The anatomical changes occurring within the aorta, to which reference has just been made, involve the presence of morbid deposit. In examining the bodies of aged persons after death, it is rare to find the internal surface of this artery entirely free from disease. Changes due to morbid deposit often occur in the middle aged, especially in males; and they are sometimes observed in young subjects. They are found when there had been, during life, no symptoms denoting disease in this situation; but they are important as leading to dilatation, aneurism, and occasionally perforation or rupture. Their agency in the production of certain physical signs is, also, to be borne in mind.

The deposit may be situated upon the free surface of the lining membrane of the vessel, forming membraniform patches, variable in number, thickness, and size, composed of a white, dense substance, sometimes of a cartilaginous firmness, closely adherent to the membrane. This substance may, possibly, in some instances, be lymph which has exuded from the vasa vasorum of the outer coat, and permeated the middle and inner tunics of the artery. According to Rokitansky, it is always derived from the blood within the artery, and is either condensed fibrin, or "an excessive deposition of the lining membrane of the vessels." This deposit in some cases extends over the whole aorta, and even into the communicating arteries. It may lead to occlusion of the latter at the points of communication with the aorta. Although this false membrane becomes, after a time, so closely adherent to the surface of the inner coat of the artery that it cannot be removed without bringing away the latter, it is not united by means of an organized attachment, and does not itself take on organization.

A more common form of deposit is that known as atheroma. This deposit takes place beneath the lining membrane of the artery. It occurs first in small, isolated points which increase and coalesce, forming patches of greater or less size. The substance of the deposit is soft and even semi-liquid, or more or less hard. It is found, on microscopical examination, to contain oil-globules in abundance with crystals of cholesterine, and, hence, it is considered as constituting a variety of fatty degeneration. It is frequently associated with fatty change of the muscular substance of the heart to a greater or less extent. The presence of this deposit involves more or less softening and looseness of the middle and lining coats of the artery. The atheromatous deposit is the seat of the calcareous matter so often observed in the bodies of those who die after the middle

period of life, not infrequently occurring during, and sometimes prior to, this period. In the progress of time, the patches of atheroma are transformed into plates or masses of a bony hardness. The lining membrane of the artery covering these plates or masses disappears, and they project into the vessel, coming in direct contact with the current of blood. The interior surface of the vessel is in this way roughened; the current of blood is broken, and the elasticity of the artery impaired or destroyed. The projections within the vessel also serve as a nucleus for the deposit of fibrin, and the calibre of the vessel may thus be considerably diminished, causing obstruction to the free passage of the blood. The transformation of atheromatous into calcareous patches, must be considered as a conservative provision for strengthening the affected portions of the artery, diminishing the liability to dilatation and rupture. If, however, the vessel be extensively calcified, and rendered thereby unyielding and inelastic, the circulation is deprived of the force derived from the recoil of the affected portion of the aorta; an additional labor falls upon the left ventricle which, in consequence, is apt to become hypertrophied. Calcified arteries were formerly said to be ossified, and the term ossification is still sometimes applied to this morbid change, incorrectly, inasmuch as the calcareous deposit lacks the characters of bony texture, resembling the latter only in density and chemical composition.

Calcareous degeneration may exist to a considerable extent without giving rise to any notable symptoms of disease. It is found after death to pervade the aorta more or less extensively, especially at and anterior to the arch, having occasioned, during life, no apparent inconvenience. But it may give rise to aortic murmurs which it is desirable to discriminate from those involving lesions of the aortic valves and orifice. With these lesions, affections of the aorta are frequently associated, but the artery may be extensively diseased without the valves and orifice being involved. How is this fact to be determined during life? The friction of the current of blood in its onward course against the inner surface of the aorta roughened by calcareous patches, causes a murmur; and the regurgitant current or retrograde movement of the column of blood, due to the recoil of the arterial coats, may also cause a murmur, even assuming that the semilunar valves are sufficient. We may thus have a systolic and a diastolic murmur, one or both, produced within the aorta, independently of either obstruction or insufficiency at the aortic orifice. It is desirable to distinguish these murmurs, for they

represent lesions which are of little consequence compared with those involving aortic contraction and regurgitation, and, cousequently, serious enlargement of the heart. A systolic murmur produced within the artery just above the orifice, may have its maximum of intensity in the second intercostal space close to the sternum, where the artery is nearest the ear of the auscultator. In this respect it does not differ from a murmur produced at the aortic orifice. It is less likely than the latter murmur to extend below the level of the third rib. It is perhaps more likely to be propagated with considerable intensity into the carotids. These differential points, it must be confessed, are not sufficient always for a positive discrimination. The aortic second sound of the heart is to be taken into consideration. This sound is not likely to be notably impaired if the aortic orifice be not the seat of lesions. At all events, an aortic murmur, whether produced at the orifice, or within the artery above, does not necessarily denote a serious morbid condition, when the aortic second sound is unimpaired. A diastolic murmur produced within the artery above the orifice, provided the semilunar valves be sufficient, is heard in the second and third intercostal spaces on the right side of the sternum. It is not propagated downward, as when it is produced by regurgitation through the aortic orifice into the cavity of the ventricle, the valves being insufficient. In the latter case, the murmur is loudest over the body of the heart and is heard often at the xiphoid cartilage, or even still lower. The integrity of the aortic second sound of the heart is important in determining that a diastolic murmur is produced within the artery alone, without involving insufficiency and regurgitation at the aortic orifice. If the aortic second sound be not notably impaired, it may be assumed that the murmur is produced within the artery. It is, however, to be considered that in proportion as the elasticity of the aorta is diminished, the intensity of the aortic second sound will be lessened. It is to be added, that the intensity or quality of a murmur produced within the aorta, is not evidence of the extent or amount of disease. Calcareous patches, few and small, may so roughen the membrane as to develop a loud rasping murmur; and, on the other hand, calcareous deposit may pervade the artery when the murmur is feeble and soft, the physical conditions, in the latter case, being less favorable for the production of sonorous vibrations. Much will depend on the power with which the left ventricle contracts, as regards the loudness and roughness of aortic murmurs; hence, other things being

equal, they are loud and rough in proportion to the amount of hypertrophy of this ventricle which may be present, and the muscular vigor of the heart.

Dilatation of the ascending aorta is a not infrequent result of atheromatous and calcareous disease. The middle and lining tunics becoming softened, attenuated, and the elasticity of the vessel impaired or lost, dilatation takes place from the distending force of the blood-currents propelled forward by the systole of the left ventricle, and backward by the recoil of the arterial coats beyond the affected portion of the aorta. This result is more apt to follow if the left ventricle become hypertrophied. The ascending portion of the arch and the sinuses of Valsalva are the points most apt to yield to the distension. In the latter situation, the dilatation is probably produced more by the retrograde than the onward current, provided the semilunar valves remain sufficient. According to Dr. Bellingham, visible pulsation of the large arteries of the neck and upper extremities, and a jerking or receding pulse, are characteristic of dilatation of the arch of the aorta. These signs have been noticed in a previous chapter as distinctive of lesions at the aortic orifice permitting regurgitation from the artery into the left ventricle. Their significance of dilatation of the aorta, disconnected from aortic insufficiency, must depend on the presence of adequate evidence that the semilunar valves remain sufficient. This evidence consists in the absence of a murmur denoting regurgitation into the ventricle, and the intensity of the aortic second sound of the heart being but little, if at all impaired. It is only under these conditions that the signs can be considered as indicating aortic dilatation. Dr. Bellingham also states that an impulse synchronous with the pulse is perceived when the ear is applied to the stethoscope laid upon the first bone of the sternum. This impulse may be per ceived thus by the ear when it is not communicated to the hand with sufficient force to be appreciable. In connection with these signs, a double rough murmur is perceived which is referable to the aorta and not to the aortic orifice. The diagnosis in some cases, as claimed by the author just mentioned, may be made out by means of this combination of physical signs; but in most cases, the diagnostic points are invalidated by the coexistence of lesions at the aortic orifice.

The foregoing diseases of the aorta, although intrinsically important, and involving pathological questions of much interest, have been passed over cursorily, because the diagnosis is generally

impracticable, and, were it practicable, they are, for the most part, not amenable to treatment. Acute aortitis, if ascertained, would call for measures to diminish the intensity of inflammation and the tendency to coagulation of the fibrin in the blood. Subacute or chronic aortitis is always latent, and it is doubtful whether, were its existence determined, therapeutical measures would be of much avail. Atheromatous deposit is not revealed either by symptoms or signs, and is dependent on a diathesis often incident to age, and the removal of which could hardly be expected. Calcareous plates or masses, and dilatation of the aorta, give rise to murmurs which, with proper attention and knowledge, may, in some instances, be referred to the aorta. The latter is the most important practical point connected with the aortic diseases which have been noticed. Murmurs, systolic and diastolic, may be generated by the currents of blood exclusively within the aorta, when the lining membrane is roughened by calcareous matter or other structural changes such as puckering of the membrane, and by alterations in the calibre of the vessel. These murmurs, if incorrectly referred to the aortic orifice, would denote serious lesions, whilst, in fact, the anatomical changes are comparatively unimportant, and perhaps innocuous. This is to be borne in mind, and it is to be determined, if practicable, in individual cases, whether aortic murmurs are produced within the artery or at the aortic orifice. Owing to the frequent coexistence of lesions situated at this orifice with diseases of the aorta, murmurs are often developed in both situations. Under these circumstances, the discrimination is difficult, and comparatively of small importance.

The subject of thoracic aneurisms claims a more extended consideration than the aortic diseases which have been noticed. To this subject, the remainder of the chapter will be devoted.

THORACIC ANEURISMS.

The term aneurism, in its broadest sense, and in accordance with its etymology,' is applicable to every species of dilatation of an arterial trunk. It is convenient, however, to exclude cases in which an artery is slightly or moderately enlarged in its whole

I aveúpvoma, a dilatation.