With the increased complexity of our modern life comes increased wear and tear on the human organism. "A man is as old as his arteries" is an old dictum, and, like many proverbs, the application to mankind today is, if anything, more pertinent than it was when the saying was first uttered. Notwithstanding the fact that the average age of mankind at death has been materially lengthened—the increase in years amounting to fourteen in the past one hundred years of history—clinicians and pathologists are agreed that the arterial degeneration known as arteriosclerosis is present to an alarming extent in persons over forty years of age. Figures in all vital statistics have shown us that all affections of the circulatory and renal systems are definitely on the increase. "Arterial diseases of various kinds, atheroma, aneurysm, etc., caused 15,685 deaths in 1915, or 23.3 per 100,000. This rate, although somewhat lower than the corresponding ones for 1912 and 1913, is higher than that for 1914, and is very much higher than that for 1900, which was 6.1."

The great group of cases of which cardiac incompetence, aneurysm, cerebral apoplexy, chronic nephritis, emphysema, and chronic bronchitis are the most frequent and important appear as terminal events in which arteriosclerosis has probably played an important part.

Thus, in the sense in which we speak of tuberculosis or pneumonia as a distinct disease, we can not so designate the diseased condition of the arteries.

Arteriosclerosis is not a disease sui generis. It is best viewed as a degeneration of the coats of the arteries, both large and small resulting in several different more or less distinct types.

These types blend one into the other and in the same patient all types may be found. Thus the sclerosis of the arteries is the result of a variety of causes, none of which is definitely known in the sense of a bacterial disease. As we shall see later, one type of arteriosclerosis has a special pathology and etiology, the syphilitic arterial changes.

Bearing in mind that arteriosclerosis (called by some "arteriocapillary fibrosis," by others "atherosclerosis") is not a true disease, it may, for convenience be defined as a chronic disease of the arteries and arterioles, characterized anatomically by increase or decrease of the thickness of the walls of the blood vessels, the initial lesion being a weakening of the middle layer caused by various toxic or mechanical agencies. This weakness of the media leads to secondary effects, which include hypertrophy or atrophy of the inner layer—and not infrequently hypertrophy of the outer layer—connective tissue formation and calcification in the vessels, and the formation of minute aneurysms along them. The term arteriocapillary fibrosis has a broader meaning, but is a cumbersome phrase, and conveys the idea that the capillary changes are an essential feature of the process, whereas these are for the most part secondary to the changes in the arteries. The veins do not always escape in the general morbid process, and when these are affected the whole condition is sometimes called vascular sclerosis or angiosclerosis.

Upon the anatomical structure of the arteries depends, as a rule, the character and extent of the arteriosclerotic lesions. For the clear comprehension of the process, it is necessary to keep in mind the essential histological differences between the aorta and the larger and smaller branches of the arterial tree.

The vascular system is often likened to a central pump, from which emanates a closed system of tubes, beginning with one large distributing pipe, which gives rise to a series of tubes, whose number is constantly increasing at the same time that their caliber is decreasing in size. From the smallest of these tubes, larger and larger vessels collect the flowing blood, until, at the pump, two large trunks of approximately the same area as the one large distributing trunk empty the blood into the heart, thus completing the circle. This is but a rough illustration, and, while possibly useful, takes into account none of the vital forces which are constantly controlling every part of the distributing system.

General Structure of the Arteries

The aorta and its branches are highly elastic tubes, having a smooth, glistening inner surface. When the arteries are cut open, they present a yellowish appearance, due to the large quantity of elastic tissue contained in the walls. The elasticity is practically perfect, being both longitudinal and transverse. The essential portion of any blood vessel is the endothelial tube, composed of flat cells cemented together by intercellular substance and having no stomata between the cells. This tube is reinforced in different ways by connective tissue, smooth muscle fibers, and fibroelastic tissue. Although the gradations from the larger to the smaller arteries and from these to the capillaries and veins are almost insensible, yet particular arteries present structural characters sufficiently marked to admit of histological differentiation.

The whole vascular system, including the heart, has an endothelial lining, which may constitute a distinct inner coat, the tunica intima, or may be without coverings, as in the case of the capillaries. The intima (Fig. 1) consists typically of endothelium, reinforced by a variable amount of fibroelastic tissue, in which the elastic fibers predominate. The tunica media is composed of intermingled bundles of elastic tissue, smooth muscle fibers, and some fibrous tissue. The adventitia or outer coat is exceedingly tough. It is usually thinner than the media, and is composed of fibroelastic tissue. This division into three coats is, however, somewhat arbitrary, as in the larger arteries particularly it is difficult to discover any distinct separation into layers.

The muscular layer varies from single scattered cells, in the arterioles, to bands of fibers making up the body of the vessel in the medium-sized arteries and veins.

There is elastic tissue in all but the smallest arteries, and it is also found in some veins. It varies in amount from a loose network to dense membranes. In the intima of the larger arteries the elastic tissue occurs as sheets, which under the microscope appear perforated and pitted, the so-called fenestrated membrane of Henle.

The nutrient vessels of the arteries and veins, the vasa vasorum, are present in all the vessels except those less than one millimeter in diameter. The vasa vasorum course in the external coat and send capillaries into the media, supplying the outer portion of the coat and the externa with nutritive material. The nutrition of the intima and inner portion of the media is obtained from the blood circulating through the vessel. Lymphatics and nerves are also present in the middle and outer layers of the vessels.

Arteries

The structure of the arteries varies notably, depending upon the size of the vessel. A cross section of the thoracic aorta reveals a dense network of elastic fibers, occupying practically all of the space between the single layer of endothelial cells and the loose elastic and connective tissue network of the outer layer. Smooth muscle fibers are seen in the middle coat, but, in comparison with the mass of elastic tissue, they appear to have only a limited function.

In a cross section of the radial artery one sees a wavy outline of intima, caused by the endothelium following the corrugations of the elastica. The endothelium is seen as a delicate line, in which a few nuclei are visible. The media is comparatively thick, and is composed of muscle cells, arranged in flat bundles, and plates of elastic tissue. Between the media and the externa the elastic tissue is somewhat condensed to form the external elastic membrane. The adventitia varies much in thickness, being better developed in the medium-sized than in the large arteries. It is composed of fibrous tissue mixed with elastic fibers.

"Followed toward the capillaries, the coats of the artery gradually diminish in thickness, the endothelium resting directly upon the internal elastic membrane so long as the latter persists, and afterward on the rapidly attenuating media. The elastica becomes progressively reduced until it entirely disappears from the middle coat, which then becomes a purely muscular tunic, and, before the capillary is reached, is reduced to a single layer of muscle cells. In the precapillary arterioles the muscle no longer forms a continuous layer, but is represented by groups of fiber cells that partially wrap around the vessel, and at last are replaced by isolated elements. After the disappearance of the muscle cells the blood vessel has become a true capillary. The adventitia shares in the general reduction, and gradually diminishes in thickness until, in the smallest arteries, it consists of only a few fibroelastic strands outside the muscle cells." (Piersol's Anatomy.)

The large arteries differ from those of medium size mainly in the fact that there is no sharp line of demarcation between the intima and the media. There is also much more elastic tissue distributed in firm bundles throughout the media, and there are fewer muscle fibers, giving a more compact appearance to the artery as seen in cross section. The predominance of elastic tissue permits of great distention by the blood forced into the artery at every heartbeat, the caliber of the tube being less markedly under the control of the vasomotor nerves than is the case in the small arteries, where the muscle tissue is relatively more developed. The adventitia of the large arteries is strong and firm, and is made up of interlacing fibroelastic tissue, of which some of the bundles are arranged longitudinally.

Veins

The walls of the veins are thinner than those of the arteries; they contain much less elastic and muscular tissue, and are, therefore, more flaccid and less contractile. Many veins, particularly those of the extremities, are provided with cup-like valves opening toward the heart. These valves, when closed, prevent the return of the blood to the periphery and distribute the static pressure of the blood column. The bulgings caused by the valves may be seen in the superficial veins of the arm and leg. There are no valves in the veins of the neck, where there is no necessity for such a protective mechanism, gravity sufficing to drain the venous blood from the cranial cavity.

Capillaries

These are endothelial tubes in the substance of the organs, the tissue of the organ giving them the necessary support. They are the final subdivisions of the blood vessels, and the vast capillary area offers the greatest amount of resistance to the blood flow, thus serving to slow the blood stream and allowing time for nutritive substances or waste products to pass from and to the blood. Usually the capillaries are arranged in the form of a network, the channels in any one tissue being of nearly uniform size, and the closeness of the mesh depending upon the organ.

As far back as 1865, Stricker observed contraction of the capillaries. This observation was apparently forgotten until revived again by Krogh recently. The latter finds that the capillaries are formed of cells which are arranged in strands encircling the vessel. The capillaries are rarely longer than 1 mm., and, according to Krogh, are capable of enormous dilatation.

The rate of flow through any capillary area is very inconstant, and the usual explanation has been that the capillaries were endothelial tubes the blood flow of which was dependent upon the contraction or dilatation of the terminal arterioles. The actual fact that in an observed capillary area some capillaries are empty renders the above explanation untenable. The color of a tissue depends upon the state of filling of the capillaries with blood.

It would seem that all the evidence now leads us to believe that the capillaries themselves are contractile and it is even possible that they may be under vasomotor control. If the anatomic structure as stated above, is correct, it would take but a slight contraction of the encircling cell to shut off completely the capillary. When the enormous capillary bed is considered, it is not inconceivable that circulating poisons may act on large areas and produce a true capillary resistance to the onflow of blood which might express itself, if long continued, in actual hypertrophy of the heart.