Arterio-Sclerosis is a term used to signify a thickening of the arterial wall, from whatever cause arising. It may occur in either a focal or a diffuse form.
In the focal form it is known as atheroma. This begins as a cellular infiltration of the subendothelial portion of the intima; the cells undergo fatty degeneration, and often the patch becomes infiltrated with lime salts. By the running together of several such patches the condition known as endarteritis deformans is produced.
Concerning the pathology of atheroma we know next to nothing. It was once thought to be due to the obliteration of the vasa vasorum, but Cowan has shown this view to be incorrect. One factor in its causation stands out, i.e. protracted high blood pressure. Except as a senile change it is, indeed, rarely met with in subjects displaying low blood pressure.
The diffuse form of arterio-sclerosis differs from atheroma in that it involves the entire circumference, and considerable portions of the length, of the vessel. Though it includes several distinct varieties, such as syphilitic endarteritis, the term for most physicians connotes a generalized thickening of the systemic arteries, either in consequence of a primary calcareous infiltration - some would not include this condition under the meaning of the word - or an increase in the actual tissue of the vessel wall. This increase involves essentially the muscular media. When the media only is affected we have the arterial hyper-myotrophy of Savill: in the majority of cases, however, the intima is thickened; less frequently, the adventitia.
Though we are still very ignorant of the pathology of arteriosclerosis, this much can be postulated of it: it is essentially due to the action of some poison, or poisons, circulating in the blood-plasma. These poisons may lead to vascular thickening in one of two ways : either directly, by causing irritative hyperplasia of the fibrous elements of the vessel wall, or indirectly, by inducing arterial hypertonus. This hypertonus involves the systemic arterioles chiefly, though it tends to implicate the entire systemic arterial tree, and, if long continued, necessarily leads to hypertrophy of the muscular media. In some cases the structural changes in the vessel wall would appear to stop here; generally, however, other changes ensue as the result of the vascular strain which is the inevitable outcome of the hypertonus, for it is obvious that the contraction of the minute arteries must send up the blood pressure in the arteries proximal to them. The strain will necessarily be felt chiefly by the media - one of the chief functions of which, indeed, is by its active contraction to resist the distensile effect of the blood pressure on the vessel wall - and by the intima, which in consequence of the pressure to which it is subjected not only thickens but tends to undergo atheromatous degeneration. The adventitia, on the other hand, protected as it usually is from the distensile pressure of the blood by the actively contracting media, may remain for the most part unchanged, even with long-continued hypertonus. It has to be remembered, however, that systemic hypertonus is rarely, if ever, quite general,1 and that when, with a widespread systemic hypertonus, certain of the arteries remain comparatively relaxed, the adventitia of those arteries will, owing to the heightened blood pressure, be subjected to considerable stretching of a rhythmic character, and will tend in consequence to undergo fibrous hyperplasia.
1 It is noteworthy that in the cases of diffuse arterio-sclerosis examined by William Russell, the muscular coat of the intra-renal arteries showed evidence of atrophy. From this we may conclude that these vessels do not share in the generalized arterial hypertonus so frequently met with in this condition, but remain, on the contrary, dilated. Such an arrangement secures a maximum supply of blood to the kidneys, for with the augmented systemic blood pressure there is diminished vascular resistance in the kidneys which, being thus abundantly flushed with blood, are so much the better able to eliminate the poisons the presence of which in the blood is the fons et origo of the arterial phenomenon under consideration. We have here, in fact, the raison d'etre of the hypertonus and high blood pressure met with in arterio-sclerosis.
While insisting on this factor of strain in the production of intimal and adventitial thickening, we are not, of course, overlooking the direct irritative effect on the vessel wall of morbid blood-plasma. That this may be an important factor in the etiology of arterio-sclerosis is abundantly shown by the fact that it is possible to get a widespread arterial thickening in subjects of comparatively low blood pressure. That, however, profound changes in the vessel wall necessarily result from the strain of long-continued high blood pressure is certain, and this, it need scarcely be said, is a fact of great therapeutic importance : practically speaking, there is but one cause of supernormal blood-pressure, namely, arteriolar hypertonus, and again but one cause of sustained hypertonus, namely, some plasmic defect. Wherefore it is manifest that in cases of arterial thickening, whether occurring in connexion with hypertonus or independently of it, our aim is to correct the morbid condition of the plasma which is responsible for the thickening.
In each class of case the dietetic indications are the same, but it is easier to test the efficacy of our treatment when hypertonus is present than when it is absent, seeing that our success in the former case is in direct proportion to the degree to which we can reduce the hypertonus, and this, happily, we now have ample means of gauging.
While there is no doubt that arterio-sclerosis is essentially due to a morbid blood state, we have still much to learn regarding the exact plasmic defects capable of producing it. Two classes of defect, however, stand out prominently in this connexion - those which occur in association with chronic renal disease and those which result from dietetic errors. It is because the constitution of the blood-plasma, and through it the condition of the blood-vessels, can be profoundly influenced by regulating the diet, that the dietetic treatment of arterio-sclerosis is of prime importance.