased extent and degree of dullness on percussion, due to tumefaction of the heart, and accumulation of blood within its cavities, is considered by Bouillard and others as a physical sign of endocarditis. Flint, however, doubts whether the cardiac enlargement often, if ever, exceeds the limit of healthy variations. He thinks if the heart is found enlarged, there must have been a previous hypertrophy. He says, “how far the size of the heart undergoes alternations during the progress of endocarditis, I am unable to say from my own observations, but it is evident that percussion cannot afford very important information with reference to this disease, except in a negative point of view, that is, by aiding in the exclusion of other cardiac affections, more especially pericarditis.”

Palpation and inspection will furnish evidence of excited action of the heart. The impulse is seen and felt to be more violent than in health, or out of proportion to the amount of febrile movement which exists. But the signs furnished you by these methods of exploration will be of little value to you except as associated with other evidence of endocardial inflammation.

Auscultation will furnish you with the only positive proof of the existence of endocarditis, and this proof is the development of the endocardial murmur.

This assertion has been substantiated by clinical experience, and you should give particular attention to its study. The murmur is usually soft, having the character of a bellows-sound. It is systolic, for it accompanies the first, or systolic sound of the heart, but you will not find it always at the commencement of the disease. In fact, its existence is considered rare in that stage. I cannot give you any certain data as to the period of inflammation in which this murmur occurs. There are conflicting opinions on this point. The time of its appearance is, however, in the opinion of all authorities, quite variable. The endocardial murmur is not, of itself, absolute proof of existing endocarditis. Previous valvular lesions may be a cause of the murmur. It occurs in consequence of blood-changes, independently of inflammatory or organic disease of the heart.

Under what circumstances then you will ask, is the presence of the murmur a diagnostic symptom of endocarditis? If you find an endocardial murmur in connection with symptoms denoting cardiac inflammation, and if acute rheumatism co-exists; and, further, if you have made previous careful explorations, and failed to discover any murmur, you may then conclude that the murmur you have detected is a sign of endocarditis. If, however, the murmur is discovered on first examination the symptom is of doubtful value.

A murmur developed by endocarditis generally continues not only throughout the duration of the disease, but even afterward. There seem to be some exceptions to this rule, for Flint says he has repeatedly known a mitral murmur to disappear entirely after recovery from rheumatism, when it was very marked during the disease. This could only occur in those rare cases in which the swelling of the valves diminishes, and the vegetations are detached and washed away, leaving the endocardial surface smooth.

I need not inform you of the cause of the murmurs alluded to. It is doubtless due to a roughness of the endo-cardial membrane covering the valves, produced by the lymph, fibrin, and vegetations; although some authors have conjectured that the murmurs were due to a spasmodic action of the papillary muscles, preventing the mitral valve from fulfilling its function – allowing regurgitation to take place.

The heart-sounds may be abnormally modified during endocarditis. Reduplications have been observed. The first sound, and sometimes the second, may be less distinct than in health, or the first sound may be wanting.


You will find that the diagnosis of endocarditis does not depend upon symptoms, but almost entirely on evidence developed by auscultation. Those of you who attempt to rely upon symptoms alone will necessarily overlook this important disease, and allow your patients to lose the aid which might be afforded in the prevention of organic disease. Never neglect this in cases of acute rheumatism. Examine your patient every day, and be on the watch for the endocardial murmur, which is the only sure evidence of this disease.

But, as I stated a few moments ago, you cannot give a positive opinion unless you have been watching for this murmur at a time before it existed, for if you heard it at the first examination, it may have previously existed from some valvular lesion of long standing. You will readily deduce from this caution, that will be very difficult, if not impossible, for you to detect endocarditis in a patient who has any organic disease of the heart.

As idiopathic endocarditis is the rarest of all diseases of the heart, I will not enter into discussion of its diagnosis. I must inform you, however, that pericarditis is so often associated with endocarditis, that you will rarely find the latter free from the former. In the diagnosis of endo-pericarditis, you will have to compare the signs of both: but, happily, the treatment of these affections is not materially different.


The prognosis of endocarditis is generally favorable, so far as any immediate danger to life is concerned. The symptoms may continue, and the condition become chronic, and cause great inconvenience, and exist for a long period. Chronic endocarditis may be suspected if the patient continues to complain of uneasiness in the heart, and that organ continues unnaturally excited. But this disease, when chronic, so nearly simulates valvular disease, that the prognosis depends on the extent of the structural lesion.

Certain accidental events may occur during endocarditis which may seriously endanger life, namely: the formation of fibrinous coagula; the detachment of vegetations or of masses of fibrin or lymph, constituting emboli; the admixture of disintegrated solid deposits; and purulent infection of the blood.

If we can judge of the prognosis from recorded clinical experiences, we can believe that, in a large majority of cases of endocarditis, recovery takes place without serious accidents. The cardiac symptoms gradually disappear. The patient, however, is generally left exposed to the evils arising from valvular disease, which may become developed at a period more or less remote, unless your treatment has prevented such a result.


The treatment of endocarditis cannot be diagnosed of so summarily as some authors have done, by asserting that there is “no essential difference” in the treatment of endocarditis and pericarditis. Not only is the treatment not the same, but the objects of treatment are dissimilar. Flint very tersely observes, that in pericarditis the compression of the heart by the accumulation of liquid within the pericardial sac is a source of distress and danger; and to prevent this accumulation, and promote its removal, are important therapeutical ends. In endocarditis, however, the action of the heart is free from all mechanical restraint. In pericarditis the inflammation is more generally diffused, and a greater effect is produced upon the muscular walls, first by excitation, and afterwards by paralysis. In endocarditis the inflammation is seated especially in the membrane connected with the valves and orifices, when it is not in contact with the muscular walls, and the latter are consequently affected in a less degree. In pericarditis the aim of the practitioner is often to avert impending death. In endocarditis there is little fear of a fatal result.

But although the two affections are so dissimilar in many respects, the general principles of management are in a great measure alike applicable to both.

The therapeutical indications in the treatment of endocarditis relate mainly to the alternations to which the membrane is exposed, and to the products of inflammation.

Your objects must be to diminish as much as possible the local effects of the inflammation; then to aid in restoration from these effects, and thus protect the organ from the remote consequences arising from incurable and progressive unsoundness. In other words, you must accomplish, if possible, the following results:

1. Abate the intensity of the inflammation.

Edwin Hale
Edwin Moses Hale 1829 – 1899 was an orthodox doctor who converted to homeopathy graduated at the Cleveland Homoeopathic Medical College to become Professor Emeritus of Materia Medica and Therapeutics at Hahnemann Medical College, editor of the North American Journal of Homeopathy and The American Homeopathic Observer and a member of the American Institute of Homeopathy. Hale was also a member of The Chicago Literary Club.

Hale wrote Lectures On Diseases Of The Heart, Materia medica and special therapeutics of the new remedies Volume 1, Materia Medica And Special Therapeutics Of The New Remedies Volume 2, Saw Palmetto: (Sabal Serrulata. Serenoa Serrulata), The Medical, Surgical, and Hygienic Treatment of Diseases of Women, New Remedies: Their Pathogenetic Effects and Therapeutic Application, Ilex Cassine : the aboriginal North American tea, Repertory to the New Remedies with Charles Porter Hart, The Characteristics of the New Remedies, Materia Medica and Special Therapeutics of the New Remedies, The Practice of Medicine, Homoeopathic Materia Medica of the New Remedies: Their Botanical Description etc.