Section V. of the Heart.

The several morbid conditions of the heart may be classified as follows:

1. Inflammation │of muscular walls. │Carditis. „ │of serous membranes. │Pericarditis. „ │ „ │Endocarditis. │ │ 2. Diseases of valves. │Thickening. „ │ „ │Ossification. „ │ „ │Atrophy. │ │ 3. Changes in the walls of the heart, │Hypertrophy. influencing the size of the cavities. │ „ │ „ │Dilation. „ │ „ │Atrophy. │ │ 4. Morbid conditions of the walls alone. │Fatty degeneration. „ │ „ │Morbid growths. „ │ „ │Ossification of │ │ coronary arteries. „ │ „ │Malformations. „ │ „ │Abscess. „ │ „ │Aneurism. „ │ „ │Rupture. │ │ 5. Displacements. │Congenital. │Ectopia cordis. „ │Pathological. │Transposition. │ │ 6. Contents of cavities. │Heart clots.

1. Inflammatory Affections.

=Carditis.= Inflammation of the muscular substance of the heart is by no means a common disease, and when present, is probably always associated either with endocarditis, or more frequently pericarditis. We may recognize this condition after death, by the light yellow color of the heart; with a relaxed, flabby, and in some instances a softened condition of the walls. Upon cutting into the muscular walls, there will be found exuding a semi-purulent fluid and often small cavities, varying in size from a pin’s head to a small pea, will be found filled with pus. This condition may involve the whole heart, or may be confined to one or more portions. Inflammation of the muscular substance of the heart, may, undoubtedly, be one of the primary causes leading to aneurism or even to rupture. The symptoms of this disease are not readily recognized during life, being always combined with inflammation of the peri- or endocardium.

=Pericarditis.= Affections of the pericardium have been noticed in the previous section.

=Endocarditis.= Inflammation of the lining membrane of the heart (endocardium) most frequently occurs in connection with an attack of articular rheumatism. It may, however, result from blows or injuries of the chest, and has been induced by violent muscular efforts. It is said also, to be often connected with some vitiated condition of the blood, as in pyæmia or Bright’s disease of the kidneys, and has been noticed also in cases of measles, typhus and puerperal fever.

Endocarditis more frequently attacks the left, than the right side of the heart. The anatomical appearances, are a loss of smoothness and transparency of the membrane, with an injected condition of its vessels. Deposits of lymph may be found adhering to the free surface at various points, or to the tendinous cords or valves, giving a roughened, or even warty appearance to all those parts. These may become detached, and swept on with the blood, and finally lodging in some of the arteries of the head or extremities, where they are known as emboli, they may become a source of serious trouble. The inflammation may extend to the muscular structure, resulting in softening or the formation of purulent cysts.

It is, however, upon those folds of the lining membrane constituting the valves, and particularly upon the left side of the heart, that the effects of endocardial inflammations are especially manifested. In this way originates most of the so-called

2. Valvular Affections of the Heart.

One of the most common of the results of inflammation extending to the valves, is

=Thickening.= This may depend either upon a deposit of lymph beneath or between the layers of membrane constituting the valves, thus rendering them thick and inflexible while the surface is left smooth, or, at the same time, a deposit upon the exterior may be found, rendering them rough and even warty in appearance, and so stiffened and irregular upon their borders as to greatly interfere with the performance of their functions, and thus permitting regurgitation to take place at the imperfectly closed opening. The tendinous cords, at the same time, may be found thickened, hardened, and contracted, or even ruptured, while the auriculo-ventricular openings may also be found greatly contracted from the thickening of the base of the valves and the fibrous tissues forming the borders of the openings. In one case the contraction on the left side of the heart was so great as scarcely to admit the little finger, while the thumb should readily pass that opening.

The semilunar valves of the aorta are liable to the same changes, their thickened condition preventing their folding back completely into the sinuses of the artery during the systolic action of the heart, or of completely closing the vessel upon pressure from above.

=Calcification.= This condition of the valves may result from a progressive change from simple thickening with fibrinous deposits, to a cartilaginous state, accompanied with so-called bony, or more properly calcareous patches, which may involve large portions of the valves. Ossification of the valves upon the right side of the heart, is but rarely found; upon the left, both the mitral and aortic valves are liable to this affection.

=Atrophy.= The aortic, pulmonary, and sometimes mitral valves, are occasionally found greatly thinned; and this condition may result either in a gradual stretching of the central portion of the valve from pressure of the blood, giving rise to aneurism of the valves, or, it may become perforated with small irregular openings, or, from its weakened condition, rupture may take place, producing sudden death. This condition appears to consist in a gradual wearing away of the substance of the valves, from unusual brittleness of their structure, the result probably of chronic inflammation.

Again, the valves may be found greatly contracted, (stenosis) hard and rigid, which will be attended with imperfect closure and consequent regurgitation. Dilatation of the orifices without any change in the valves, may also be found, resulting in the same imperfect closure.

Disease of the valves of the heart, by obstructing the orifices, is likely to result in

3. Changes Affecting the Size of the Cavities.

=Hypertrophy.= Hypertrophy of the heart, is a condition in which there is an increased thickness of its walls, and generally also enlargement of its cavities. Yet there may be thickening—very rarely however—with a diminution in the size of the cavities. It may affect both sides of the heart, but is frequently confined to the left ventricle.

The main cause of hypertrophy of the heart, is the existence of some obstruction to the circulation, either in the heart, or some portion of the arterial system, as by aneurism, pressure of tumors, etc., or by disease of the kidneys. It is most frequently, however, associated with disease of the valves or large arteries. It may sometimes result from continued functional excitement, and generally accompanies cases of partial adhesion of the surfaces of the pericardium, while complete adhesion is more likely to be followed by dilatation or atrophy. On the right side of the heart, hypertrophy is usually the result of some obstruction to the circulation through the lungs, as in an emphysematous condition of that organ.

The following measurements, &c., of the normal heart, will serve as a guide in judging of cases of enlargement:

Size. Lænnec has stated, that the heart in its normal condition, is about the size of the closed fist of the individual. This comparison, however, is not very satisfactory. It will be usually found to measure about 5 inches in length, 3½ in its greatest width, and 2½ in its extreme thickness, from its anterior to its posterior surface.

Weight. From an examination of four hundred cases, the average weight was found to be 9½ ounces in the male, and 8¼ ounces in the female. In a robust, muscular male, the heart may, however, be found to weigh as much as 12 ounces, and still be normal in all its parts.

Thickness of Walls. Right auricle, 1 line; left, 1½ lines. Right ventricle, 1½ lines, and left, a little over 5 lines, or half an inch, at its middle, being a little thinner both at the base and apex.

Size of Orifices. Circumference of auriculo-ventricular opening of the right side, nearly 4 inches; of left side, 3½ inches; of the pulmonary artery, 2⅝ inches; of aorta, 2⅜ inches.

When enlarged, the heart may be found measuring 6 to 7 inches in length, as much in breadth, and 12 to 16 inches in circumference. The weight may also be increased to 15, 20 or 25 ounces, and the walls may increase in thickness to nearly a-half inch, and upon the left to over an inch.

Hypertrophy of the heart, has been divided into three forms:—1st, simple hypertrophy; 2d, eccentric; and 3d, concentric hypertrophy.

In the first form, the walls are thickened, while the cavities remain unchanged. (Simple hypertrophy.)

In the second form, the thickening of the walls is attended with an enlargement or dilatation of the cavities. (Eccentric hypertrophy.)

In the third form, the thickening is attended with a diminution in the capacity of the cavities. (Concentric hypertrophy.)

It has been observed in cases where an examination has been made very soon after a sudden, violent death, attended with loss of blood, as in decapitation, etc., that the cavities have been nearly obliterated, while the walls were greatly thickened. By maceration for a few days, the ventricles have become relaxed to their natural size and capacity. This state of the heart has been observed in persons in whom, during life, none of the symptoms of disease of the heart had been manifested, and hence the condition is to be considered as the immediate effect of the peculiar character of the cause of death.

=Dilatation.= Dilatation of the cavities of the heart, is a condition which may also result from the presence of obstacles or impediments to the circulation, as from ossification of the valves; narrowing of the pulmonary or aortic orifices; employments requiring powerful muscular efforts; and in consolidation, tubercular induration, emphysematous condition of the lungs, or fatty degeneration.

The muscular substance is usually soft and flaccid, sometimes of a violet color, again pale and yellowish. The thinning may be so great, as to reduce the thickest part of the left ventricle to two lines or even less, when the walls will appear to be composed of but little more than a thin layer of fat covered with the pericardium.

Three forms of dilatation are recognized: active, simple and passive.

Active dilatation is associated with hypertrophy of walls, constituting eccentric hypertrophy.

In simple hypertrophy, the walls retain their normal thickness, while the shape may be changed according to the cavity affected.

Passive dilatation, on the other hand, is accompanied with thinning of the walls, and usually results from fatty degeneration, atrophy, or some other change in the muscular fibre.

=Atrophy.= In this condition there is a uniform decrease in the size of the heart. Its cavities becomes small, and its walls thin. It usually attends diseases accompanied with great impoverishment of the blood, as in cancer, diabetes, etc., or may result from obstruction of the coronary arteries from calcification, atheroma or thrombi.

Paget mentions a case where the heart of a cancerous man, fifty years old, weighed only five ounces, four drachms; and that of a diabetic woman, which weighed only five ounces, one drachm. It is usually accompanied with a general wasting of the tissues and organs of the body, and frequently will be found associated with fatty degeneration, which will now be noticed.

4. Morbid Condition of the Walls Alone.

=Fatty Degeneration.= Two forms of fatty diseases of the heart have been recognized. In the first, which should be known as “fatty growth,” to distinguish from “fatty degeneration,” there is an unusual quantity of adipose matter in those parts of the heart where more or less is usually found, viz.:—Along the furrows through which the vessels run, and particularly about the base of the heart. The fatty masses may dip more or less into the substance of the walls, displacing the muscular fibres, although the latter are generally normal in color and density, even when imbedded in masses of fat. This condition may be found in persons who are otherwise thin, as well as in the obese.

But the more frequent form of fatty disease, is that known as fatty degeneration. In this, we find upon opening the heart, that it has lost the reddish-brown color characteristic of the muscular fibre in its normal condition, and is pale, soft and flabby. The whole organ feels soft, doughy and inelastic, much like a heart beginning to decompose. If the wall of the left ventricle be partly cut through, the remainder is easily torn, and the surfaces have a granulated appearance.

Upon the inner surface, beneath the endocardium, numerous small thickly set spots, or sometimes wavy lines, of a pale buff, or light yellow color, may be noticed. This appearance does not depend upon a deposit of fat among the muscular fibres, but rather upon a change in that tissue; and an examination with the microscope, will show fatty degeneration of the fibre.

This condition of the heart, may involve the whole organ, or may be confined to one or more portions. It is much less common in the auricles, than in the ventricles, and more frequent in the left ventricle than in the right. It will be generally found more advanced in the upper portion of the septum of the ventricles, and in the large, fleshy columns of the left side; or it may be found in these columns alone, which accounts for the occasional rupture of the latter.

Fatty Degeneration may be associated with fatty growth, or with hypertrophy, or thinning and dilatation, and may be the cause of rupture. The general character of softness, paleness, and mottled color, should lead to suspicion of the existence of this disease, when a microscopic examination being resorted to, the conclusion would be decisive. A small portion of fibre, examined with a power of 300 or 400 diameters, will present, in fatty degeneration, instead of the striated appearance of the normal fibre, a granular appearance, with numerous minute oil globules scattered through the fibre. In the palest part of the heart, the disease will be generally most advanced; but even here, the microscope will show some fibres in a healthy condition, while others around them are rendered completely granular.

Exhausting diseases of various kinds, typhus and other severe fevers, phosphorus poisoning, etc., may result in this peculiar condition of the heart.

5. Morbid Growths.

Under this head may be placed tumors, cancers, melanosis, and hydatids.

=Tumors= of various kinds are occasionally found in connection with the heart. Fibrous tumors of a small size may develop within the muscular walls, while syphilitic growths, cysts, and tubercular deposits may also, in rare cases, be discovered.

=Cancer.= Cancer of the heart has been noticed in two forms—epithelial and medullary. A man, fifty-eight years old, had an epithelial cancer of the eye, which was removed. Two years after, the man died with a large cancerous tumor over the parotid gland. A post-mortem examination revealed a cancerous mass, about an inch and a-half in diameter, imbedded in the apex of the right ventricle and septum of the heart. A microscopic examination revealed its epithelial character.

Medullary cancer of the heart has been usually found associated with the same disease in the lungs and liver, and forms an investing mass which may involve the whole organ.

=Melanosis= of the heart presents the same character as in other parts of the body, and is considered but a variety of the medullary cancer, pigmentary matter being added. It may be developed upon the surface, or may infiltrate the substance of the whole organ.

=Hydatids= have been occasionally found in the heart, the most of which have probably been animal in their character, (acephalocysts.) A female, forty years old, who had been suffering pain in the region of the heart for some months, suddenly died, after running rapidly up stairs. One ounce of fluid was found in the pericardium. A considerable tumor was found at the apex of the heart, which slightly fluctuated. This tumor was about three inches in diameter, globular in form, and encroached considerably upon the cavity of the right ventricle. When laid open, it was found to contain a large number of small cysts or hydatids, varying in size from that of a small pea to that of a pigeon’s egg, the space between which was filled with a soft curdlike substance, of a yellow color.

=Ossification of Coronary Arteries.= That condition of the arteries of the heart usually termed ossification is more properly one of calcification, consisting of a deposit of hard, gritty, calcareous matter, in which there is none of the true character of real bone, no trace of bone-corpuscle or vascular canals ever being discovered in them. Chemical analysis has shown the deposits to be composed of 50 parts of animal matter, with 47½ of the phosphate and 2 of the carbonate of lime in every 100. This matter being deposited in circular layers, the artery becomes gradually converted into a hard, bony-like tube, which may be traced with the finger along the grooves of the heart through which the coronary artery runs. This is peculiarly a disease of old people, and may accompany a similar condition of the arch of the aorta or of the semilunar valves, and by interfering with the proper nutrition of the heart may result in other forms of disease, as fatty degeneration, dilatation, &c.

=Abscess.= Abscess of the heart, may unquestionably follow an attack of carditis, or inflammation of the muscular substance. The cut surface of the heart in these cases, not unfrequently shows small cavities containing a purulent fluid, and in some instances a distinct abscess is found.

A man, sixty years old, was suddenly attacked, while at work, with coma and great feebleness, followed by death on the third day. The left ventricle being opened, an abscess was discovered near the apex, irregular in form, and containing a bloody, purulent-looking fluid. The coronary arteries were much ossified.

=Malformations= of the heart, are extremely rare in adults, or even in children that have passed the early days of infancy. They consist frequently in arrest of development of the auricular septum, or, in other words, of a patulous foramen ovale, which, by permitting of a mixture of arterial and venous blood upon the left side of the heart, results in early death. I have in several instances found this foramen imperfectly closed in the adult heart, but the opening has been so small—barely sufficient to permit the passage of a probe—as to offer little or no obstacle to the proper performance to the heart’s function. Malformation of the heart is undoubtedly one of the many causes of death in utero, which might be demonstrated by a post-mortem examination.

=Aneurism.= Partial aneurism, or false aneurism of the heart, consists in the formation of a sac or pouch, in some portion of the walls of the organ, communicating with the cavity of the chamber, in the walls of which it has been formed. They may form in any part of the muscular walls of the heart, but are more frequent in the left ventricle. They would seem to result from a separation of some of the muscular fibres, when, by their retraction, a cavity or pouch, of a rounded or oval form results, which, in some instances, has its walls composed of the pericardium alone, there being a complete destruction of the muscular fibres.

The interior of these pouches, may be found filled with layers of coagulated fibrinous deposits, as in the case of aneurism of arteries; or, if they communicate with the ventricular cavity by a large opening, they may be filled with a simple soft clot of blood.

The size of these aneurismal pouches, vary from that of a cherry, to a pigeon’s egg, or larger, when they change much the usual figure of the heart, by their projection upon the external surface.

The following conditions have been supposed to favor the formation of these aneurismal sacs:—1st, softening of the muscular tissue of the heart; 2d, ulceration of the lining membrane; and 3d, rupture of the muscular fibres.

=Rupture= of the walls of the heart sometimes happens, producing sudden death. It may result from severe contusions of the chest, in which case, the auricles are more likely to give way. More frequently, rupture will result from softening of the walls in fatty degeneration or ulceration, or from the bursting of an aneurism of the heart, or from stenosis of the aorta. In the latter cases, the left ventricle will be usually the seat of the rupture.

6. Displacements.

Changes of Position of the heart, are by no means unfrequent. They may be congenital in their origin, or the result of disease in the surrounding organs. Of congenital displacement, we may mention first:

Ectopia Cordis, where, from some arrest of development, in the inclosing parts, the heart may be found in some position other than its normal one. From deficiency of the sternum and ribs, the heart has been found protruding from the chest, (ectopia pectoralis,) or from absence or deficiency of the diaphragm, it may be found in the abdomen with the abdominal viscera. Such cases live but a short time after birth.

Transposition of the heart is found in those cases where all the viscera, abdominal and thoracic, are exactly reversed in position. A case of this kind was discovered in the dissecting-room a few years ago, by Dr. R. B. Weaver, demonstrator of anatomy, in the Hahnemann Medical College. The heart was here upon the right side, the aorta curving to the left; the liver upon the left; the stomach with its pylorus to the left; the colon commencing in the left iliac fossa; in short, everything completely reversed in position. The subject was a female of about thirty years, and undoubtedly suffered no inconvenience from the abnormal positions.

The more frequent displacements of the heart, however, are those resulting from disease in the surrounding structures. It may be crowded from its normal position, by pleuritic effusions, accumulations of air (pneumothorax), or even by a highly emphysematous lung. Displacements may also result from the presence of aneurismal or other tumors in the chest; curvatures of the spine; or from a hernial protrusion of some of the abdominal viscera through an opening in the diaphragm; or the presence of tumors, enlarged viscera, dropsies, etc., within the abdomen.

7. Contents of the Cavities.

=Heart Clots.= This subject is one that has until recently, been but imperfectly understood; and now even, our knowledge relating to it, is by no means complete. Enough is known, however, to convince us that heart clots, are a more frequent cause of sudden death, than has been heretofore supposed.

Having in a recent paper, read before the Philadelphia County Homœopathic Medical Society, quite fully treated of this subject, I shall here merely transcribe the leading points of the same.

Fibrinous heart clots, polypus of the heart, or fatty deposits, as they are sometimes called, differ from ordinary clots of blood, in the absence of the blood corpuscles, and hence, presenting the buff color characteristic of the coagulated fibrin of the blood. Ordinary blood clots, with the corpuscles entangled with the fibrin—and hence presenting the red color of blood—are usually found in the cavities of the heart and large blood-vessels after death, but in greater quantity upon the right side.

Color. The shade of color presented by the fibrinous clot varies in different cases. While buff is the prevailing color, the shade varies from a light drab to a decided yellow.

Consistency. In this respect a good deal of variation is also found; the difference depending, probably, in part upon the character of the disease, and in part upon the rapidity or slowness of the formation; those of a rapid or very recent formation, having a soft, fatty, or jelly-like character; while, on the other hand, those of a more gradual formation, and with more sthenic forms of disease, acquire a considerable degree of density, the surface presenting a smooth appearance, as if acted upon by a current of blood, and in all respects resembling the dense fibrinous masses, found blocking up the cavities of aneurismal tumors.

Position. In every case reported below, the clot has been on the right side of the heart, although in some, a small, soft clot has been found on the left. I am not sure that I have ever found one of these clots on the left side of the heart of such a size and consistency, or under such circumstances, as to have led me to suppose that it might have been a cause of death.

The body of the clot is usually found in the ventricle, extending from this, either up into the pulmonary artery, or through the opening into the auricle. In all cases, the clot has been more or less entangled with the tendinous cords of the valves and muscular columns of the heart, requiring, in some instances, considerable force to tear it away from its attachments.

Time of formation. An important question to be decided in regard to these heart clots, is the time of their formation. Are they ante or post-mortem in their origin? And upon the solution of this query depends the conclusion as to whether they are the cause or the result of death in the cases where found. That a fibrinous clot may sometimes be formed in the coagulation of the blood outside of the body, is a fact well known; as in the blood drawn from patients suffering from acute inflammatory affections, where, from the retarding of the coagulation, the blood corpuscles, from their greater specific gravity, have time to fall towards the bottom of the vessel, thus giving the “buffy coat” to the upper portion of the clot. The same cause—retarded coagulation—unquestionably may give rise to a clot in the heart after death, presenting the same character, viz., with the upper portion, of the buff, fibrinous character, while the lower portion, from the presence of corpuscles, will present the appearance of an ordinary blood clot. Such clots are not unfrequently found after death.

But have we any evidence that the fibrin of the blood may be deposited, forming clots within the vessels during life? In proof of this, we have only to refer to the result of the application of a ligature to an artery; where the interval between the point of application and the first vessel coming off above, will be filled with a fibrinous clot, which performs an important part in the closing up of the vessel; or, to the well-known deposits of fibrinous layers within aneurismal tumors, sufficient, in many cases, to so fill up the sac as to result in a cure; therefore, the favoring conditions being present, it is not unreasonable to claim that fibrinous clots may form within the heart, of such size and in such positions as to be an immediate cause of death.

Causes. In looking for the causes, or conditions promoting the formation of these fibrinous deposits, we have to consider, first, variations in the character of the blood itself; and secondly, peculiarities in its circulation and in the circulatory apparatus. Fibrin, one of the normal constituents of the blood, is estimated by physiologists as forming from 2 to 3 parts in 1000, while it may fall as low as 1, or rise to 7½ parts. We find it reduced to the minimum quantity in all diseases which present a hæmorrhagic tendency, as in true typhus, yellow fever, certain malignant forms of disease, and as the effect of many poisons, both animal and vegetable. In these cases, the loss of fibrin results in the effusion of blood into the tissues, producing petechial spots, or upon the mucous surfaces, giving rise to epistaxis, black vomit, hæmaturia, etc., while very feeble, if any, coagulation of the blood will be found after death.

In scurvy, however, where we have a condition of the blood not unlike that above referred to, there appears to be a marked tendency to the formation of clots, as has been noticed by many observers, and as has been verified by Dr. J. C. Morgan, in several cases which came under his notice while in the army.

But it is in cases where there is at least a relative increase of fibrin, that heart clots are more liable to form. Such a condition we find in cases where, while the fibrin remains normal in quantity, the water of the blood, the menstruum in which the fibrin is held in solution, is below the normal standard, this reduction favoring the tendency to deposit. Thus, in all cases where there has been an exhausting and rapid flux from the bowels, as in cholera, or excessive purging from drastic cathartics, or from the colliquative sweating of phthisis, we have the favoring condition, and death may be the immediate result of a fibrinous clot in the heart.

The most favorable condition, however, for the formation of heart clots, is undoubtedly that in which there is an absolute increase of fibrin, and this we find in a large number of diseases marked by acute inflammatory symptoms; as in pleurisy, pneumonia, diphtheria, croup, acute rheumatism, erysipelas, puerperal fever, etc. In a large number of deaths from these diseases, a post-mortem examination would undoubtedly bring to light a heart clot, which has at least served to hasten, if it has not been the immediate cause of the fatal termination.

Again, the formation of heart clots is evidently promoted by any circumstances or conditions, resulting in great feebleness or languor of the circulation, independent of variations in the amount of fibrin. A complete stasis of the blood is certain to be followed by coagulation; as in employment of pressure in the treatment of aneurism; so in cases of great prostration of the powers of life, attended with extreme feebleness of the circulation, as 1st. In cases of shock, where life is not immediately destroyed; 2d. In certain cases of poisoning, as by opium, where the action of the heart is greatly depressed; and 3d. In syncope, either with or without loss of blood. In all of these cases the danger of the formation of the heart clot is very great, and probably in a large number this is the immediate cause of death.

It is a fact well established, that loss of blood, either by hæmorrhages or venesection, is followed by an increased coagulability of that fluid; hence, the fearful hæmorrhages which sometimes attend parturition, if accompanied with syncope, are in great danger of being followed by the formation of the heart clot, and thus ending in death.

Another circumstance tending to promote the formation of fibrinous clots in the heart, is evidently to be found in the peculiar formation of the valves guarding the auriculo-ventricular openings. It is well known how fibrin may be collected from fresh blood, by beating the same with a bundle of twigs, the latter soon becoming coated with shreds of fibrin; so the chordæ tendineæ and fleshy columns of the heart, between which the blood is continually being driven, affords convenient points for collecting the same from the feebly circulating or overcharged blood; and from the close intermingling of the tendinous cords, with the substance of the clot, it is probably upon these that the deposit first begins to form.

In explanation of the fact that fibrinous clots are almost universally found on the right or venous side of the heart, notwithstanding that arterial blood is richer in fibrin than venous, the following has been suggested to my mind: First. While venous blood contains a smaller proportion of fibrin, may not its deoxydized condition favor the more ready deposit of this substance, than by the more highly vitalized arterial blood? Second. The feebler muscular power of the right side of the heart would necessarily be attended with a slower circulation through its cavities, the partial stasis of the blood giving another condition favorable for the formation of a clot; and Third. The valves of the right side of the heart, present three flaps or folds, instead of two as on the left, and hence, with their numerous tendinous cords, offer an increased number of obstructing points, around which the deposit may be made. These several circumstances would seem sufficient to account for the admitted fact.

Symptoms. The symptoms attending the formation of fibrinous clots in the heart, are usually sudden in their accession, frequently attended with a chill, and marked by great oppression in breathing, coldness of surface, and pallor of face and lips, the latter symptom distinguishing from the dyspnœa attending croup, asthma, pneumonia, etc., where the face is livid from venous congestion. The pulse is usually rapid and feeble; the action of the heart labored, palpitating, and sometimes intermitting, while auscultation will reveal a tumultuous churning-like action, the normal sounds being quite undistinguishable.

Pulsation of the jugulars will be present in most cases, and where the clot greatly obstructs the play of the tricuspid valves, a double pulsation will be likely to be noticed. In the last stage, a copious cold perspiration appears upon the whole surface of the body.

As might be anticipated, fibrinous formations, while of small size, are sometimes washed away from their attachments and swept on with the current of blood into the arteries and carried to distant parts of the body, as is sometimes the case also in aneurism, thus producing the embolic masses often found blocking up arteries in different parts of the body. When upon the right side, the embolus would be carried into the pulmonary artery, obstructing the circulation through the lungs, and producing symptoms more or less grave, according to the size of the clot. Upon the left side of the heart, from the greater force of the circulation, these bodies are probably more frequently swept away from their attachments and carried into the aorta, and thus on, perhaps, through the carotids to the head, or into the subclavian, or down the aorta, finally lodging in some of the branches of the lower extremities. Convulsions, paralysis, etc., are not unfrequently produced by the lodgment of emboli in some of the arteries of the brain, while, when carried into the arteries of the extremities, pain, falling of temperature, impairment of sensation, contraction of muscles, atrophy, and even gangrene may result.

The following examples will serve to illustrate the class of cases to which I refer:

CASE I.—Death from Heart Clot in Anæmia.

A lad, 11 years old, and very anæmic, went to school in the morning in his usual health; while there was taken with a chill. On his way home vomited freely. The chill lasted for a long time, and was accompanied with an oppression in breathing, which gradually increased through the day and night, and until the time of my first visit at 11 o’clock A. M. the next day. I then found him extremely pallid, lips bloodless, perspiring freely, suffering from great restlessness and distress, with extreme dyspnœa; mind wandering, pulse irregular and feeble; action of the heart very tumultuous, the normal sounds being unrecognizable. In the neck noticed a rapid rolling pulsation of the jugulars, which presented two beats to one of the artery at the wrist.

At my second visit, made at 4 o’clock P. M., the patient had just expired.

The autopsy, made twenty hours after death, gave the following results: Upon opening the abdomen found the liver presenting a dark mottled appearance, and highly congested; other abdominal organs natural; pericardium contained about one ounce of serum. Upon opening the right auricle of the heart, found a firm fibrinous mass, extending downwards through the ventricular opening, and which, upon the latter cavity being opened, was found firmly attached to the tricuspid valves, and entangled with the fleshy columns and tendinous cords.

The presence of such a body in this position, and with such attachments, it was evident, must have so interfered with the passage of the blood from the auricle to the ventricle, as, upon the contraction of the former cavity, to have caused a backward pressure into the veins, and thus have produced the first of the double pulsations of the jugulars.

Again, the position of this clot, preventing the closure of the valves upon the contraction of the ventricle, there would have been a regurgitation into the auricle, and the same backward flow into the veins, thus producing the second pulsation of the jugulars seen during life.

CASE II.—Death from Heart Clot in Pregnancy.

A lady, 28 or 30 years old, also very anæmic, and three months pregnant, had been suffering occasional fainting spells. For some days before her decease she had suffered from dyspnœa, and on that day, after ascending a flight of stairs, fell upon the floor, and before a physician could be obtained breathed her last. A post-mortem showed all the thoracic and abdominal viscera in a healthy condition, while the right side of the heart contained a large fibrinous clot, with attachments similar to those found in Case I.

CASE III.—Death from Heart Clot in Diphtheria.

A boy, 3 years old, had an attack of diphtheria. The case presented no unfavorable symptoms until about the fourth day, when he was taken with great restlessness and oppression in breathing, and while sitting on the chamber at stool, suddenly died. The autopsy here again revealed the heart clot, as in the other cases.

CASE IV.—Death from Heart Clot in Consumption.

A man, 30 years of age, a furrier by trade, was suffering from tubercular disease of the lungs. He had never given up his work, though he was much reduced in flesh, had a bad cough, diarrhœa, and night sweats. While at his employment, he was one day taken with great oppression, increased cough, etc., and in twenty-four hours expired.

The post-mortem showed that, while the upper portion of both lungs contained large deposits of tubercles, there were no abscesses, and the lower portions presented sufficient sound lung tissue to have maintained life. Upon opening the heart the usual fibrinous clot was found in the right ventricle, extending upwards into the auricle.

CASE V.—Death from Heart Clot in Rheumatism.

A strong colored man, of 25 years, had an attack of inflammatory rheumatism. The disease presented the usual characters, the inflammation wandering from joint to joint. During the second week he was suddenly attacked with great difficulty in breathing, violent and irregular action of the heart, and great distress, followed by rapid prostration and death. The post-mortem examination revealed thickened tricuspid valves, with a firm clot of large size adhering to the same.

CASE VI.—Death from Heart Clot in Debility.

A gentleman, 55 years old, who had been for some time in feeble health, was taken, upon rising in the morning, with oppression and distress in the region of the heart, dying in twelve hours. The heart clot was found here, as in the other cases, upon the right side of the heart.

CASE VII.—Heart Clot in Death from Over-dose of Morphia.

A gentleman, of about 50 years, a physician, was found one morning dead in his bed. His health had been previously good, excepting that he was troubled with neuralgia which gave him sleepless nights, and for which he sometimes took morphia. On the night previous to his death he came home and retired at a late hour. An open bottle of morphia and small spatula were found on his desk next morning, the spatula showing evidence of having been thrust deeply into the morphia, and probably a large and over-dose carelessly removed and taken. The autopsy here again revealed a large and firm fibrinous heart clot.

CASE VIII.—Death from Heart Clot in Acute Gastritis.

A lady of about 60 years, had an attack of acute gastritis, but was considered convalescing, and her physician (Dr. Martin) made his last visit in the evening. The next morning she was found dead in her bed. The post-mortem showed the spleen somewhat enlarged, and its capsule greatly thickened. Other organs healthy, while the heart contained an unusually large fibrinous clot, which has been preserved in the College Museum.

The above include the more marked cases of death that have come under my notice, where that result could, in my mind, be fairly attributed to the formation of fibrinous clots in the heart.

The following inferences may, we think, be fairly deduced from the several cases reported:

First. In some instances the fibrinous clots are apparently the sole cause of death. (Cases 1, 2, and 3.)

Second. In other, and a larger number of diseases, as in acute rheumatism, pneumonia, croup, etc., which otherwise would recover, a fatal termination results from the formation of heart clots. (Cases 3 and 5.)

Third. In still other diseases, which are of themselves necessarily fatal, as in phthisis, cholera, etc., death is often hastened by these formations. (Case 4.)