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The pathology of arteriosclerosis.


According to Warfield, "Arteriosclerosis may 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 and mechanical agencies."

Before discussing the structure of the lesions we will consider the etiology. To begin with, two broad divisions of arteriosclerosis may be made: The first is the congenital form, so-called, or that which results from inherited tendency. This is based upon the theory that some people are not endowed with as good arterial tissue with which to begin life as they should have, on account of the constitutional diseases or habits of their ancestors. Consequently unless they escape the etiological factors of acquired arteriosclerosis they show sclerotic changes at a very early age. But if the tendency were known by guarding their living they might postpone the process for some time.

The second class is the acquired form, and it is, in fact, generally the only one we consider. The main factors in the etiology of this form is the triad: Tension, toxins and time. Probably as far as we now know in the order named. Hypertension is now believed to hold first place, although some seem inclined to place toxins first. But hypertension seems to be a cause rather than a result of arteriosclerosis. Among the etiological factors may be mentioned age. As time passes on the integrity of the arterial tissue seems to wane, but other things being equal probably the better the arterial tissue in the beginning the longer it resists these time elements.

Sex: The males seem far more prone to arterial disease than women.

Race: The Negro seems to be the victim more frequently than his white brother.

Occupation: The fact is that any occupation which requires either absorption of toxic substances, or prolonged muscular labor will hasten markedly the onset of arterial disease.

Infectious diseases, on account of the circulating toxins, seem to have a marked effect according to the length of time that they have acted. Other causes that may be mentioned are: Syphilis, chronic drug intoxications, over-eating, mental strain, muscular overwork and renal disease.

Having considered the main causes briefly, we will now turn to the pathological anatomy. The order of frequency in which arteries are affected is probably as follows: Aorta, splenic, femoral, iliac, coronary arteries of the heart, arteries of the brain, uterine, subclavian, brachial, ulnar and radial arteries.

The whole subject of the pathology of arteriosclerosis has been much enriched by the practical application of blood pressure instruments clinically upon man and study of experimental lesions produced by drugs and micro-organisms upon the aortas of rabbits. Simple atheroma, which shows small whitish plaques on the retina due to fatty degeneration, must not be confused with the lesions of arteriosclerosis, as they have no significance, except the danger of clot formation upon the eroded surface.

It is customary to differentiate three types of arteriosclerosis, namely, (1) nodular; (2) diffuse; (3) senile; but this is not a classification of distinct types, as they often exist in various grades in the same individual. It is better, perhaps, to separate the three groups into (1) nodular; (2) diffuse or senile; and (3) syphilitic.

In the nodular form the lesions are found on the aorta and large branches, particularly at or near the orifices of branching vessels. These nodules may increase in size forming large, slightly raised plaques of yellowish white color. The initial lesion is in the media, consisting of an actual dissolution of this coat with rupture of the elastic fibers and infiltration with small round cells. There is thus a weak spot in the artery and, layer upon layer of intimal cells form over the injured place in an attempt to strengthen it, and at the same time there is a thickening of the connective tissue of the adventitia. The blood supply to the inner portion of the media comes from the blood stream itself, and as the intimal growth takes place the blood supply is cut off and this leads to softening in these places. These may rupture, leaving ulcerated places, or calcification may take place. The changes in the intima constitute the effort on the part of nature to repair a defect in the vessel wall which is to compensate for the weakened media and the widened lumen.

Two processes may take place due to hypertension: First, a dilatation and thinning of the arterial walls; second, a thickening and intimal hypertrophy. If the strain is pronounced there is dilatation. If only moderate, there is thickening of the walls, diverse manifestations of a common cause.

In the diffuse or senile type the aorta may appear smooth, but it is markedly dilated, particularly the thoracic portion which is elongated, as evidenced by its slight tortuosity, and it has lost the greater part of its elasticity. Associated with such changes in the aorta and its larger branches is marked sclerosis of the smaller arteries. Intimal fibrosis is common, together with hypertrophy and fibrosis of the middle coat, with sometimes, periarterial thickening. Calcification of the media is found and is preceded by hypertrophy of the media. In the radial artery the media, as usual, is affected first. The muscle cells undergo degeneration, and either marked thickening takes place or sacculation results, depending upon the severity of the exciting cause. Calcification of the media is common. This occasionally takes the form of rings encircling the vessel, because of the alternation in this artery of the circular muscle bundles with the circular yellow elastic fibers. This gives to the examining finger the sensation of feeling a string of fine beads. If calcification does not take place the vessel may become tortuous in character, due the loss of its elasticity.

The syphilitic form seems to have its seat of election in the aorta, just above the aortic valves, and in the ascending portion of the arch. There are semi-translucent, hyaline-like plaques which have a tendency to form in groups, and instead of undergoing an atheromatous change, as in the ordinary nodular form, they are prone to scar formation and puckering, so that microscopically the nature of the process may, as a rule, be readily diagnosed. Microscopically, the process is found to be a subacute inflammation of the media. There is marked round cell infiltration around some of the branches of the vasa vasorum and absorption of the tissue elements of the middle coat. This is accompanied by hypertrophy of the intimal tissue, and there follows a degeneration of the deeper portions of this new tissue and new capillaries are formed, which have their origin in the inflammatory area in the media. This granulation tissue in the process of healing contracts and forms the characteristic scars on the aorta. When the process is more acute, actual destruction instead of reparative processes takes place, resulting in aneurysmal dilatation at the weakened spot. Spirochete pallidae have been found in the degenerated media and in small gummata, which were situated beneath the intima. A large percentage of patients with cardio-vascular disease give the Wassermann reaction. In cases of aortic insufficiency the reaction is said to be present in almost every case. Obliterating endarteritis may occur in such organs as the kidney, liver, spleen and intestines. This generally occurs in the smaller arteries, and is an irregular thickening, with deposits of lime salts in the walls. Occasionally such an obliterating process takes place in a larger artery and a thrombus forms, but by a process of central softening new channels permeate the thrombus and the function of the vessel is restored to some extent.


DR. A. S. TUCHLER: I would like to take issue with the statement the doctor makes as to the cause. It was always my idea, and we have been taught that it is the sedentary habits that lead to hypertension, while the doctor's paper, as I understand it, says those who are accustomed to severe muscular labor are sufferers from that condition. I have observed that the ordinary working man that works hard, whether a boiler maker, a machinist, or what not, can eat three times a day and drink his beer and whiskey and indulge in food without any danger to himself. He needs an abundance of proteids to give him energy to do his work. But let us of sedentary habits indulge in that and hypertension will be pronounced in a short time. Therefore, that is an important feature that I do not like to see passed by without bringing out that particular point.

DR. SAXTON: Perhaps I have as great opportunity for observing conditions among the laboring class of the far South as any of you. They are almost entirely of the laboring class, and yet I find a great many cases of arteriosclerosis. So it is not clear, in my mind, that sedentary habits or working habits are really the cause of arteriosclerosis. So far as the real condition that brings about arteriosclerosis, I think it is easier for us to treat the condition when it exists than to get a good clear idea of the cause. I do not know, but I will have to say as I did yesterday, "We don't know nothin' and we don't know that."

DR. COX: I think that the doctor who has just spoken is correct, that we don't know nothin, but there is a good deal of work being done on this line, and the drift seems to be toward the idea that hypertension is the cause and not the result. A man might work hard and not be under the strain that would cause hypertension. There are so many factors that enter into blood pressure that relative blood pressure has very little effect. It is the continued blood pressure that makes the difference.

National Eclectic Medical Association Quarterly, Vol. 7, 1915-16, was edited by William Nelson Mundy, M.D.

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