Disturbances of the Heart / Discussion of the Treatment of the Heart in Its Various Disorders, With a Chapter on Blood Pressure

by Oliver T. Osborne

Hypertension is generally a prelude to arteriosclerosis, and everything which tends to increase tension promotes the disease; everything which tends to diminish tension more or less inhibits the disease. Therefore a subsecretion of the thyroid predisposes to arteriosclerosis, and increased secretion of the suprarenals predisposes to arteriosclerosis, the thyroid furnishing vasodilator substance and the suprarenals vasopressor substance to the blood. Furthermore. if these secretions are abnormal, protein metabolism is more or less disturbed.

While arteriosclerosis often occurs coincidently with gout, and gout apparently may be a cause of arteriosclerosis, still the two diseases are widely dissociated, and the causes are not the same.

Although the arterial pressure has been high before arteriosclerosis developed, and may remain high for some time in the arteries, unless the heart fails, the distal peripheral pressure, as in the fingers and toes, may be poor in spite of the high blood pressure. When the left heart begins to fail, pendent edema readily occurs.

PATHOLOGY

The pathology of arteriosclerosis is a thickening and diminishing elasticity of the arteries, beginning with the inner coat and gradually spreading and involving all the coats, the larger arteries often developing calcareous deposits or thickened cartilaginous plates—an atheroma. If the thickening of the walls of the smaller vessels advances, their caliber is diminished, and there may even be complete obstruction (endarteritis obliterans). On the other hand, some arteries, especially if the calcareous deposits are considerable, may become weakened in spots and dilation may occur, causing either smaller or larger aneurysms.

Histologically the disease is a connective tissue formation beginning first as a round-cell infiltration in the subendothelial layer of the intima. This process does not advance homogeneously; one side of an artery may be more affected than the other, and the lumen may be narrowed at one side and not at the other, allowing the artery to expand irregularly from the force of the heart beat. As the disease continues, the internal elastic layer is lost, the muscular coat begins to atrophy, and then small calcareous granules may begin to be deposited, which may form into plates. In the large arteries, the advance of the process differs somewhat. There may be more actual inflammatory signs, fatty degeneration may occur, and even a necrosis may take place.

However generally distributed arteriosclerosis is, in some regions the disease is more advanced than in others, and in those regions the most serious symptoms will occur. The regions which can stand the disease least well are the brain and coronary arteries, and next perhaps the legs, at the distal parts at least, where the circulation is always at a disadvantage if the patient is up and about.

SYMPTOMS

The symptoms are increased tension, which means, sooner or later, hypertrophy of the left ventricle and an accentuated closure of the aortic valve. This alone means more and more tendency to aortic irritation and aortic valve irritation, with inflammation, and later deposits of calcareous material, perhaps with stiffening of the aortic valve and narrowing, aortic stenosis being the result. If such a patient with the disease advanced to this stage must overwork, or sustains any severe muscle strain, an aneurysm of the aorta may occur. In the meantime, with the advancing degeneration of the cerebral arteries, some sudden cerebral congestion, caused by leaning over, lifting, vomiting or hard coughing, may rupture a cerebral vessel, and all the symptoms of apoplexy are present. If small hemorrhages occur in the arterioles of the extremities, of course the prognosis is not serious. Sometimes some of the smaller vessels of the brain may become obstructed and cerebral degeneration occur. If distal vessels become obstructed, as of the toes or feet, gangrene takes place unless the obstruction occurs at a place where the collateral circulation could save the part from such a death. These are some of the ultimate results of serious and final arteriosclerosis. The more frequent result, when the disease has not advanced so far, is a failing heart, either from degenerative myocarditis, coronary sclerosis or dilatation, with all the symptoms of coronary sclerosis and angina pectoris, or with the symptoms of failing circulation.

With high blood pressure to the point of beginning endarteritis, a gradually increasing force of the apex beat occurs, the aortic closure is accentuated as just described, the pulse is slow, the tensity of the arteries depends on the stage of the disease, and when the disease is actually present, the palpable arteries do not collapse on pressure. They soon lose their elasticity, and if this occurs in parts which are soft and flexible, the arteries become more or less tortuous by the force of the blood current twisting and bending them, owing to the irregularity of their hardening. The extremities readily become numb, or the part "goes to sleep," as it is termed. This occurs frequently at night. Sooner or later some edema of the feet and legs occurs in the latter part of the day. Sometimes abdominal colic attacks occur, caused by disturbed circulation. Various disturbances of metabolism may occur, depending on the circulation in the different organs or on coincident disease, and the liver, pancreas and kidneys may be affected.