CHAPTER XIV

AORTIC STENOSIS

Pathogenesis-Morbid Anatomy-Effects on the Heart and Circulation-Compen. sation: its duration and failure-Symptoms-Complications-Mode of Termi. nation-Physical Signs-Diagnosis-Estimation of degree of Stenosis.

ETIOLOGICAL PATHOLOGY

AORTIC stenosis arises under precisely the same pathological conditions as aortic incompetence. The chief causes, therefore, of aortic stenosis are: (1) endocarditis due to rheumatism, the zymotic fevers, syphilis, etc.; (2) endocarditis due to prolonged muscular strain; (3) atheroma which may attack the aortic valve primarily, or, as most commonly happens, by extension from the aorta.

Aortic stenosis is occasionally observed as a congenital malformation.

The morbid changes lead to thickening, rigidity, and retraction of the semilunar cusps, with more or less induration and constriction of the fibrous aortic ring.

The segments of the valve sometimes become adherent to one another, and thus diminish the size of the orifice, or they may be the seat of abundant vegetations, which obstruct the passage of blood through the opening.

Atheromatous disease of the valve sometimes leads to more or less complete calcification of the semilunar cusps and basal ring. The cusps of the valve are consequently unable to fall back completely during the ventricular systole, so that a variable degree of obstruction is produced at the aortic opening.

In a very large proportion of cases aortic stenosis is combined with incompetence of the valve, owing to the inability of the thickened and rigid segments to adequately close the narrowed orifice.

Indeed, pure aortic obstruction is one of the rarest of cardiac lesions, but it will be convenient to include in this description those forms of aortic disease in which stenosis is the predominant feature.

PATHOLOGICAL RESULTS

Effects on the Heart and Circulation

The effect of aortic stenosis is to interfere with the passage of blood from the left ventricle into the aorta during systole.

The difficulty experienced by the left ventricle in the expulsion of its contents calls for an increased display of force, which, under favourable circumstances, leads to hypertrophy of its walls. If, by this means, the volume of blood propelled into the aorta during each systole does not fall below the normal, compensation is established. It will therefore appear that in aortic stenosis compensation depends solely on hypertrophy of the left ventricle.

If the constriction of the opening is attended by incompetence of the valve, a variable degree of dilatation of the left ventricle is also produced, for the reasons which were given in the previous chapter.

Uncomplicated aortic stenosis may endure for many years without giving rise to any appreciable disturbance of the circulation; indeed, it sometimes happens that the lesion is not discovered until after death from other causes.

Compensation is maintained longer in aortic stenosis than in any other form of valvular disease, but in the absence of a definite exciting cause failure of the heart is rarely recovered from.

The breakdown of compensation usually depends on progressive constriction of the aortic orifice, or on interference with the blood supply to the heart through the coronary arteries, or on the occurrence of a complication.

The left ventricle becomes unable to completely empty itself at each systole, and consequently undergoes dilatation from incomplete emptying, i.e. from failure.

A variable degree of arterial anæmia ensues, and the dilatation of the left ventricle, if continued, leads to muscular and relative incompetence of the mitral valve, followed by pulmonic engorgement, dilatation of the right heart, general venous congestion, and dropsy.

The occurrence of mitral regurgitation in the course of aortic stenosis may depend also on chronic forcing of the mitral valve by the high pressure which prevails in the left ventricle, or on concomitant structural disease at the mitral orifice.

SYMPTOMS

So long as compensation is good, the subjects of aortic stenosis remain free from symptoms until the degree of narrowing becomes sufficiently great to seriously interfere with the supply of blood to the aorta and systemic vessels. The patient then begins to suffer from headache, giddiness, syncopal attacks, and other symptoms of disordered cerebral circulation.

Anæmia is developed, and the defective supply of blood to the systemic arteries leads to interference with nutrition and coldness of the extremities associated with general nervous and muscular debility. As compensation begins to fail, dyspnoea, palpitation, pain, which may have anginal characters, and other symptoms of cardiac insufficiency make their appearance.

The dilatation of the left ventricle which accompanies failure of compensation is attended by regurgitation through the mitral orifice, together with the signs and symptoms of pulmonic and systemic venous congestion.

As a rule death takes place slowly from gradual failure of the ventricles. A sudden termination is sometimes observed as the result of syncope, embolism, or the rupture of a cerebral vessel.

The complications of aortic stenosis do not require special consideration, since they resemble, for the most part, those described in connection with aortic incompetence.

PHYSICAL SIGNS

Physiognomy. The appearance presented by the subjects of aortic stenosis is in no way characteristic until the disease has made considerable progress, when the signs of anæmia are gradually developed. The complexion then acquires the sallow or greyishwhite hue described under aortic regurgitation, and the skin and mucous membranes become pallid.

A bluish tinge affecting the lips, cheeks, and extremities, etc., may be noticed after failure of the left ventricle has occurred, and is due to insufficient aëration of the blood following leakage through the mitral valve and the consequent production of pulmonic congestion.

Pulse. So long as compensation is maintained the pulse is slow and regular both in force and frequency. The artery is small and can be felt between the beats, but, as a rule, is easily compressible.

The pulse wave is small, long, and well sustained; it rises gradually and falls slowly.

Both the anacrotic and the bisferiens pulse may be found in association with aortic stenosis, but it cannot be said that either pulse is pathognomonic of this lesion.

The exact significance of these pulses has not yet been fully worked out, but, speaking generally, the indication in either event is organic disease at the orifice or along the course of the aorta.

HEART

Inspection.-Bulging of the præcordial region is not uncommon. The apex beat is displaced downwards and slightly outwards.

Palpation. The impulse of the left ventricle conveys to the hand the impression of a slow, deliberate, forcible thrust. A thrill, systolic in time, is sometimes palpable over the base of the heart.

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Percussion. The area of cardiac dulness is increased chiefly downwards and to the left, and corresponds with the enlargement of the left ventricle.

Auscultation. At the base of the heart, over the aortic cartilage, the first sound is accompanied, or more or less replaced, by a loud, rough, and rasping murmur, which is conducted upwards along the right sternal edge into the neck. The murmur is usually audible over the upper portion of the thorax and along the course of both carotid arteries. It can frequently be heard at the apex, and occasionally over the whole præcordium.

The murmur usually has the characters above indicated, but in some instances it is soft and blowing, in others musical.

As a rule the bruit occupies the whole of the interval between the commencement of the first sound and the occurrence of the second sound. The second sound over the aortic cartilage is commonly muffled and indistinct, and is sometimes more or less replaced by a diastolic murmur.

The first sound at the apex is usually dull and ill defined, and may be accompanied by a systolic bruit of mitral origin.

The establishment of mitral regurgitation, which, as already explained, takes place sooner or later in the course of aortic stenosis, is followed by the signs and symptoms of pulmonic engorgement, portal and systemic venous congestion, and dropsy.

The occurrence of this train of events in association with aortic stenosis, in the absence of a definite existing cause, indicates failure of the left ventricle and the breakdown of compensation, and is usually of the worst possible augury.

DIAGNOSIS

In the diagnosis of aortic stenosis much more importance attaches to the character of the pulse and to the changes in the left ventricle than to the presence of a systolic murmur in the aortic area, inasmuch as the latter sign may be observed in various other conditions, chief among which are rigidity, roughening, or fenestration of one or more of the cusps of the aortic valve, dilatation or aneurism of the aorta, anæmia, and acute or sub-acute aortitis.

A systolic basic murmur, due to the roughening and rigidity of the aortic cusps, that is caused by atheroma is almost certainly accompanied by accentuation of the second sound, and is therefore not likely to be mistaken for the bruit of aortic stenosis. Again, fenestration of an aortic cusp, or a shred of fibrin hanging from some portion of the valve, would not give rise to any modification of the pulse, or to enlargement of the left ventricle.

In dilatation of the aorta the volume of the pulse is larger than in aortic stenosis. Moreover, the presence of pulsation and dulness in the intercostal spaces to the right of the sternum above the level of the third or second rib, together with the well-marked and charac

teristic accentuation of the second sound, which is invariably observed in aortic dilatation so long as the aortic valve is competent, would suffice for the recognition of the lesion.

The presence of pressure signs would establish the diagnosis of aortic aneurism.

The systolic aortic murmur due to anæmia is soft and blowing in character, and does not substitute itself for the first sound, as in aortic stenosis. Moreover, the murmur in the aortic area is usually, if not always, preceded and accompanied by a venous hum in the neck and a systolic bruit in the pulmonic area. Furthermore, the age and general condition of the patient, together with the absence of the signs of cardiac hypertrophy, or of any special modification in the volume of the pulse, renders the differential diagnosis between anæmia and aortic obstruction comparatively easy.

The determination of the nature of the lesion producing aortic stenosis depends on the age, sex, and history of the patient, and on the condition of the peripheral vessels. The cardiac physical signs do not, as a rule, afford much information in this respect, though Constantin Paul considers that the systolic bruit of aortic obstruction due to atheroma tends to spread laterally rather than vertically. If the obstruction at the aortic opening caused by atheroma is due merely to rigidity of the segments of the valve, the second sound is usually accentuated.

The appearance of an aortic systolic murmur accompanied by irregular pyrexia, retrosternal pain and rapid cardiac failure would be strongly suggestive of aortitis.

ESTIMATION OF THE DEGREE OF NARROWING

IN AORTIC STENOSIS

The degree of constriction in aortic stenosis is determined by means of the character of the pulse, and the extent of the hypertrophy of the left ventricle.

1. The pulse.—A moderate degree of arterial constriction with a pulse of fair size is compatible with an inconsiderable amount of narrowing at the aortic orifice. This inference is strengthened if it is found that a sudden additional strain thrown on the heart leads merely to increased force and frequency of the pulse.

On the other hand, a small vessel with great diminution in the volume of the pulse is indicative of severe aortic obstruction.

2. The degree of hypertrophy of the left ventricle.-So long as compensation is maintained, the extent of the ventricular hypertrophy is a measure of the degree of stenosis which obtains. Nevertheless it cannot be too strongly insisted upon that the indications afforded by the pulse altogether outweigh the evidence supplied by the condition of the left ventricle in estimating the degree of narrowing in cases of aortic stenosis.